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ESP: PubMed Auto Bibliography 19 Jul 2026 at 01:53 Created:
Microbiome
It has long been known that every multicellular organism coexists with large prokaryotic ecosystems — microbiomes — that completely cover its surfaces, external and internal. Recent studies have shown that these associated microbiomes are not mere contamination, but instead have profound effects upon the function and fitness of the multicellular organism. We now know that all MCEs are actually functional composites, holobionts, composed of more prokaryotic cells than eukaryotic cells and expressing more prokaryotic genes than eukaryotic genes. A full understanding of the biology of "individual" eukaryotes will now depend on an understanding of their associated microbiomes.
Created with PubMed® Query: microbiome[tiab] NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2026-07-17
Human salivary microbiome as a potential non-invasive biomarker for early-onset colorectal cancer screening: a prospective study.
BMC microbiology pii:10.1186/s12866-026-05397-7 [Epub ahead of print].
BACKGROUND: The incidence of early-onset colorectal cancer (EOCRC) has been increasing in recent years, the carcinogenesis of which has been linked to oral microbiota alterations. However, it is unknown if the salivary microbiome could help detect EOCRC. Therefore, we aimed to determine whether salivary microbiome profiles can distinguish patients with EOCRC from healthy individuals and to evaluate their diagnostic performance as a non-invasive screening tool.
METHODS: We collected saliva samples from 65 EOCRC patients and 63 control individuals, the microbiota of which was assessed using high-throughput 16S ribosomal RNA gene V3-V4 region sequencing. We then profiled the saliva microbiota and developed EOCRC screening models using machine learning (ML) algorithms.
RESULTS: The alpha diversity was comparable between salivary microbiomes of the EOCRC patients and control individuals, while the beta diversity exhibited statistical difference between two groups. A differential analysis of the genus-level saliva microbial communities revealed that, in the EOCRC patients, Prevotella, Actinomyces, and Corynebacterium were more abundant, whereas Fusobacterium, Haemophilus, norank_o__Absconditabacteriales_SR1, norank_c__Gracilibacteria, Peptococcus, Eikenella, and Eubacterium_yurii_group were less abundant. Furthermore, in developing the EOCRC screening model based on the salivary microbiome, the neural network model showed the best performance, achieving an AUC of 0.780 and a recall of 0.929, showing potential for distinguishing EOCRC patients from control individuals in this cohort.
CONCLUSIONS: This study first highlights the potential dysbiosis of salivary microbiota in EOCRC patients and suggests that salivary microbiome-based biomarkers may serve as potential non-invasive tools for EOCRC screening. Additional research with larger sample sizes would help to further validate these findings.
TRIAL REGISTRATION: This study was registered with the Chinese Clinical Trial Registry (registration number: ChiCTR2400087634) on July 31, 2024, retrospectively registered.
Additional Links: PMID-42469627
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PubMed:
Citation:
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@article {pmid42469627,
year = {2026},
author = {Zhen, J and Dong, M and Li, Y and Cao, B and Liao, F and Lin, D and Zhang, J and Liu, C and Zheng, X and Dong, W},
title = {Human salivary microbiome as a potential non-invasive biomarker for early-onset colorectal cancer screening: a prospective study.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05397-7},
pmid = {42469627},
issn = {1471-2180},
support = {82170549//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: The incidence of early-onset colorectal cancer (EOCRC) has been increasing in recent years, the carcinogenesis of which has been linked to oral microbiota alterations. However, it is unknown if the salivary microbiome could help detect EOCRC. Therefore, we aimed to determine whether salivary microbiome profiles can distinguish patients with EOCRC from healthy individuals and to evaluate their diagnostic performance as a non-invasive screening tool.
METHODS: We collected saliva samples from 65 EOCRC patients and 63 control individuals, the microbiota of which was assessed using high-throughput 16S ribosomal RNA gene V3-V4 region sequencing. We then profiled the saliva microbiota and developed EOCRC screening models using machine learning (ML) algorithms.
RESULTS: The alpha diversity was comparable between salivary microbiomes of the EOCRC patients and control individuals, while the beta diversity exhibited statistical difference between two groups. A differential analysis of the genus-level saliva microbial communities revealed that, in the EOCRC patients, Prevotella, Actinomyces, and Corynebacterium were more abundant, whereas Fusobacterium, Haemophilus, norank_o__Absconditabacteriales_SR1, norank_c__Gracilibacteria, Peptococcus, Eikenella, and Eubacterium_yurii_group were less abundant. Furthermore, in developing the EOCRC screening model based on the salivary microbiome, the neural network model showed the best performance, achieving an AUC of 0.780 and a recall of 0.929, showing potential for distinguishing EOCRC patients from control individuals in this cohort.
CONCLUSIONS: This study first highlights the potential dysbiosis of salivary microbiota in EOCRC patients and suggests that salivary microbiome-based biomarkers may serve as potential non-invasive tools for EOCRC screening. Additional research with larger sample sizes would help to further validate these findings.
TRIAL REGISTRATION: This study was registered with the Chinese Clinical Trial Registry (registration number: ChiCTR2400087634) on July 31, 2024, retrospectively registered.},
}
RevDate: 2026-07-17
Correction: Altered microbial cargo in fecal microbiome-derived outer membrane vesicles as novel biomarkers for vascular dementia.
BMC microbiology, 26(1):.
Additional Links: PMID-42469646
PubMed:
Citation:
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@article {pmid42469646,
year = {2026},
author = {Li, X and Wei, W and Wei, S and Xu, W and Mo, L and Wang, J and Zhu, H and Liu, Z and Jin, F},
title = {Correction: Altered microbial cargo in fecal microbiome-derived outer membrane vesicles as novel biomarkers for vascular dementia.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {},
pmid = {42469646},
issn = {1471-2180},
}
RevDate: 2026-07-17
Metabolome-microbiome convergence under circadian disruption accelerates mammary tumorigenesis: multi-omics integration insights.
BMC cancer pii:10.1186/s12885-026-16546-6 [Epub ahead of print].
Circadian rhythm disruption (CRD), common in shift work and jet lag, promotes mammary tumorigenesis through coordinated reprogramming of tumor metabolism and the local microbiome. CRD increased immunosuppressive metabolites - kynurenic acid, spermidine, and argininosuccinic acid - that suppressed effector T-cell activity and drove macrophage polarization toward anti-inflammatory phenotypes. 16S rRNA sequencing revealed enrichment of immune-modulatory Firmicutes and Bacilli within CRD tumors. Experimental and multi-omics integrative analyses strongly support metabolome-microbiome crosstalk driving immune suppression under CRD. Inhibition of arginase-1 (ARG1) with nor-NOHA restored cytotoxic T-cell responses and reduced lung metastases. These findings establish metabolome-microbiome interactions as a central mechanism of CRD-induced immunosuppression and metastasis, revealing potential therapeutic targets for circadian disruption-associated breast cancer.
Additional Links: PMID-42469677
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PubMed:
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@article {pmid42469677,
year = {2026},
author = {Sarkar, M and Ogunlusi, O and Stewart, T and Muller, E and Seeley, EH and Sarkar, TR},
title = {Metabolome-microbiome convergence under circadian disruption accelerates mammary tumorigenesis: multi-omics integration insights.},
journal = {BMC cancer},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12885-026-16546-6},
pmid = {42469677},
issn = {1471-2407},
abstract = {Circadian rhythm disruption (CRD), common in shift work and jet lag, promotes mammary tumorigenesis through coordinated reprogramming of tumor metabolism and the local microbiome. CRD increased immunosuppressive metabolites - kynurenic acid, spermidine, and argininosuccinic acid - that suppressed effector T-cell activity and drove macrophage polarization toward anti-inflammatory phenotypes. 16S rRNA sequencing revealed enrichment of immune-modulatory Firmicutes and Bacilli within CRD tumors. Experimental and multi-omics integrative analyses strongly support metabolome-microbiome crosstalk driving immune suppression under CRD. Inhibition of arginase-1 (ARG1) with nor-NOHA restored cytotoxic T-cell responses and reduced lung metastases. These findings establish metabolome-microbiome interactions as a central mechanism of CRD-induced immunosuppression and metastasis, revealing potential therapeutic targets for circadian disruption-associated breast cancer.},
}
RevDate: 2026-07-17
Laminaria extract reshapes the gut microbiota and TCA cycle-centered metabolic profiles associated with immune modulation in Hu lambs.
BMC veterinary research pii:10.1186/s12917-026-05742-y [Epub ahead of print].
BACKGROUND: The global push to restrict antibiotic use in livestock has intensified the need for effective, safe feed additives, particularly for young lambs, which are highly susceptible to post-weaning diarrhea and immune dysfunction due to an underdeveloped intestinal barrier. Laminaria extract, rich in bioactive polysaccharides, has emerged as a promising candidate; however, its functional mechanisms in ruminants remain poorly understood. This study therefore investigated the effects of dietary Laminaria extract supplementation on growth performance, immune parameters, gut microbiota, and fecal metabolomic profiles in lambs.
METHODS: Lambs were randomly assigned to five groups: a basal control (CON), three Laminaria extract doses (LL, 1 g/kg; LM, 3 g/kg; LH, 6 g/kg), and a diclazuril positive control (DIC). Growth performance was evaluated via body weight and average daily gain (ADG). Serum immune cytokines were measured by ELISA, gut microbiota via 16S rRNA sequencing, and fecal metabolomics by UPLC-MS, followed by integrative correlation and pathway analyses.
RESULTS: Dietary Laminaria supplementation improved growth performance and immune markers in a dose-dependent manner, with the high-dose (6 g/kg) group exhibiting the most pronounced effects. Specifically, the high-dose group showed a 217.47% increase in ADG compared with the CON group (p < 0.05). Microbiome analysis revealed a selective enrichment of beneficial genera, particularly Prevotella and Muribaculum, in the supplemented groups, with the highest relative abundances observed at the 6 g/kg dosage. Furthermore, untargeted metabolomics revealed that the high-dose group exhibited the most substantial upregulation in the relative abundances of tricarboxylic acid (TCA) cycle intermediates, with citrate and α-ketoglutarate showing 2.93-fold and 2.95-fold increases in peak intensity, respectively (p < 0.05). Concurrently, elevated relative signal intensities of short-chain fatty acids (SCFAs) were detected in the high-dose group, further supporting the metabolic benefits of Laminaria supplementation.
CONCLUSION: This study confirmed that 3-6 g/kg dietary Laminaria extract improves growth and immunity of Hu lambs by enriching Prevotella and Muribaculum, activating TCA cycle metabolism. Low dosage prioritized antioxidant improvement, while high dosage exerted superior growth-promoting effects, supporting Laminaria extract as a natural antibiotic alternative for lambs.
Additional Links: PMID-42469845
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PubMed:
Citation:
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@article {pmid42469845,
year = {2026},
author = {Lin, M and Li, J and Chen, J and Zhen, A and Wajiha, W and Li, S and Li, X and Zhang, S and Tan, S and Zhao, J and Jian, F},
title = {Laminaria extract reshapes the gut microbiota and TCA cycle-centered metabolic profiles associated with immune modulation in Hu lambs.},
journal = {BMC veterinary research},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12917-026-05742-y},
pmid = {42469845},
issn = {1746-6148},
support = {No. 2023YFD1801200//National Key Research and Development Program of China/ ; No. CARS-38//the China Agriculture (Sheep and Goats) Research System/ ; },
abstract = {BACKGROUND: The global push to restrict antibiotic use in livestock has intensified the need for effective, safe feed additives, particularly for young lambs, which are highly susceptible to post-weaning diarrhea and immune dysfunction due to an underdeveloped intestinal barrier. Laminaria extract, rich in bioactive polysaccharides, has emerged as a promising candidate; however, its functional mechanisms in ruminants remain poorly understood. This study therefore investigated the effects of dietary Laminaria extract supplementation on growth performance, immune parameters, gut microbiota, and fecal metabolomic profiles in lambs.
METHODS: Lambs were randomly assigned to five groups: a basal control (CON), three Laminaria extract doses (LL, 1 g/kg; LM, 3 g/kg; LH, 6 g/kg), and a diclazuril positive control (DIC). Growth performance was evaluated via body weight and average daily gain (ADG). Serum immune cytokines were measured by ELISA, gut microbiota via 16S rRNA sequencing, and fecal metabolomics by UPLC-MS, followed by integrative correlation and pathway analyses.
RESULTS: Dietary Laminaria supplementation improved growth performance and immune markers in a dose-dependent manner, with the high-dose (6 g/kg) group exhibiting the most pronounced effects. Specifically, the high-dose group showed a 217.47% increase in ADG compared with the CON group (p < 0.05). Microbiome analysis revealed a selective enrichment of beneficial genera, particularly Prevotella and Muribaculum, in the supplemented groups, with the highest relative abundances observed at the 6 g/kg dosage. Furthermore, untargeted metabolomics revealed that the high-dose group exhibited the most substantial upregulation in the relative abundances of tricarboxylic acid (TCA) cycle intermediates, with citrate and α-ketoglutarate showing 2.93-fold and 2.95-fold increases in peak intensity, respectively (p < 0.05). Concurrently, elevated relative signal intensities of short-chain fatty acids (SCFAs) were detected in the high-dose group, further supporting the metabolic benefits of Laminaria supplementation.
CONCLUSION: This study confirmed that 3-6 g/kg dietary Laminaria extract improves growth and immunity of Hu lambs by enriching Prevotella and Muribaculum, activating TCA cycle metabolism. Low dosage prioritized antioxidant improvement, while high dosage exerted superior growth-promoting effects, supporting Laminaria extract as a natural antibiotic alternative for lambs.},
}
RevDate: 2026-07-18
Coffee as a polypharmacological modulator of mitochondrial health: from molecular mechanisms to translational implications.
Journal of translational medicine pii:10.1186/s12967-026-08662-5 [Epub ahead of print].
BACKGROUND: Coffee is one of the most widely consumed beverages worldwide, yet its biological effects have often been attributed primarily to caffeine. Emerging evidence suggests that coffee contains a complex array of bioactive compounds, including chlorogenic acids, trigonelline, diterpenes, and melanoidins that collectively exert pleiotropic effects on cellular metabolism. However, a comprehensive framework linking the full spectrum of coffee-derived bioactives to mitochondrial health and chronic disease prevention is still lacking.
MAIN BODY: This review proposes an integrated perspective on coffee as a systemic "mitochondrial network optimizer." We present this model as an integrative framework and hypothesis rather than an established causal model. We synthesize molecular, pre-clinical, and clinical evidence suggesting that coffee bioactives converge on key regulatory nodes, namely the AMPK/SIRT1/PGC-1α axis, Nrf2/ARE antioxidant pathway, PINK1/Parkin-mediated mitophagy, and mitochondrial calcium signaling to coordinately enhance mitochondrial biogenesis, quality control, redox defense, and metabolic efficiency. These multi-targeted mechanisms provide a plausible biological basis for the consistent epidemiological associations between moderate coffee consumption and reduced risk of metabolic diseases (type 2 diabetes, non-alcoholic fatty liver disease), neurodegenerative disorders (Parkinson's, Alzheimer's), and cardiovascular conditions. Furthermore, we critically examine key determinants of response heterogeneity, including non-linear hormetic dose-response relationships, inter-individual variability (CYP1A2 genotype, gut microbiota, sex), and the impact of coffee processing and brewing methods on bioactive composition.
CONCLUSIONS: Collectively, these findings support the hypothesis that coffee may serve as a paradigm of polypharmacological dietary intervention that targets fundamental pathways of mitochondrial resilience. Moving beyond reductionist views centered on single compounds, we propose that the holistic effects of coffee are best understood through systems-level modulation of mitochondrial homeostasis. Future research should prioritize precision nutrition approaches stratified by genotype, microbiome, and metabolic phenotype, to translate these mechanistic insights into personalized dietary recommendations and the development of mitochondria-targeted nutraceuticals. We caution that this integrative framework requires direct validation in human causal studies.
Additional Links: PMID-42469894
Publisher:
PubMed:
Citation:
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@article {pmid42469894,
year = {2026},
author = {Jiang, Z and Ding, Y},
title = {Coffee as a polypharmacological modulator of mitochondrial health: from molecular mechanisms to translational implications.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-08662-5},
pmid = {42469894},
issn = {1479-5876},
support = {LQ24H160009//Zhejiang Provincial National Natural Science Foundation of China/ ; LHZY24H020002//Hangzhou Joint Fund of the Zhejiang Provincial Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Coffee is one of the most widely consumed beverages worldwide, yet its biological effects have often been attributed primarily to caffeine. Emerging evidence suggests that coffee contains a complex array of bioactive compounds, including chlorogenic acids, trigonelline, diterpenes, and melanoidins that collectively exert pleiotropic effects on cellular metabolism. However, a comprehensive framework linking the full spectrum of coffee-derived bioactives to mitochondrial health and chronic disease prevention is still lacking.
MAIN BODY: This review proposes an integrated perspective on coffee as a systemic "mitochondrial network optimizer." We present this model as an integrative framework and hypothesis rather than an established causal model. We synthesize molecular, pre-clinical, and clinical evidence suggesting that coffee bioactives converge on key regulatory nodes, namely the AMPK/SIRT1/PGC-1α axis, Nrf2/ARE antioxidant pathway, PINK1/Parkin-mediated mitophagy, and mitochondrial calcium signaling to coordinately enhance mitochondrial biogenesis, quality control, redox defense, and metabolic efficiency. These multi-targeted mechanisms provide a plausible biological basis for the consistent epidemiological associations between moderate coffee consumption and reduced risk of metabolic diseases (type 2 diabetes, non-alcoholic fatty liver disease), neurodegenerative disorders (Parkinson's, Alzheimer's), and cardiovascular conditions. Furthermore, we critically examine key determinants of response heterogeneity, including non-linear hormetic dose-response relationships, inter-individual variability (CYP1A2 genotype, gut microbiota, sex), and the impact of coffee processing and brewing methods on bioactive composition.
CONCLUSIONS: Collectively, these findings support the hypothesis that coffee may serve as a paradigm of polypharmacological dietary intervention that targets fundamental pathways of mitochondrial resilience. Moving beyond reductionist views centered on single compounds, we propose that the holistic effects of coffee are best understood through systems-level modulation of mitochondrial homeostasis. Future research should prioritize precision nutrition approaches stratified by genotype, microbiome, and metabolic phenotype, to translate these mechanistic insights into personalized dietary recommendations and the development of mitochondria-targeted nutraceuticals. We caution that this integrative framework requires direct validation in human causal studies.},
}
RevDate: 2026-07-18
CmpDate: 2026-07-18
Human skin microbiota and postpartum depression: A bidirectional Mendelian randomization study.
Medicine, 105(29):e49660.
Postpartum depression (PPD) is a common mental health disorder after childbirth. Although microbiome research in PPD has mainly focused on the gut, the role of skin microbiota remains unclear. We used Mendelian randomization (MR) to assess potential causal associations between skin microbiota and PPD. A bidirectional 2-sample MR analysis used genome-wide association study (GWAS) summary statistics. Genetic instruments for skin microbial features were obtained from a published skin microbiota GWAS, and PPD data were derived from 67,205 mothers (7604 cases, 59,601 controls). Instruments were selected at P <1 × 10-5, linkage disequilibrium-clumped, harmonized, and filtered for weak instruments (F statistic <10). Because this microbiome threshold is exploratory, Benjamini-Hochberg false discovery rate correction was applied within taxonomic levels. The inverse-variance weighted method was primary, complemented by weighted median and mode-based methods. Heterogeneity, pleiotropy, and outliers were assessed using Cochran Q, MR-Egger intercept, and MR-PRESSO. Three skin microbial taxa showed nominal associations with PPD. Higher genetically predicted Acinetobacter on the dorsal forearm (dry skin; 9 single nucleotide polymorphisms [SNPs]; mean F = 22.12) and Proteobacteria in the antecubital fossa (moist skin; 6 SNPs; mean F = 23.44) were associated with increased PPD risk, whereas Betaproteobacteria in the antecubital fossa (11 SNPs; mean F = 21.54) was associated with decreased risk. Associations were directionally consistent, with no substantial heterogeneity or horizontal pleiotropy. After multiple-testing assessment, the findings were exploratory rather than definitive. Reverse MR did not support an effect of PPD on the identified skin microbiota. This MR study provides exploratory genetic evidence linking specific skin microbial features to PPD risk. The findings extend microbiota-related hypotheses beyond the gut microbiome but require validation in larger microbiome GWAS datasets, longitudinal cohorts, and mechanistic studies before clinical or causal conclusions are drawn.
Additional Links: PMID-42469996
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PubMed:
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@article {pmid42469996,
year = {2026},
author = {Huang, C and Zhang, S and Lu, Z},
title = {Human skin microbiota and postpartum depression: A bidirectional Mendelian randomization study.},
journal = {Medicine},
volume = {105},
number = {29},
pages = {e49660},
doi = {10.1097/MD.0000000000049660},
pmid = {42469996},
issn = {1536-5964},
support = {2025CGW051//Public Welfare Research Project of Jiaxing/ ; 2026CFY084//Public Welfare Research Project of Jiaxing/ ; },
mesh = {Humans ; Female ; *Skin Microbiome ; Genome-Wide Association Study ; Polymorphism, Single Nucleotide ; *Mendelian Randomization Analysis ; *Depression, Postpartum/microbiology/genetics ; *Skin/microbiology ; Acinetobacter/genetics/isolation & purification ; Proteobacteria/genetics/isolation & purification ; *Microbiota ; },
abstract = {Postpartum depression (PPD) is a common mental health disorder after childbirth. Although microbiome research in PPD has mainly focused on the gut, the role of skin microbiota remains unclear. We used Mendelian randomization (MR) to assess potential causal associations between skin microbiota and PPD. A bidirectional 2-sample MR analysis used genome-wide association study (GWAS) summary statistics. Genetic instruments for skin microbial features were obtained from a published skin microbiota GWAS, and PPD data were derived from 67,205 mothers (7604 cases, 59,601 controls). Instruments were selected at P <1 × 10-5, linkage disequilibrium-clumped, harmonized, and filtered for weak instruments (F statistic <10). Because this microbiome threshold is exploratory, Benjamini-Hochberg false discovery rate correction was applied within taxonomic levels. The inverse-variance weighted method was primary, complemented by weighted median and mode-based methods. Heterogeneity, pleiotropy, and outliers were assessed using Cochran Q, MR-Egger intercept, and MR-PRESSO. Three skin microbial taxa showed nominal associations with PPD. Higher genetically predicted Acinetobacter on the dorsal forearm (dry skin; 9 single nucleotide polymorphisms [SNPs]; mean F = 22.12) and Proteobacteria in the antecubital fossa (moist skin; 6 SNPs; mean F = 23.44) were associated with increased PPD risk, whereas Betaproteobacteria in the antecubital fossa (11 SNPs; mean F = 21.54) was associated with decreased risk. Associations were directionally consistent, with no substantial heterogeneity or horizontal pleiotropy. After multiple-testing assessment, the findings were exploratory rather than definitive. Reverse MR did not support an effect of PPD on the identified skin microbiota. This MR study provides exploratory genetic evidence linking specific skin microbial features to PPD risk. The findings extend microbiota-related hypotheses beyond the gut microbiome but require validation in larger microbiome GWAS datasets, longitudinal cohorts, and mechanistic studies before clinical or causal conclusions are drawn.},
}
MeSH Terms:
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Humans
Female
*Skin Microbiome
Genome-Wide Association Study
Polymorphism, Single Nucleotide
*Mendelian Randomization Analysis
*Depression, Postpartum/microbiology/genetics
*Skin/microbiology
Acinetobacter/genetics/isolation & purification
Proteobacteria/genetics/isolation & purification
*Microbiota
RevDate: 2026-07-18
Recent developments in the therapeutic management of acid-related gastrointestinal diseases.
Expert review of gastroenterology & hepatology [Epub ahead of print].
INTRODUCTION: Acid-related gastrointestinal diseases, particularly gastroesophageal reflux disease (GERD) and peptic ulcer disease (PUD), remain major global health burdens despite decades of proton pump inhibitor (PPI)-based therapy. Persistent symptoms, nocturnal acid breakthrough, refractory disease, antibiotic resistance in Helicobacter pylori infection, and interindividual pharmacogenomic variability continue to limit current management strategies.
AREAS COVERED: This review summarizes therapeutic advances in acid-related diseases with a focus on articles published between 2020 and 2025, and on potassium-competitive acid blockers (P-CABs), mucosal protective agents, adjunctive pharmacotherapies, endoscopic anti-reflux interventions, and precision medicine studies. Literature from randomized controlled trials, meta-analyses, international guidelines, and observational studies was reviewed to evaluate efficacy, safety, and clinical positioning of emerging therapies in GERD, PUD, and H. pylori eradication. The search was conducted in Pubmed.
EXPERT OPINION: P-CABs, particularly vonoprazan, represent the most important advance in acid suppression in recent decades, offering faster, more potent, and more predictable acid inhibition than PPIs. Precision approaches integrating GERD phenotyping, pharmacogenomics, and antibiotic susceptibility testing are shifting management toward individualized care. However, long-term safety data, cost-effectiveness analyses, and robust comparative trials remain limited. Future progress will likely depend on combining phenotype-directed pharmacologic, endoscopic, and microbiome-informed strategies supported by artificial intelligence-driven diagnostics and treatment selection.
Additional Links: PMID-42470089
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PubMed:
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@article {pmid42470089,
year = {2026},
author = {Lanas-Gimeno, A and Lanas, A},
title = {Recent developments in the therapeutic management of acid-related gastrointestinal diseases.},
journal = {Expert review of gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1080/17474124.2026.2706854},
pmid = {42470089},
issn = {1747-4132},
abstract = {INTRODUCTION: Acid-related gastrointestinal diseases, particularly gastroesophageal reflux disease (GERD) and peptic ulcer disease (PUD), remain major global health burdens despite decades of proton pump inhibitor (PPI)-based therapy. Persistent symptoms, nocturnal acid breakthrough, refractory disease, antibiotic resistance in Helicobacter pylori infection, and interindividual pharmacogenomic variability continue to limit current management strategies.
AREAS COVERED: This review summarizes therapeutic advances in acid-related diseases with a focus on articles published between 2020 and 2025, and on potassium-competitive acid blockers (P-CABs), mucosal protective agents, adjunctive pharmacotherapies, endoscopic anti-reflux interventions, and precision medicine studies. Literature from randomized controlled trials, meta-analyses, international guidelines, and observational studies was reviewed to evaluate efficacy, safety, and clinical positioning of emerging therapies in GERD, PUD, and H. pylori eradication. The search was conducted in Pubmed.
EXPERT OPINION: P-CABs, particularly vonoprazan, represent the most important advance in acid suppression in recent decades, offering faster, more potent, and more predictable acid inhibition than PPIs. Precision approaches integrating GERD phenotyping, pharmacogenomics, and antibiotic susceptibility testing are shifting management toward individualized care. However, long-term safety data, cost-effectiveness analyses, and robust comparative trials remain limited. Future progress will likely depend on combining phenotype-directed pharmacologic, endoscopic, and microbiome-informed strategies supported by artificial intelligence-driven diagnostics and treatment selection.},
}
RevDate: 2026-07-18
The Vape, the Mouth, and the Mycobiome: A Comparative Metagenomic Analysis.
Journal of dental research [Epub ahead of print].
Electronic nicotine delivery systems (ENDS), including e-cigarettes, are increasingly marketed as safer alternatives to combustible tobacco, yet their effects on oral health remain underexplored. Although the role of ENDS in creating dysbiotic oral bacterial communities is documented, effects on the oral mycobiome remain underexplored. This study compared the subgingival fungal communities of 123 periodontally and systemically healthy e-cigarette-only users, smokers, dual users, former smokers, and never-smokers using whole-genome shotgun sequencing for functional profiling. Taxonomic assignment using Kraken 2 and the PlusPF database identified 98 fungal taxa, and functional annotation with the Kyoto Encyclopedia of Genes and Genomes identified 2,960 fungal genes. Cross-domain bacterial-fungal interactions were interrogated using a correlation threshold of |r| ≥ 0.7 and P ≤ 0.001. E-cigarette users demonstrated a significantly higher α-diversity than smokers and never-smokers did (P < 0.001; P < 0.005) and a mycobiome enriched with Candida albicans, Aspergillus oryzae, and Schizosaccharomyces pombe. Functional profiling revealed enrichment of genes encoding or DNA repair, xenobiotic degradation, membrane transport, and stress response. The mycobiome of dual users and former smokers using e-cigarettes did not differ from that of e-cigarette users. Cross-kingdom networks identified 5- to 10-fold higher bacterial-fungal connectivity in e-cigarette users, with fungi capable of enhanced stress tolerance, DNA repair capacity, and metabolic adaptability acting as network anchors. Our data support an association between e-cigarette use and remodeling of the oral mycobiome and microbiome, driven by enhanced polymicrobial interactions and increased functional complexity, suggesting that assumptions regarding the biological neutrality of e-cigarette aerosols warrant further investigation.
Additional Links: PMID-42470286
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PubMed:
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@article {pmid42470286,
year = {2026},
author = {Nikam, R and Kalani, K and Beverly, M and Kumar, PS},
title = {The Vape, the Mouth, and the Mycobiome: A Comparative Metagenomic Analysis.},
journal = {Journal of dental research},
volume = {},
number = {},
pages = {220345261450182},
doi = {10.1177/00220345261450182},
pmid = {42470286},
issn = {1544-0591},
abstract = {Electronic nicotine delivery systems (ENDS), including e-cigarettes, are increasingly marketed as safer alternatives to combustible tobacco, yet their effects on oral health remain underexplored. Although the role of ENDS in creating dysbiotic oral bacterial communities is documented, effects on the oral mycobiome remain underexplored. This study compared the subgingival fungal communities of 123 periodontally and systemically healthy e-cigarette-only users, smokers, dual users, former smokers, and never-smokers using whole-genome shotgun sequencing for functional profiling. Taxonomic assignment using Kraken 2 and the PlusPF database identified 98 fungal taxa, and functional annotation with the Kyoto Encyclopedia of Genes and Genomes identified 2,960 fungal genes. Cross-domain bacterial-fungal interactions were interrogated using a correlation threshold of |r| ≥ 0.7 and P ≤ 0.001. E-cigarette users demonstrated a significantly higher α-diversity than smokers and never-smokers did (P < 0.001; P < 0.005) and a mycobiome enriched with Candida albicans, Aspergillus oryzae, and Schizosaccharomyces pombe. Functional profiling revealed enrichment of genes encoding or DNA repair, xenobiotic degradation, membrane transport, and stress response. The mycobiome of dual users and former smokers using e-cigarettes did not differ from that of e-cigarette users. Cross-kingdom networks identified 5- to 10-fold higher bacterial-fungal connectivity in e-cigarette users, with fungi capable of enhanced stress tolerance, DNA repair capacity, and metabolic adaptability acting as network anchors. Our data support an association between e-cigarette use and remodeling of the oral mycobiome and microbiome, driven by enhanced polymicrobial interactions and increased functional complexity, suggesting that assumptions regarding the biological neutrality of e-cigarette aerosols warrant further investigation.},
}
RevDate: 2026-07-18
Plasma metabolomic signatures of heterogeneous multimorbidity trajectories in ageing: a population-based cohort study.
GeroScience [Epub ahead of print].
Age-related disease burden accumulates heterogeneously from later midlife to older age, but the biology underlying these divergent trajectories is poorly understood. We analysed 7199 adults aged 40 years and over in the Tsuruoka Metabolomics Cohort Study, Japan, with baseline fasting plasma metabolomics (94 metabolites measured by capillary electrophoresis-mass spectrometry) and linked health insurance claims. Monthly cumulative Charlson Comorbidity Index scores were constructed from aligned cohort entry to 60 months to capture accumulation of newly documented Charlson conditions after follow-up start. K-means clustering identified six trajectories of claims-recorded disease burden, and ordinal logistic regression related metabolites to ordered trajectory severity with adjustment for demographic and lifestyle factors. Six trajectories ranged from minimal accumulation to rapid progression. Nineteen metabolites were associated with greater trajectory severity after false discovery rate correction. Glutamate showed the strongest positive association (odds ratio, 1.18 per standard deviation; 95% confidence interval, 1.12-1.24), whereas cysteine-glutathione disulfide showed the strongest inverse association (odds ratio, 0.89; 95% confidence interval, 0.86-0.93). Eighteen of these metabolites were also associated with time to first newly documented Charlson disease. Disease-specific analyses linked glutamate to diabetes with complications, mild liver disease, and cerebrovascular disease. Exploratory cluster-specific analyses identified hippurate as a distinctive marker of a late-acceleration trajectory. These findings implicate amino acid metabolism, redox balance, and microbiome-host interactions as candidate biological pathways underlying heterogeneous patterns of age-related disease accumulation, and warrant replication in independent cohorts. These signals may inform biomarker development for accelerated disease-burden accumulation.
Additional Links: PMID-42470521
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@article {pmid42470521,
year = {2026},
author = {Toki, R and Iba, C and Omoto, Y and Matsumoto, M and Iida, M and Edagawa, S and Harada, S and Hirata, A and Miyagawa, N and Miyake, A and Hirayama, A and Sugimoto, M and Sato, A and Amano, K and Soga, T and Arakawa, K and Takebayashi, T},
title = {Plasma metabolomic signatures of heterogeneous multimorbidity trajectories in ageing: a population-based cohort study.},
journal = {GeroScience},
volume = {},
number = {},
pages = {},
pmid = {42470521},
issn = {2509-2723},
support = {JP24390168//Japan Society for the Promotion of Science/ ; JP15H04778//Japan Society for the Promotion of Science/ ; 25670303//Japan Society for the Promotion of Science/ ; },
abstract = {Age-related disease burden accumulates heterogeneously from later midlife to older age, but the biology underlying these divergent trajectories is poorly understood. We analysed 7199 adults aged 40 years and over in the Tsuruoka Metabolomics Cohort Study, Japan, with baseline fasting plasma metabolomics (94 metabolites measured by capillary electrophoresis-mass spectrometry) and linked health insurance claims. Monthly cumulative Charlson Comorbidity Index scores were constructed from aligned cohort entry to 60 months to capture accumulation of newly documented Charlson conditions after follow-up start. K-means clustering identified six trajectories of claims-recorded disease burden, and ordinal logistic regression related metabolites to ordered trajectory severity with adjustment for demographic and lifestyle factors. Six trajectories ranged from minimal accumulation to rapid progression. Nineteen metabolites were associated with greater trajectory severity after false discovery rate correction. Glutamate showed the strongest positive association (odds ratio, 1.18 per standard deviation; 95% confidence interval, 1.12-1.24), whereas cysteine-glutathione disulfide showed the strongest inverse association (odds ratio, 0.89; 95% confidence interval, 0.86-0.93). Eighteen of these metabolites were also associated with time to first newly documented Charlson disease. Disease-specific analyses linked glutamate to diabetes with complications, mild liver disease, and cerebrovascular disease. Exploratory cluster-specific analyses identified hippurate as a distinctive marker of a late-acceleration trajectory. These findings implicate amino acid metabolism, redox balance, and microbiome-host interactions as candidate biological pathways underlying heterogeneous patterns of age-related disease accumulation, and warrant replication in independent cohorts. These signals may inform biomarker development for accelerated disease-burden accumulation.},
}
RevDate: 2026-07-18
CmpDate: 2026-07-18
Species-Specific Bacterial Associations Emerge From Stochastically Assembled Microbiomes in Northeastern American Fireflies.
Molecular ecology, 35(14):e70473.
Many insects harbour microbial communities that can profoundly influence the biology of their host. Yet, the relative contribution of random exposure (i.e., stochastic) events and deterministic ecological factors in shaping these communities remains unclear for most taxa. We examined microbiome assembly across 344 firefly (Coleoptera: Lampyridae) specimens from the Northeastern United States, spanning 12 species and species groups, and generating a high-resolution dataset through deep 16S rRNA gene amplicon sequencing and quantitative PCR. To formally assess the balance between stochastic and deterministic forces, we applied integrative statistical approaches, including an innovative null-modelling framework based on the normalized stochasticity ratio (NST) index. We hypothesized that firefly microbiome assembly is dominated by stochastic processes driven by unpredictable microbial exposures. Consistent with this, we observed elevated NST values for most bacteria, coupled with high intraspecific variability in bacterial abundance and composition. However, microbiomes were more similar among closely related fireflies and unusually prevalent mollicute strains showed low NST values, species-specific associations and retention across geography and host development. While adult bioluminescence and diet could not be directly linked to microbiome abundance or composition, considering seasonal factors and intra-host anatomy within host species revealed patterns explaining some of the intraspecific microbiome variation. These results show that deterministic processes, likely arising from host-specific microbial filtering mechanisms, act alongside stochastic forces to shape firefly-microbe associations. By integrating broad field sampling with quantitative bacterial load estimates and comprehensive microbiome analyses, this study clarifies how evolutionary history, ecology and chance jointly govern microbiome assembly in a diverse insect lineage.
Additional Links: PMID-42470666
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@article {pmid42470666,
year = {2026},
author = {Béchade, B and Lower, SE and Nichols, SR and Dabbert, TJ and Ravenscraft, A},
title = {Species-Specific Bacterial Associations Emerge From Stochastically Assembled Microbiomes in Northeastern American Fireflies.},
journal = {Molecular ecology},
volume = {35},
number = {14},
pages = {e70473},
doi = {10.1111/mec.70473},
pmid = {42470666},
issn = {1365-294X},
support = {//University of Texas at Arlington/ ; //Bucknell University/ ; },
mesh = {Animals ; *Microbiota/genetics ; RNA, Ribosomal, 16S/genetics ; Species Specificity ; *Bacteria/genetics/classification ; *Fireflies/microbiology ; Sequence Analysis, DNA ; Stochastic Processes ; DNA, Bacterial/genetics ; New England ; },
abstract = {Many insects harbour microbial communities that can profoundly influence the biology of their host. Yet, the relative contribution of random exposure (i.e., stochastic) events and deterministic ecological factors in shaping these communities remains unclear for most taxa. We examined microbiome assembly across 344 firefly (Coleoptera: Lampyridae) specimens from the Northeastern United States, spanning 12 species and species groups, and generating a high-resolution dataset through deep 16S rRNA gene amplicon sequencing and quantitative PCR. To formally assess the balance between stochastic and deterministic forces, we applied integrative statistical approaches, including an innovative null-modelling framework based on the normalized stochasticity ratio (NST) index. We hypothesized that firefly microbiome assembly is dominated by stochastic processes driven by unpredictable microbial exposures. Consistent with this, we observed elevated NST values for most bacteria, coupled with high intraspecific variability in bacterial abundance and composition. However, microbiomes were more similar among closely related fireflies and unusually prevalent mollicute strains showed low NST values, species-specific associations and retention across geography and host development. While adult bioluminescence and diet could not be directly linked to microbiome abundance or composition, considering seasonal factors and intra-host anatomy within host species revealed patterns explaining some of the intraspecific microbiome variation. These results show that deterministic processes, likely arising from host-specific microbial filtering mechanisms, act alongside stochastic forces to shape firefly-microbe associations. By integrating broad field sampling with quantitative bacterial load estimates and comprehensive microbiome analyses, this study clarifies how evolutionary history, ecology and chance jointly govern microbiome assembly in a diverse insect lineage.},
}
MeSH Terms:
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Animals
*Microbiota/genetics
RNA, Ribosomal, 16S/genetics
Species Specificity
*Bacteria/genetics/classification
*Fireflies/microbiology
Sequence Analysis, DNA
Stochastic Processes
DNA, Bacterial/genetics
New England
RevDate: 2026-07-18
B vitamin-mediated interactions in synthetic microbial communities.
Current opinion in microbiology, 93:102799 pii:S1369-5274(26)00093-7 [Epub ahead of print].
Microbial communities drive fundamental processes across the globe, from biogeochemical cycling to human health. Yet, their complexity often obscures mechanistic understanding. Synthetic communities (SynComs) have emerged as powerful tools to distill this complexity into tractable, rationally designed systems to study community function. Metabolic interactions - competition and sharing of resources between organisms - are a frequent focus of these controlled studies. The role of B vitamin cross-feeding remains a critical frontier because B vitamins are required in trace quantities for metabolism, but not all organisms can make their own, necessitating cross-feeding interactions. Here, we review recent advances in microbial ecology that use SynComs to investigate B vitamin-mediated interactions through mechanistic approaches across scales, domains of life, environments, and disciplines. We highlight key findings that demonstrate how auxotrophy, obligate cross-feeding networks, precursor sharing, exploitation and interference competition, and cell lysis together encompass B vitamin interactions. Collectively, these processes demonstrate how microbial B vitamin exchanges drive macroscale community functions like host-microbiome interdependencies. The mechanistic insights into microbial community interactions synthesized from these integrative approaches provide foundational insight into the structure and function of natural microbial communities, advancing the potential to engineer microbiomes for therapeutic and environmental applications.
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@article {pmid42470720,
year = {2026},
author = {Suazo, DD and Wang, E and Taga, ME},
title = {B vitamin-mediated interactions in synthetic microbial communities.},
journal = {Current opinion in microbiology},
volume = {93},
number = {},
pages = {102799},
doi = {10.1016/j.mib.2026.102799},
pmid = {42470720},
issn = {1879-0364},
abstract = {Microbial communities drive fundamental processes across the globe, from biogeochemical cycling to human health. Yet, their complexity often obscures mechanistic understanding. Synthetic communities (SynComs) have emerged as powerful tools to distill this complexity into tractable, rationally designed systems to study community function. Metabolic interactions - competition and sharing of resources between organisms - are a frequent focus of these controlled studies. The role of B vitamin cross-feeding remains a critical frontier because B vitamins are required in trace quantities for metabolism, but not all organisms can make their own, necessitating cross-feeding interactions. Here, we review recent advances in microbial ecology that use SynComs to investigate B vitamin-mediated interactions through mechanistic approaches across scales, domains of life, environments, and disciplines. We highlight key findings that demonstrate how auxotrophy, obligate cross-feeding networks, precursor sharing, exploitation and interference competition, and cell lysis together encompass B vitamin interactions. Collectively, these processes demonstrate how microbial B vitamin exchanges drive macroscale community functions like host-microbiome interdependencies. The mechanistic insights into microbial community interactions synthesized from these integrative approaches provide foundational insight into the structure and function of natural microbial communities, advancing the potential to engineer microbiomes for therapeutic and environmental applications.},
}
RevDate: 2026-07-16
TAAR Immunopharmacology.
Handbook of experimental pharmacology [Epub ahead of print].
Trace amine-associated receptors (TAARs) were originally identified as G protein-coupled receptors involved in monoaminergic signaling within the central nervous system. However, accumulating evidence indicates that TAARs, particularly TAAR1 and TAAR2, are also expressed in the immune system, including circulating leukocytes, lymphocytes, macrophages, and microglia. This chapter reviews current evidence regarding TAAR expression, functional pharmacology, and potential translational relevance within the immune system.Expression studies support a predominant TAAR1/TAAR2 pattern across both innate and adaptive immune-cell populations. Functional studies indicate that TAAR signaling can modulate inflammatory responses through chemotaxis, cytokine production, and immunoglobulin secretion. However, these effects are highly context-dependent, preventing a simple classification of TAAR signaling as either pro-inflammatory or anti-inflammatory.The chapter also discusses the emerging role of TAAR signaling in the pathophysiology of diseases, including inflammatory bowel disease, methamphetamine-associated immune dysfunction during HIV infection, multiple sclerosis, Parkinson's disease, fibromyalgia, and hematological malignancies.Despite growing interest in TAAR immunopharmacology, the current evidence remains largely preclinical and methodologically heterogeneous. Major limitations include incomplete protein-level validation, reliance on immortalized cell lines or mixed-cell populations, species-specific pharmacology of available ligands, and limited understanding of physiological trace amine signaling under basal conditions. Further integrative studies will be required to clarify TAAR pathophysiological significance and determine whether TAAR-targeted strategies may have translational relevance in immune-mediated disorders.
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@article {pmid42463873,
year = {2026},
author = {Magnesa, A and Pacini, A and Rutigliano, G},
title = {TAAR Immunopharmacology.},
journal = {Handbook of experimental pharmacology},
volume = {},
number = {},
pages = {},
pmid = {42463873},
issn = {0171-2004},
abstract = {Trace amine-associated receptors (TAARs) were originally identified as G protein-coupled receptors involved in monoaminergic signaling within the central nervous system. However, accumulating evidence indicates that TAARs, particularly TAAR1 and TAAR2, are also expressed in the immune system, including circulating leukocytes, lymphocytes, macrophages, and microglia. This chapter reviews current evidence regarding TAAR expression, functional pharmacology, and potential translational relevance within the immune system.Expression studies support a predominant TAAR1/TAAR2 pattern across both innate and adaptive immune-cell populations. Functional studies indicate that TAAR signaling can modulate inflammatory responses through chemotaxis, cytokine production, and immunoglobulin secretion. However, these effects are highly context-dependent, preventing a simple classification of TAAR signaling as either pro-inflammatory or anti-inflammatory.The chapter also discusses the emerging role of TAAR signaling in the pathophysiology of diseases, including inflammatory bowel disease, methamphetamine-associated immune dysfunction during HIV infection, multiple sclerosis, Parkinson's disease, fibromyalgia, and hematological malignancies.Despite growing interest in TAAR immunopharmacology, the current evidence remains largely preclinical and methodologically heterogeneous. Major limitations include incomplete protein-level validation, reliance on immortalized cell lines or mixed-cell populations, species-specific pharmacology of available ligands, and limited understanding of physiological trace amine signaling under basal conditions. Further integrative studies will be required to clarify TAAR pathophysiological significance and determine whether TAAR-targeted strategies may have translational relevance in immune-mediated disorders.},
}
RevDate: 2026-07-16
A network-based meta-analysis of the honeybee gut microbiome: geographic, seasonal, and pesticide-associated shifts.
Scientific reports pii:10.1038/s41598-026-62172-4 [Epub ahead of print].
The honeybee (Apis mellifera) gut microbiome is essential for pollinator health, yet its functional responses to environmental stressors remain poorly understood. We conducted a global meta-analysis of honeybee gut microbiomes from seven geographic regions, including newly generated data from Armenia, and applied a novel co-abundance network approach, tsantsR, to uncover community-level co-abundance patterns and functional adaptations. We identified a conserved core of six and ten phylotypes in 16 S and WGS datasets, respectively. In Armenia, seasonal and environmental factors, such as urbanization, were linked to compositional shifts, including higher relative abundance of Commensalibacter in autumn and of Bombilactobacillus in urban colonies. Analysis of pesticide and dietary exposure revealed distinct microbial responses. Oxalic acid and neonicotinoid exposure were associated with shifts in opportunistic pathogens, including Klebsiella, Hafnia-Obesumbacterium, and Serratia. In contrast, the herbicide glyphosate was linked to a potential adaptive response characterized by disruption of core taxa such as Snodgrassella alvi and upregulation of pathways hypothesized to be involved in glyphosate degradation, primarily linked to enrichment of Pseudomonas.
Additional Links: PMID-42463890
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@article {pmid42463890,
year = {2026},
author = {Vardazaryan, N and Adunts, L and Bazukyan, I and Zakharyan, M and Liu, H and Melkonian, C and Nersisyan, L},
title = {A network-based meta-analysis of the honeybee gut microbiome: geographic, seasonal, and pesticide-associated shifts.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-62172-4},
pmid = {42463890},
issn = {2045-2322},
support = {24AA-1F065//HESC MESCS RA/ ; 24FP-2I061//HESC MESCS RA/ ; 2022 to IB//Yerevan State University/ ; },
abstract = {The honeybee (Apis mellifera) gut microbiome is essential for pollinator health, yet its functional responses to environmental stressors remain poorly understood. We conducted a global meta-analysis of honeybee gut microbiomes from seven geographic regions, including newly generated data from Armenia, and applied a novel co-abundance network approach, tsantsR, to uncover community-level co-abundance patterns and functional adaptations. We identified a conserved core of six and ten phylotypes in 16 S and WGS datasets, respectively. In Armenia, seasonal and environmental factors, such as urbanization, were linked to compositional shifts, including higher relative abundance of Commensalibacter in autumn and of Bombilactobacillus in urban colonies. Analysis of pesticide and dietary exposure revealed distinct microbial responses. Oxalic acid and neonicotinoid exposure were associated with shifts in opportunistic pathogens, including Klebsiella, Hafnia-Obesumbacterium, and Serratia. In contrast, the herbicide glyphosate was linked to a potential adaptive response characterized by disruption of core taxa such as Snodgrassella alvi and upregulation of pathways hypothesized to be involved in glyphosate degradation, primarily linked to enrichment of Pseudomonas.},
}
RevDate: 2026-07-16
Enhanced biodiesel wastewater treatment using moving bed biofilm reactor (MBBR) and improved applicability to subsequent coagulation process.
Scientific reports pii:10.1038/s41598-026-62982-6 [Epub ahead of print].
Biodiesel wastewater (BDW) is a high-strength industrial effluent rich in organic matter, oils, and suspended solids, posing significant challenges for conventional treatment processes. In this study, a pilot-scale moving bed biofilm reactor (MBBR) was operated continuously for three months to evaluate its performance in treating biodiesel wastewater (BDW) and its impact on the efficiency of subsequent coagulation. The MBBR achieved sustained chemical oxygen demand (COD) and total organic carbon (TOC) removal under fluctuating influent conditions, with average removal rates of 74.79% and 81.37%, respectively. Microbial community analysis based on 16 S rRNA gene sequencing revealed a diverse biofilm community in the MBBR carriers, with Bacteroidetes, Saccharibacteria_TM7, Proteobacteria, and Firmicutes as major phyla. At the genus level, Saccharimonas, Chryseobacterium, and Proteiniphilum were the predominant taxa. In addition, MBBR pre-treatment substantially enhanced the performance of downstream coagulation using ferrous sulfate. The COD removal efficiency by coagulation increased more than 2.5-fold after MBBR treatment (from 13.35% to 34.29%), along with notable enhancements in TOC and SS removal. These enhancements may be associated with biological modification of wastewater characteristics during MBBR pretreatment, which improved the conditions for particle aggregation during subsequent coagulation. By linking continuous pilot-scale MBBR operation, carrier-associated biofilm characterization, and downstream FeSO4 coagulation response, this study provides practical insight into the integration of biofilm-based pretreatment with existing physicochemical treatment processes for high-strength industrial wastewater.
Additional Links: PMID-42463891
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@article {pmid42463891,
year = {2026},
author = {Lee, SC and Cho, K and Lee, CG and Kim, SB and Choi, N},
title = {Enhanced biodiesel wastewater treatment using moving bed biofilm reactor (MBBR) and improved applicability to subsequent coagulation process.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-62982-6},
pmid = {42463891},
issn = {2045-2322},
support = {RS-2025-02214066//Korea Environmental Industry and Technology Institute/ ; },
abstract = {Biodiesel wastewater (BDW) is a high-strength industrial effluent rich in organic matter, oils, and suspended solids, posing significant challenges for conventional treatment processes. In this study, a pilot-scale moving bed biofilm reactor (MBBR) was operated continuously for three months to evaluate its performance in treating biodiesel wastewater (BDW) and its impact on the efficiency of subsequent coagulation. The MBBR achieved sustained chemical oxygen demand (COD) and total organic carbon (TOC) removal under fluctuating influent conditions, with average removal rates of 74.79% and 81.37%, respectively. Microbial community analysis based on 16 S rRNA gene sequencing revealed a diverse biofilm community in the MBBR carriers, with Bacteroidetes, Saccharibacteria_TM7, Proteobacteria, and Firmicutes as major phyla. At the genus level, Saccharimonas, Chryseobacterium, and Proteiniphilum were the predominant taxa. In addition, MBBR pre-treatment substantially enhanced the performance of downstream coagulation using ferrous sulfate. The COD removal efficiency by coagulation increased more than 2.5-fold after MBBR treatment (from 13.35% to 34.29%), along with notable enhancements in TOC and SS removal. These enhancements may be associated with biological modification of wastewater characteristics during MBBR pretreatment, which improved the conditions for particle aggregation during subsequent coagulation. By linking continuous pilot-scale MBBR operation, carrier-associated biofilm characterization, and downstream FeSO4 coagulation response, this study provides practical insight into the integration of biofilm-based pretreatment with existing physicochemical treatment processes for high-strength industrial wastewater.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-17
The effect of SSRI/SNRI antidepressant treatment on the gut microbiota of patients with major depressive disorder.
Communications medicine, 6(1):.
BACKGROUND: The gut microbiome has been linked to major depressive disorder (MDD), yet it remains unclear whether antidepressant treatment influences these associations. This study aimed to clarify the role of serotonin reuptake inhibitors (SSRI/SNRI) in shaping gut microbiome changes observed in MDD.
METHODS: We conducted cross-sectional analyses in two independent patient cohorts (total N = 1802) and a meta-analysis across both cohorts, comparing the gut microbiome of MDD patients with and without SSRI/SNRI treatment.
RESULTS: Here we show that SSRI/SNRI treatment is consistently associated with reduced Clostridium sensu stricto 1 abundance. This effect is specific to SSRI/SNRI treatment and not observed with other psychotropic medications. Importantly, reductions in Clostridium sensu stricto 1 in MDD compared to unaffected controls are explained by SSRI/SNRI medication status.
CONCLUSIONS: Antidepressant treatment is an important factor shaping gut microbiome alterations linked to MDD, underscoring the need to account for medication effects and potentially informing future microbiome-based strategies to improve treatment response.
Additional Links: PMID-42463908
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Citation:
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@article {pmid42463908,
year = {2026},
author = {Natasha, EE and Mulder, D and Fehse, L and Winter, NR and Fisch, L and Welzel, M and Bang, C and Meinert, S and Flinkenflügel, K and Borgers, T and Goltermann, J and Leehr, EJ and Culmsee, C and Stein, F and Thomas-Odenthal, F and Usemann, P and Teutenberg, L and Nenadic, I and Straube, B and Alexander, N and Jamalabadi, H and Jansen, A and Nitsch, R and Lügering, A and Franke, A and Dannlowski, U and Kircher, T and Heider, D and Hahn, T and Vrijsen, JN and van Eijndhoven, P and Tendolkar, I and Reif, A and Edwin Thanarajah, S and Matura, S and Arias Vasquez, A and Bloemendaal, M},
title = {The effect of SSRI/SNRI antidepressant treatment on the gut microbiota of patients with major depressive disorder.},
journal = {Communications medicine},
volume = {6},
number = {1},
pages = {},
pmid = {42463908},
issn = {2730-664X},
support = {82601081//EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ ; },
abstract = {BACKGROUND: The gut microbiome has been linked to major depressive disorder (MDD), yet it remains unclear whether antidepressant treatment influences these associations. This study aimed to clarify the role of serotonin reuptake inhibitors (SSRI/SNRI) in shaping gut microbiome changes observed in MDD.
METHODS: We conducted cross-sectional analyses in two independent patient cohorts (total N = 1802) and a meta-analysis across both cohorts, comparing the gut microbiome of MDD patients with and without SSRI/SNRI treatment.
RESULTS: Here we show that SSRI/SNRI treatment is consistently associated with reduced Clostridium sensu stricto 1 abundance. This effect is specific to SSRI/SNRI treatment and not observed with other psychotropic medications. Importantly, reductions in Clostridium sensu stricto 1 in MDD compared to unaffected controls are explained by SSRI/SNRI medication status.
CONCLUSIONS: Antidepressant treatment is an important factor shaping gut microbiome alterations linked to MDD, underscoring the need to account for medication effects and potentially informing future microbiome-based strategies to improve treatment response.},
}
RevDate: 2026-07-16
Distinct site-specific bacterial microbiota within and between skin physiologic types in healthy Koreans: a pilot study.
Scientific reports pii:10.1038/s41598-026-62903-7 [Epub ahead of print].
Human skin is classified into sebaceous, moist, and dry, which influence the skin microbiome. However, variation within each type is poorly understood and may depend more on anatomical site than physiologic type. We analyzed bacterial communities from eight anatomical sites in ten healthy Korean adults using 16 S rRNA V1-V3 sequencing. Multivariate analysis showed that the anatomical site explained more variation in the microbiome than physiologic type. In dry skin, Cutibacterium was enriched in the dorsal forearm, whereas Kocuria was dominant on the sole. Within moist skin, Staphylococcus showed site-associated compositional differences, while the neck showed a trend toward higher Cutibacterium. Sebaceous scalp sites were rich in Lawsonella and had less Cutibacterium than facial sites. Despite limited species-level resolution of the V1-V3 region, heterogeneity was observed within the same physiologic type, indicating that anatomical site is an important determinant of microbiome structure. These results indicate distinct bacterial community structures both between and within physiologic skin types. These findings provide baseline insights into site-specific host-microbe interactions in healthy skin.
Additional Links: PMID-42463922
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@article {pmid42463922,
year = {2026},
author = {Kim, SY and Trần, TQT and Nam, KH and Yun, SK and Park, J},
title = {Distinct site-specific bacterial microbiota within and between skin physiologic types in healthy Koreans: a pilot study.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-62903-7},
pmid = {42463922},
issn = {2045-2322},
support = {2022R1F1A1074286//National Research Foundation of the Korean government (Ministry of Science and ICT)/ ; RS-2023-KH136575//Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI) by the Ministry of Health and Welfare of the Republic of Korea/ ; },
abstract = {Human skin is classified into sebaceous, moist, and dry, which influence the skin microbiome. However, variation within each type is poorly understood and may depend more on anatomical site than physiologic type. We analyzed bacterial communities from eight anatomical sites in ten healthy Korean adults using 16 S rRNA V1-V3 sequencing. Multivariate analysis showed that the anatomical site explained more variation in the microbiome than physiologic type. In dry skin, Cutibacterium was enriched in the dorsal forearm, whereas Kocuria was dominant on the sole. Within moist skin, Staphylococcus showed site-associated compositional differences, while the neck showed a trend toward higher Cutibacterium. Sebaceous scalp sites were rich in Lawsonella and had less Cutibacterium than facial sites. Despite limited species-level resolution of the V1-V3 region, heterogeneity was observed within the same physiologic type, indicating that anatomical site is an important determinant of microbiome structure. These results indicate distinct bacterial community structures both between and within physiologic skin types. These findings provide baseline insights into site-specific host-microbe interactions in healthy skin.},
}
RevDate: 2026-07-17
Divergent responses of rhizosphere microbial diversity and co-occurrence patterns to elevation and season in Quercus franchetii from the Yuanmou dry‑hot valley, Southwest China.
BMC microbiology pii:10.1186/s12866-026-05364-2 [Epub ahead of print].
BACKGROUND: Dry-hot valleys suffer from severe ecological stress, with the rhizosphere being an essential microhabitat for plant adaptation. Elevation and seasonal changes are key drivers shaping rhizosphere microbial diversity and community composition. However, their impacts on rhizosphere bacteria and fungi associated with Quercus franchetii in dry-hot valleys remain poorly understood.
RESULT: Bacterial α-diversity exhibited a V-shaped pattern along the elevational gradient, whereas fungal α-diversity generally declined with increasing elevation. Seasonal effects were pronounced, with both bacterial and fungal diversity higher in the rainy season. Soil pH had strong positive correlations with bacterial α-diversity, and both soil pH and water content were associated with variations in bacterial and fungal community composition. Bacterial co-occurrence networks were more complex than fungal networks. Rainy-season networks had higher natural connectivity, and higher random and targeted robustness AUC. Actinobacteriota, Acidobacteriota, and Ascomycota acted as keystone taxa stabilizing network interactions. Functional predictions indicated that bacterial communities were predominantly chemoheterotrophic, whereas fungal communities were dominated by symbiotrophic guilds.
CONCLUSIONS: Elevational gradients exert a stronger influence than seasonal variation on rhizosphere microbial diversity and composition. Soil pH and water content are key environmental filters shaping microbial assemblages. Microbial networks maintain ecosystem functions through seasonally modulated connectivity and cooperation. Keystone taxa may mediate network stability and functional resilience under spatiotemporal environmental variation. These results provide a basis for predicting microbial responses to environmental change in dry-hot valleys.
Additional Links: PMID-42464079
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PubMed:
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@article {pmid42464079,
year = {2026},
author = {Xie, X and Li, G and Wu, J and Liu, C and Yue, H and Zhang, D},
title = {Divergent responses of rhizosphere microbial diversity and co-occurrence patterns to elevation and season in Quercus franchetii from the Yuanmou dry‑hot valley, Southwest China.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05364-2},
pmid = {42464079},
issn = {1471-2180},
support = {KFJ-BRP-017-47//the Strategic Biological Resources Capacity Building Project, Chinese Academy of Sciences/ ; 6321A5//Technology Research of Ecological Restoration for Arid River Valley in Yunnan Province/ ; },
abstract = {BACKGROUND: Dry-hot valleys suffer from severe ecological stress, with the rhizosphere being an essential microhabitat for plant adaptation. Elevation and seasonal changes are key drivers shaping rhizosphere microbial diversity and community composition. However, their impacts on rhizosphere bacteria and fungi associated with Quercus franchetii in dry-hot valleys remain poorly understood.
RESULT: Bacterial α-diversity exhibited a V-shaped pattern along the elevational gradient, whereas fungal α-diversity generally declined with increasing elevation. Seasonal effects were pronounced, with both bacterial and fungal diversity higher in the rainy season. Soil pH had strong positive correlations with bacterial α-diversity, and both soil pH and water content were associated with variations in bacterial and fungal community composition. Bacterial co-occurrence networks were more complex than fungal networks. Rainy-season networks had higher natural connectivity, and higher random and targeted robustness AUC. Actinobacteriota, Acidobacteriota, and Ascomycota acted as keystone taxa stabilizing network interactions. Functional predictions indicated that bacterial communities were predominantly chemoheterotrophic, whereas fungal communities were dominated by symbiotrophic guilds.
CONCLUSIONS: Elevational gradients exert a stronger influence than seasonal variation on rhizosphere microbial diversity and composition. Soil pH and water content are key environmental filters shaping microbial assemblages. Microbial networks maintain ecosystem functions through seasonally modulated connectivity and cooperation. Keystone taxa may mediate network stability and functional resilience under spatiotemporal environmental variation. These results provide a basis for predicting microbial responses to environmental change in dry-hot valleys.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
From signals to systems: the epigenetic-microbiome-mitochondrial axis in IBD pathogenesis.
Gut microbes, 18(1):2692755.
Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is increasingly recognized not merely as an immune-mediated disorder, but as a systems-level condition arising from dynamic interactions among host genetics, environmental exposures, the gut microbiome, and epigenetic regulation. While genetic susceptibility confers risk, accumulating evidence indicates that epigenetic mechanisms act as molecular integrators that translate environmental and microbial signals into sustained transcriptional programs governing immune tolerance, epithelial integrity and tissue repair. Concurrently, intestinal dysbiosis, characterized by loss of short-chain fatty acid-producing commensals and expansion of pro-inflammatory taxa, reshapes host metabolism and chromatin states through microbial-derived metabolites including short-chain fatty acids, secondary bile acids, and tryptophan catabolites. These metabolites affect epigenetic enzymes and modulate the epigenetic chromatin landscape as well as mitochondrial bioenergetics, linking microbial ecology to inflammatory gene regulation. In turn, epigenetic alterations in epithelial and immune compartments influence antimicrobial defense, barrier function, and cytokine networks, thereby sculpting microbial community organization. This bidirectional microbiome-epigenome dialogue creates self-reinforcing circuits that can either sustain mucosal homeostasis or drive chronic inflammation and colitis-associated tumorigenesis. In this review, we synthesize emerging insights into the microbiome-epigenome-mitochondrial axis in IBD and propose a conceptual framework in which metabolic, microbial, and genome-mediated signals converge to determine disease trajectory. We discuss how this integrative perspective may assist biomarker discovery and therapeutic innovation, including epigenetic modulators and microbiota-targeted interventions. Understanding IBD as a dynamically regulated host-microbe ecosystem may accelerate the development of precision strategies aimed at restoring resilient mucosal equilibrium.
Additional Links: PMID-42464117
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PubMed:
Citation:
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@article {pmid42464117,
year = {2026},
author = {Kazemifard, N and Shahrokh, S and Dimitrov, G and Totonchi, M and Dimitrov, S},
title = {From signals to systems: the epigenetic-microbiome-mitochondrial axis in IBD pathogenesis.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2692755},
doi = {10.1080/19490976.2026.2692755},
pmid = {42464117},
issn = {1949-0984},
mesh = {Humans ; *Epigenesis, Genetic ; *Inflammatory Bowel Diseases/microbiology/genetics/metabolism ; *Mitochondria/metabolism/genetics ; Animals ; *Gastrointestinal Microbiome ; Dysbiosis/microbiology ; Intestinal Mucosa/microbiology ; },
abstract = {Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is increasingly recognized not merely as an immune-mediated disorder, but as a systems-level condition arising from dynamic interactions among host genetics, environmental exposures, the gut microbiome, and epigenetic regulation. While genetic susceptibility confers risk, accumulating evidence indicates that epigenetic mechanisms act as molecular integrators that translate environmental and microbial signals into sustained transcriptional programs governing immune tolerance, epithelial integrity and tissue repair. Concurrently, intestinal dysbiosis, characterized by loss of short-chain fatty acid-producing commensals and expansion of pro-inflammatory taxa, reshapes host metabolism and chromatin states through microbial-derived metabolites including short-chain fatty acids, secondary bile acids, and tryptophan catabolites. These metabolites affect epigenetic enzymes and modulate the epigenetic chromatin landscape as well as mitochondrial bioenergetics, linking microbial ecology to inflammatory gene regulation. In turn, epigenetic alterations in epithelial and immune compartments influence antimicrobial defense, barrier function, and cytokine networks, thereby sculpting microbial community organization. This bidirectional microbiome-epigenome dialogue creates self-reinforcing circuits that can either sustain mucosal homeostasis or drive chronic inflammation and colitis-associated tumorigenesis. In this review, we synthesize emerging insights into the microbiome-epigenome-mitochondrial axis in IBD and propose a conceptual framework in which metabolic, microbial, and genome-mediated signals converge to determine disease trajectory. We discuss how this integrative perspective may assist biomarker discovery and therapeutic innovation, including epigenetic modulators and microbiota-targeted interventions. Understanding IBD as a dynamically regulated host-microbe ecosystem may accelerate the development of precision strategies aimed at restoring resilient mucosal equilibrium.},
}
MeSH Terms:
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Humans
*Epigenesis, Genetic
*Inflammatory Bowel Diseases/microbiology/genetics/metabolism
*Mitochondria/metabolism/genetics
Animals
*Gastrointestinal Microbiome
Dysbiosis/microbiology
Intestinal Mucosa/microbiology
RevDate: 2026-07-17
Clinical randomized comparative study of Laifu Chengqi Decoction enema for treating postoperative peritonitis in children with complicated appendicitis.
BMC pediatrics pii:10.1186/s12887-026-07329-w [Epub ahead of print].
BACKGROUND: Laifu Chengqi Decoction (LF-CQD) is a traditional Chinese medicine enema rooted in classic heat-clearing and purgative formulas traditionally used to relieve abdominal distention, resolve stasis, and restore bowel motility. Its components (e.g., Laifuzi and Dahuang) provide plausible pro-motility and anti-inflammatory actions, supporting its culturally grounded use as a postoperative adjunct in pediatric perforated appendicitis. This study aimed to evaluate the clinical efficacy of LF-CQD enemas in the treatment of postoperative peritonitis in children.
METHODS: This prospective randomized controlled trial included 118 children with perforated appendicitis complicated by peritonitis. The LF-CQD group received LF-CQD retention enemas for 5 days, whereas the control group was administered saline enemas. The primary outcome was time to first passage of flatus (a core marker of gastrointestinal recovery). Key secondary outcomes included time to bowel sound resumption, time to oral intake, preoperative and postoperative day (POD) 3 and 7 inflammatory marker levels, complication rates at 6-month follow-up, antibiotic use, and length of hospital stay.
RESULTS: Gastrointestinal function recovery was significantly faster in the LF-CQD group than in the control group [bowel sound resumption (p < 0.001), flatus (p < 0.001), and oral intake (p < 0.001)]. On POD7, the LF-CQD group exhibited significantly lower inflammatory marker levels than the control group (C-reactive protein level: p < 0.001). Exploratory post-hoc analyses showed greater relative reductions (ΔCRP/ΔWBC) in the LFCQD group at all timepoints (all p < 0.05). Complication rates for intra-abdominal abscess (8.5% vs. 25.4%, p = 0.008) and adhesive intestinal obstruction (5.1% vs. 22%, p = 0.003) were reduced, and antibiotic use duration was shorter (p < 0.001).
CONCLUSIONS: LFCQD enema serves as a safe, well-tolerated adjuvant intervention for children with postoperative peritonitis secondary to complicated perforated appendicitis. It accelerates gastrointestinal function recovery and alleviates postoperative inflammation. However, being a single-center trial with a modest sample size, it yielded large treatment effects for intra-abdominal abscess, adhesive intestinal obstruction, and length of hospital stay; thus, these effect sizes warrant cautious interpretation and require validation in large-scale multicenter trials. Exploratory post hoc analyses also indicated reduced systemic inflammatory marker levels in the intervention group. We hypothesize that LFCQD may modulate inflammatory signaling cascades and promote gut microbiota homeostasis to drive these clinical improvements. However, as no direct assessment of these pathways or metagenomic profiling of the intestinal microbiome was performed during this trial, these mechanistic proposed mechanistic pathways remain speculative and unconfirmed. In conclusion, this study demonstrates clinical associations between LFCQD enema and improved postoperative outcomes, but does not establish definitive causal molecular mechanisms.
TRIAL REGISTRATION: International Traditional Medicine Clinical Trial Registry; ITMCTR2025001634. Retrospectively registered on July 24, 2025, which constitutes an methodological limitation of this trial. All primary and secondary outcomes, inclusion and exclusion criteria, and core study procedures were precisely predefined and finalized in 2019 at the study design stage, prior to the initiation of patient enrollment in January 2020. No post-hoc additions, deletions, or modifications to any trial outcomes were made after patient recruitment, data collection, or statistical analysis. The retrospective registration was merely delayed due to institutional administrative procedures for traditional Chinese medicine clinical trials, without any alteration to the originally designed trial endpoints. The updated Supplementary Material 1 provides a detailed item-by-item comparison between the registered protocol and manuscript-reported outcomes, confirming full consistency and integrity of all pre-specified endpoints.
Additional Links: PMID-42464224
Publisher:
PubMed:
Citation:
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@article {pmid42464224,
year = {2026},
author = {Zhang, G and Wang, Y and Liu, S and Wu, X and Fu, H and Sun, D},
title = {Clinical randomized comparative study of Laifu Chengqi Decoction enema for treating postoperative peritonitis in children with complicated appendicitis.},
journal = {BMC pediatrics},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12887-026-07329-w},
pmid = {42464224},
issn = {1471-2431},
support = {2025KJ061//Tianjin Municipal Education Commission Scientific Research Project/ ; },
abstract = {BACKGROUND: Laifu Chengqi Decoction (LF-CQD) is a traditional Chinese medicine enema rooted in classic heat-clearing and purgative formulas traditionally used to relieve abdominal distention, resolve stasis, and restore bowel motility. Its components (e.g., Laifuzi and Dahuang) provide plausible pro-motility and anti-inflammatory actions, supporting its culturally grounded use as a postoperative adjunct in pediatric perforated appendicitis. This study aimed to evaluate the clinical efficacy of LF-CQD enemas in the treatment of postoperative peritonitis in children.
METHODS: This prospective randomized controlled trial included 118 children with perforated appendicitis complicated by peritonitis. The LF-CQD group received LF-CQD retention enemas for 5 days, whereas the control group was administered saline enemas. The primary outcome was time to first passage of flatus (a core marker of gastrointestinal recovery). Key secondary outcomes included time to bowel sound resumption, time to oral intake, preoperative and postoperative day (POD) 3 and 7 inflammatory marker levels, complication rates at 6-month follow-up, antibiotic use, and length of hospital stay.
RESULTS: Gastrointestinal function recovery was significantly faster in the LF-CQD group than in the control group [bowel sound resumption (p < 0.001), flatus (p < 0.001), and oral intake (p < 0.001)]. On POD7, the LF-CQD group exhibited significantly lower inflammatory marker levels than the control group (C-reactive protein level: p < 0.001). Exploratory post-hoc analyses showed greater relative reductions (ΔCRP/ΔWBC) in the LFCQD group at all timepoints (all p < 0.05). Complication rates for intra-abdominal abscess (8.5% vs. 25.4%, p = 0.008) and adhesive intestinal obstruction (5.1% vs. 22%, p = 0.003) were reduced, and antibiotic use duration was shorter (p < 0.001).
CONCLUSIONS: LFCQD enema serves as a safe, well-tolerated adjuvant intervention for children with postoperative peritonitis secondary to complicated perforated appendicitis. It accelerates gastrointestinal function recovery and alleviates postoperative inflammation. However, being a single-center trial with a modest sample size, it yielded large treatment effects for intra-abdominal abscess, adhesive intestinal obstruction, and length of hospital stay; thus, these effect sizes warrant cautious interpretation and require validation in large-scale multicenter trials. Exploratory post hoc analyses also indicated reduced systemic inflammatory marker levels in the intervention group. We hypothesize that LFCQD may modulate inflammatory signaling cascades and promote gut microbiota homeostasis to drive these clinical improvements. However, as no direct assessment of these pathways or metagenomic profiling of the intestinal microbiome was performed during this trial, these mechanistic proposed mechanistic pathways remain speculative and unconfirmed. In conclusion, this study demonstrates clinical associations between LFCQD enema and improved postoperative outcomes, but does not establish definitive causal molecular mechanisms.
TRIAL REGISTRATION: International Traditional Medicine Clinical Trial Registry; ITMCTR2025001634. Retrospectively registered on July 24, 2025, which constitutes an methodological limitation of this trial. All primary and secondary outcomes, inclusion and exclusion criteria, and core study procedures were precisely predefined and finalized in 2019 at the study design stage, prior to the initiation of patient enrollment in January 2020. No post-hoc additions, deletions, or modifications to any trial outcomes were made after patient recruitment, data collection, or statistical analysis. The retrospective registration was merely delayed due to institutional administrative procedures for traditional Chinese medicine clinical trials, without any alteration to the originally designed trial endpoints. The updated Supplementary Material 1 provides a detailed item-by-item comparison between the registered protocol and manuscript-reported outcomes, confirming full consistency and integrity of all pre-specified endpoints.},
}
RevDate: 2026-07-17
Aspartame and asthma: immunomodulatory effects on airway inflammation.
Respiratory research pii:10.1186/s12931-026-03820-1 [Epub ahead of print].
BACKGROUND AND OBJECTIVE: Asthma is a heterogeneous inflammatory airway disease influenced by genetic and environmental factors, including diet. Aspartame, a widely used artificial sweetener, has been implicated in immunometabolic changes that may affect asthma risk, but the potential role evidence remains limited. We aimed to examine the association between aspartame intake and asthma outcomes using integrated human analyses and complementary animal experiments.
METHODS: Human data were obtained from 1021 adolescents in the Taiwan Puberty Longitudinal Study. Aspartame consumption, assessed using a validated food frequency questionnaire, was categorized as none, low, or high based on median intake. Asthma status was determined based on physician diagnosis and symptom history. In parallel, BALB/c mice were sensitized with house dust mite (HDM) extract and administered oral aspartame at 15, 30, or 60 mg/kg/day for 10 weeks. Immunological, microbiome, metabolic, and histopathological parameters were evaluated.
RESULTS: Low aspartame consumption was significantly associated with higher odds of asthma (odds ratio = 2.852; 95% confidence interval: 1.038-8.014; p = 0.0369). In mice, aspartame exposure increased serum IgE levels, airway inflammation, and MMP-12 and MCP-1 expression. Although lung function changes were not statistically significant, histological analyses revealed more pronounced goblet cell hyperplasia, peribronchial collagen deposition, and eosinophilic infiltration, especially in the 60 mg/kg group. Aspartame also reduced microbial α-diversity and altered microbial composition. Short-chain fatty acids profiling revealed significantly decreased isobutyric, hexanoic, and heptanoic acid levels in aspartame-treated mice.
CONCLUSIONS: Aspartame intake exacerbates asthma-related immunological, microbial, and histological disturbances.
Additional Links: PMID-42464261
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PubMed:
Citation:
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@article {pmid42464261,
year = {2026},
author = {Utami, FA and Huang, SY and Liu, YH and Hsu, JW and Mazariegos, JRR and Nguyen, NN and Huang, SW and Weng, CM and Chuang, HC and Huang, CH and Tsai, WL and Chen, YC},
title = {Aspartame and asthma: immunomodulatory effects on airway inflammation.},
journal = {Respiratory research},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12931-026-03820-1},
pmid = {42464261},
issn = {1465-993X},
support = {113-2628-B-038-006-MY3//National Science and Technology Council/ ; 112TMU-TMUH-02-1 and 113TMU-TMUH-01//Taipei Medical University Hospital/ ; },
abstract = {BACKGROUND AND OBJECTIVE: Asthma is a heterogeneous inflammatory airway disease influenced by genetic and environmental factors, including diet. Aspartame, a widely used artificial sweetener, has been implicated in immunometabolic changes that may affect asthma risk, but the potential role evidence remains limited. We aimed to examine the association between aspartame intake and asthma outcomes using integrated human analyses and complementary animal experiments.
METHODS: Human data were obtained from 1021 adolescents in the Taiwan Puberty Longitudinal Study. Aspartame consumption, assessed using a validated food frequency questionnaire, was categorized as none, low, or high based on median intake. Asthma status was determined based on physician diagnosis and symptom history. In parallel, BALB/c mice were sensitized with house dust mite (HDM) extract and administered oral aspartame at 15, 30, or 60 mg/kg/day for 10 weeks. Immunological, microbiome, metabolic, and histopathological parameters were evaluated.
RESULTS: Low aspartame consumption was significantly associated with higher odds of asthma (odds ratio = 2.852; 95% confidence interval: 1.038-8.014; p = 0.0369). In mice, aspartame exposure increased serum IgE levels, airway inflammation, and MMP-12 and MCP-1 expression. Although lung function changes were not statistically significant, histological analyses revealed more pronounced goblet cell hyperplasia, peribronchial collagen deposition, and eosinophilic infiltration, especially in the 60 mg/kg group. Aspartame also reduced microbial α-diversity and altered microbial composition. Short-chain fatty acids profiling revealed significantly decreased isobutyric, hexanoic, and heptanoic acid levels in aspartame-treated mice.
CONCLUSIONS: Aspartame intake exacerbates asthma-related immunological, microbial, and histological disturbances.},
}
RevDate: 2026-07-17
Highly penetrative nanocarrier modulates tumor bacteria to enhance oxygen-free photo immunotherapy in spinal metastatic cancer.
Journal of nanobiotechnology pii:10.1186/s12951-026-04810-7 [Epub ahead of print].
Microbiome and transcriptome analyses revealed that Fusobacterium nucleatum (F.n) in clinical samples is associated with immune suppression and poor prognosis in triple-negative breast cancer spinal metastasis. However, its preferential localization in hypoxic tumor regions limits the efficacy of conventional antimicrobial therapies, which poorly penetrate solid tumors and function suboptimally under anaerobic conditions. Developing strategies that enable deep tumor penetration, eliminate anaerobic bacteria, and induce immunogenic cell death remains a major challenge. In this study, a novel charge-enrichment and light-activated biomimetic nanosystem, designated as polyion liquid-bridged eosin Y (PIL-BEY), was developed. On one hand, interionic hydrogen bonding and dynamic electrostatic interactions within polyionic liquids reduce the surface energy of the nanoprobe and synergistically remodel the dense tumor stromal microenvironment via photodynamic therapy, thereby facilitating the deep intratumoral penetration and accumulation of PIL-BEY. On the other hand, the novel photosensitizer BEY generates reactive oxygen species via electron transfer under hypoxic conditions, thereby effectively eradicating bacteria within hypoxic tumor regions. The resulting pathogen-associated molecular patterns, together with damage-associated molecular patterns, activate dendritic cells, promote cytotoxic T lymphocyte infiltration, trigger immunogenic cell death, and induce systemic antitumor immune responses with durable immune memory. This oxygen-independent, dual-functional nanoplatform offers a promising strategy for treating invasive metastatic tumors.
Additional Links: PMID-42464276
Publisher:
PubMed:
Citation:
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@article {pmid42464276,
year = {2026},
author = {Jia, C and Lu, H and Wang, J and Hu, A and Aji, A and Chen, Q and Liang, B and Ma, Y and Wu, Z and Xue, F and Jiang, L and Dong, J},
title = {Highly penetrative nanocarrier modulates tumor bacteria to enhance oxygen-free photo immunotherapy in spinal metastatic cancer.},
journal = {Journal of nanobiotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12951-026-04810-7},
pmid = {42464276},
issn = {1477-3155},
support = {2024D031//Fujian Provincial Natural Science Foundation of China/ ; yg2023-27//Medical Engineering fund of Fudan University and Shanghai Oriental Talent Program/ ; No. 81972508, 82172738, 82272457, 82472396//National Natural Science Foundation of China/ ; },
abstract = {Microbiome and transcriptome analyses revealed that Fusobacterium nucleatum (F.n) in clinical samples is associated with immune suppression and poor prognosis in triple-negative breast cancer spinal metastasis. However, its preferential localization in hypoxic tumor regions limits the efficacy of conventional antimicrobial therapies, which poorly penetrate solid tumors and function suboptimally under anaerobic conditions. Developing strategies that enable deep tumor penetration, eliminate anaerobic bacteria, and induce immunogenic cell death remains a major challenge. In this study, a novel charge-enrichment and light-activated biomimetic nanosystem, designated as polyion liquid-bridged eosin Y (PIL-BEY), was developed. On one hand, interionic hydrogen bonding and dynamic electrostatic interactions within polyionic liquids reduce the surface energy of the nanoprobe and synergistically remodel the dense tumor stromal microenvironment via photodynamic therapy, thereby facilitating the deep intratumoral penetration and accumulation of PIL-BEY. On the other hand, the novel photosensitizer BEY generates reactive oxygen species via electron transfer under hypoxic conditions, thereby effectively eradicating bacteria within hypoxic tumor regions. The resulting pathogen-associated molecular patterns, together with damage-associated molecular patterns, activate dendritic cells, promote cytotoxic T lymphocyte infiltration, trigger immunogenic cell death, and induce systemic antitumor immune responses with durable immune memory. This oxygen-independent, dual-functional nanoplatform offers a promising strategy for treating invasive metastatic tumors.},
}
RevDate: 2026-07-17
Microbiota-derived metabolite landscapes modulate Fusobacterium fitness and colorectal cancer cell behaviour.
Gut pathogens pii:10.1186/s13099-026-00859-9 [Epub ahead of print].
BACKGROUND: Gut microbiota dysbiosis is increasingly viewed as a disruption of microbial metabolic functions rather than only a shift in microbial composition. Microbiota-derived metabolites not only shape microbial ecology but also directly influence surrounding host tissues by modulating epithelial cell signaling, inflammation, and tumor-associated processes. Among dysbiosis-associated microbes, Fusobacterium is consistently enriched in colorectal cancer (CRC) and contributes to tumor progression, yet the ecological factors regulating its expansion and interaction with host tissues remain unclear. Here, we investigated how microbiome-derived metabolite environments associated with healthy and dysbiotic microbial communities influence Fusobacterium fitness and colorectal epithelial cell behavior.
METHODS: CRC-associated dysbiosis was generated using an orthotopic murine CRC model combined with antibiotic-induced microbiota perturbation. Gut microbial communities were profiled using 16 S rRNA gene sequencing. Metabolite-enriched supernatants derived from healthy gut microbiota, oral microbiota, dysbiotic microbiota and probiotic cultures were evaluated for their effects on CRC-associated bacteria and Fusobacterium sp. growth, adhesion and invasion. These metabolite supernatants were applied to colorectal cancer cells and their effects on viability (MTT assay), migration (scratch assay), apoptosis (Annexin V-FITC flow cytometry), and inflammatory signaling (Western blot analysis of inflammatory markers) were evaluated.
RESULTS: CRC-associated dysbiosis showed reduced microbial diversity with enrichment of opportunistic taxa including Fusobacterium and depletion of beneficial commensals such as Lactobacillus and Bifidobacterium. Metabolite-enriched supernatants from healthy gut and oral microbiota suppressed Fusobacterium growth by 55-65% and reduced bacterial adhesion and invasion in epithelial cells. In epithelial models, these metabolite environments reduced CRC viability to 60% of untreated control, with comparatively smaller effects observed in non-cancerous epithelial cells. They also inhibited cell migration, accompanied by suppression of inflammatory signaling pathways including IL-6, IL-1β, NF-κB, and HIF-1α. In contrast, conditioned media from dysbiotic cancer-microbiota interactions increased tumor cell viability to 120-140% of controls. These findings suggest an association between microbiota-derived metabolite landscapes, pathobiont fitness and epithelial responses under CRC-associated dysbiosis.
Additional Links: PMID-42464327
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PubMed:
Citation:
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@article {pmid42464327,
year = {2026},
author = {Dhiman, C and Kumar, A and Sonak, SS and Erukulla, P and Nimbarte, VD and Narayan, KP},
title = {Microbiota-derived metabolite landscapes modulate Fusobacterium fitness and colorectal cancer cell behaviour.},
journal = {Gut pathogens},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13099-026-00859-9},
pmid = {42464327},
issn = {1757-4749},
abstract = {BACKGROUND: Gut microbiota dysbiosis is increasingly viewed as a disruption of microbial metabolic functions rather than only a shift in microbial composition. Microbiota-derived metabolites not only shape microbial ecology but also directly influence surrounding host tissues by modulating epithelial cell signaling, inflammation, and tumor-associated processes. Among dysbiosis-associated microbes, Fusobacterium is consistently enriched in colorectal cancer (CRC) and contributes to tumor progression, yet the ecological factors regulating its expansion and interaction with host tissues remain unclear. Here, we investigated how microbiome-derived metabolite environments associated with healthy and dysbiotic microbial communities influence Fusobacterium fitness and colorectal epithelial cell behavior.
METHODS: CRC-associated dysbiosis was generated using an orthotopic murine CRC model combined with antibiotic-induced microbiota perturbation. Gut microbial communities were profiled using 16 S rRNA gene sequencing. Metabolite-enriched supernatants derived from healthy gut microbiota, oral microbiota, dysbiotic microbiota and probiotic cultures were evaluated for their effects on CRC-associated bacteria and Fusobacterium sp. growth, adhesion and invasion. These metabolite supernatants were applied to colorectal cancer cells and their effects on viability (MTT assay), migration (scratch assay), apoptosis (Annexin V-FITC flow cytometry), and inflammatory signaling (Western blot analysis of inflammatory markers) were evaluated.
RESULTS: CRC-associated dysbiosis showed reduced microbial diversity with enrichment of opportunistic taxa including Fusobacterium and depletion of beneficial commensals such as Lactobacillus and Bifidobacterium. Metabolite-enriched supernatants from healthy gut and oral microbiota suppressed Fusobacterium growth by 55-65% and reduced bacterial adhesion and invasion in epithelial cells. In epithelial models, these metabolite environments reduced CRC viability to 60% of untreated control, with comparatively smaller effects observed in non-cancerous epithelial cells. They also inhibited cell migration, accompanied by suppression of inflammatory signaling pathways including IL-6, IL-1β, NF-κB, and HIF-1α. In contrast, conditioned media from dysbiotic cancer-microbiota interactions increased tumor cell viability to 120-140% of controls. These findings suggest an association between microbiota-derived metabolite landscapes, pathobiont fitness and epithelial responses under CRC-associated dysbiosis.},
}
RevDate: 2026-07-17
Chemical prophage induction selectively removes Vibrio from a pelagic Sargassum-derived multispecies biofilm.
Environmental microbiome pii:10.1186/s40793-026-00925-4 [Epub ahead of print].
BACKGROUND: Pelagic Sargassum has undergone significant range expansion and dramatic blooms in the Atlantic over the past 15 years. This alga's microbiome provides symbiotic functions that are believed to contribute to its ecological success. Recent research shows that Sargassum-associated bacteria are enriched in integrated prophages compared to the surrounding seawater and that these prophages are inducible by chemical and ultraviolet treatment.
RESULTS: Here, we investigated a Sargassum-derived in vitro multispecies biofilm encompassing the dominant heterotrophic microbial members associated with Sargassum to probe the impacts of prophage induction on the composition of Sargassum microbiomes. Induction was quantified by coverage-based virus-to-host ratios in chemically induced treatments with Mitomycin C and non-induced controls, and the community composition and metabolic profiles were analyzed after Mitomycin C treatment. Chemical induction led to a significant increase in abundance and virus-to-host ratio of viral genomes linked to Vibrio metagenome-assembled genomes. This was accompanied by altered biofilm community composition, with a reduction in Vibrio bacterial abundance that opened niche space for other biofilm members in the genera Pseudoalteromonas, Alteromonas, and Cobetia. The induced Vibrio-associated phages encoded genes involved in quorum sensing, biofilm formation, virulence, and host metabolism. Induction led to the depletion of 17 metabolic modules, including functions related to energy metabolism and nitrogen utilization.
CONCLUSION: Due to the high frequency of lysogeny in the Sargassum microbiome and the susceptibility of prophages to chemical and ultraviolet light induction, these results suggest that prophage integration and induction are mechanisms that contribute to structuring the Sargassum microbiome and its functional profiles, potentially aiding in microbiome flexibility in changing environmental contexts.
Additional Links: PMID-42464402
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PubMed:
Citation:
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@article {pmid42464402,
year = {2026},
author = {Stiffler, AK and Varona, NS and Wallace, BA and Silveira, CB},
title = {Chemical prophage induction selectively removes Vibrio from a pelagic Sargassum-derived multispecies biofilm.},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-026-00925-4},
pmid = {42464402},
issn = {2524-6372},
support = {2023349872//National Science Foundation Graduate Research Fellowship Program/ ; 2023353157//National Science Foundation Graduate Research Fellowship Program/ ; 80NSSC23K0676/NASA/NASA/United States ; 2424579//National Science Foundation/ ; },
abstract = {BACKGROUND: Pelagic Sargassum has undergone significant range expansion and dramatic blooms in the Atlantic over the past 15 years. This alga's microbiome provides symbiotic functions that are believed to contribute to its ecological success. Recent research shows that Sargassum-associated bacteria are enriched in integrated prophages compared to the surrounding seawater and that these prophages are inducible by chemical and ultraviolet treatment.
RESULTS: Here, we investigated a Sargassum-derived in vitro multispecies biofilm encompassing the dominant heterotrophic microbial members associated with Sargassum to probe the impacts of prophage induction on the composition of Sargassum microbiomes. Induction was quantified by coverage-based virus-to-host ratios in chemically induced treatments with Mitomycin C and non-induced controls, and the community composition and metabolic profiles were analyzed after Mitomycin C treatment. Chemical induction led to a significant increase in abundance and virus-to-host ratio of viral genomes linked to Vibrio metagenome-assembled genomes. This was accompanied by altered biofilm community composition, with a reduction in Vibrio bacterial abundance that opened niche space for other biofilm members in the genera Pseudoalteromonas, Alteromonas, and Cobetia. The induced Vibrio-associated phages encoded genes involved in quorum sensing, biofilm formation, virulence, and host metabolism. Induction led to the depletion of 17 metabolic modules, including functions related to energy metabolism and nitrogen utilization.
CONCLUSION: Due to the high frequency of lysogeny in the Sargassum microbiome and the susceptibility of prophages to chemical and ultraviolet light induction, these results suggest that prophage integration and induction are mechanisms that contribute to structuring the Sargassum microbiome and its functional profiles, potentially aiding in microbiome flexibility in changing environmental contexts.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
Eukaryotic and bacterial gut communities vary along a lifestyle-associated urbanization gradient: comparative analysis of Germany and Madagascar.
Gut microbes, 18(1):2701492.
Intestinal eukaryotes, often neglected in gut microbiome studies, play crucial roles in human health and cause life-threatening diseases affecting millions worldwide. This neglect has also been driven by the underrepresentation of samples from regions with a high prevalence of (parasitic) intestinal eukaryotes. As a result, the overall understanding of how intestinal eukaryotes vary among broad lifestyle and socioeconomic differences, remains limited. Addressing this gap is increasingly urgent given the global rise of urbanization and industrialization and their profound effects on lifestyle, pathogen exposure, and environmental factors. We characterized the diversity and composition of eukaryotic and bacterial microbiota in 1387 fecal samples from Madagascar (Andina, Ankazomborona, Tsiroanomandidy) and Germany (Kiel), spanning a composite gradient of urbanization-associated lifestyles. Using a parallel approach of 18S V4-V5 rRNA and 16S V3-V4 rRNA amplicon gene sequencing, we identified distinct regional patterns in eukaryotic and bacterial community composition. Malagasy cohorts showed higher prevalence of helminths (e.g. Schistosoma, Necator) and protozoa (e.g. Entamoeba, Dientamoeba). Notably, the diversity of particularly food-associated fungi increased along the composite urbanization-associated lifestyle gradient, peaking in samples from Germany. Bacterial 16S amplicon sequencing confirmed and extended known geographical differences, showing a dominance of Bacteroides in Germany versus Prevotella and Firmicutes in Madagascar. This work highlights the importance of integrating eukaryotic and prokaryotic data, as well as considering different lifestyle-associated factors in microbiome research. We further highlight the need for deeper investigation into the role of dietary and environmental fungi in the human gut ecosystem.
Additional Links: PMID-42464572
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PubMed:
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@article {pmid42464572,
year = {2026},
author = {Saalfrank, J and Rühlemann, MC and Rausch, P and Hey, JC and Rakotoarivelo, RA and Rasamoelina, T and Rakotozandrindrainy, R and Randriamampionona, N and Schwarz, NG and Razafindrakoto, R and Fusco, D and Franke, A and Bang, C},
title = {Eukaryotic and bacterial gut communities vary along a lifestyle-associated urbanization gradient: comparative analysis of Germany and Madagascar.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2701492},
doi = {10.1080/19490976.2026.2701492},
pmid = {42464572},
issn = {1949-0984},
mesh = {Madagascar ; Humans ; Germany ; *Urbanization ; *Bacteria/classification/genetics/isolation & purification ; *Gastrointestinal Microbiome ; Feces/microbiology/parasitology ; Animals ; Life Style ; *Eukaryota/classification/isolation & purification/genetics ; RNA, Ribosomal, 16S/genetics ; Female ; Male ; Adult ; Adolescent ; Young Adult ; Child ; Fungi/classification/genetics/isolation & purification ; },
abstract = {Intestinal eukaryotes, often neglected in gut microbiome studies, play crucial roles in human health and cause life-threatening diseases affecting millions worldwide. This neglect has also been driven by the underrepresentation of samples from regions with a high prevalence of (parasitic) intestinal eukaryotes. As a result, the overall understanding of how intestinal eukaryotes vary among broad lifestyle and socioeconomic differences, remains limited. Addressing this gap is increasingly urgent given the global rise of urbanization and industrialization and their profound effects on lifestyle, pathogen exposure, and environmental factors. We characterized the diversity and composition of eukaryotic and bacterial microbiota in 1387 fecal samples from Madagascar (Andina, Ankazomborona, Tsiroanomandidy) and Germany (Kiel), spanning a composite gradient of urbanization-associated lifestyles. Using a parallel approach of 18S V4-V5 rRNA and 16S V3-V4 rRNA amplicon gene sequencing, we identified distinct regional patterns in eukaryotic and bacterial community composition. Malagasy cohorts showed higher prevalence of helminths (e.g. Schistosoma, Necator) and protozoa (e.g. Entamoeba, Dientamoeba). Notably, the diversity of particularly food-associated fungi increased along the composite urbanization-associated lifestyle gradient, peaking in samples from Germany. Bacterial 16S amplicon sequencing confirmed and extended known geographical differences, showing a dominance of Bacteroides in Germany versus Prevotella and Firmicutes in Madagascar. This work highlights the importance of integrating eukaryotic and prokaryotic data, as well as considering different lifestyle-associated factors in microbiome research. We further highlight the need for deeper investigation into the role of dietary and environmental fungi in the human gut ecosystem.},
}
MeSH Terms:
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Madagascar
Humans
Germany
*Urbanization
*Bacteria/classification/genetics/isolation & purification
*Gastrointestinal Microbiome
Feces/microbiology/parasitology
Animals
Life Style
*Eukaryota/classification/isolation & purification/genetics
RNA, Ribosomal, 16S/genetics
Female
Male
Adult
Adolescent
Young Adult
Child
Fungi/classification/genetics/isolation & purification
RevDate: 2026-07-17
Meta-Analysis of DNA methylation and gut microbiome data in preterm birth reveals epigenetic and microbial biomarkers for early diagnosis and probiotic-based intervention.
Archives of physiology and biochemistry [Epub ahead of print].
Background: Globally, preterm birth continues to be a major contributor to neonatal morbidity and mortality. Developing early diagnostics and focused interventions requires an understanding of the molecular and microbiome factors causing preterm birth and also the identification of biomarkers. Methods: We integrated gut microbiome and DNA methylation data to identify biomarkers of preterm birth. Analysis of GSE120458 revealed 1,609 differentially methylated regions involved in immune, hormonal, and neurodevelopmental pathways. Microbiome profiling identified five altered genera: Faecalibacterium prausnitzii, Streptococcus, Blautia faecis, Gemella, and Agathobacter. Taxon Set Enrichment Analysis revealed that these genera were found to be associated with systemic diseases like diabetes, obesity, and inflammatory bowel disease. Results: We identified 1,649 genes targeted by 33 microbial metabolites, with 17 overlapping methylated genes indicating microbiome-epigenome interactions. These genes were linked to neuroimmune and synaptic pathways. Conclusion: Hub genes may serve as biomarkers for early intervention. Overall, the results connect microbial metabolism with epigenetic regulation in preterm birth.
Additional Links: PMID-42464791
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@article {pmid42464791,
year = {2026},
author = {Li, L and Wang, C and Liu, C and Dong, Y},
title = {Meta-Analysis of DNA methylation and gut microbiome data in preterm birth reveals epigenetic and microbial biomarkers for early diagnosis and probiotic-based intervention.},
journal = {Archives of physiology and biochemistry},
volume = {},
number = {},
pages = {1-13},
doi = {10.1080/13813455.2026.2699137},
pmid = {42464791},
issn = {1744-4160},
abstract = {Background: Globally, preterm birth continues to be a major contributor to neonatal morbidity and mortality. Developing early diagnostics and focused interventions requires an understanding of the molecular and microbiome factors causing preterm birth and also the identification of biomarkers. Methods: We integrated gut microbiome and DNA methylation data to identify biomarkers of preterm birth. Analysis of GSE120458 revealed 1,609 differentially methylated regions involved in immune, hormonal, and neurodevelopmental pathways. Microbiome profiling identified five altered genera: Faecalibacterium prausnitzii, Streptococcus, Blautia faecis, Gemella, and Agathobacter. Taxon Set Enrichment Analysis revealed that these genera were found to be associated with systemic diseases like diabetes, obesity, and inflammatory bowel disease. Results: We identified 1,649 genes targeted by 33 microbial metabolites, with 17 overlapping methylated genes indicating microbiome-epigenome interactions. These genes were linked to neuroimmune and synaptic pathways. Conclusion: Hub genes may serve as biomarkers for early intervention. Overall, the results connect microbial metabolism with epigenetic regulation in preterm birth.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
Gut Microbiome Alterations in Cancer and Non-cancer Adults: A Cross-Sectional Metagenomic Study.
Technology in cancer research & treatment, 25:15330338261470516.
IntroductionPrevious studies found associations between cancer and the gut microbiome. Thus, we aimed to investigate the gut microbiome composition in adults with and without cancer to try to identify specific microbes that may be associated with cancer in a cross-sectional, observational, and retrospective study.MethodsStool samples from sixty participants, n=20 controls, n=25 with aggressive cancer, and n=15 with non-aggressive cancer were analyzed using Metagenomic Next Generation Sequencing. Mann-Whitney U test tests were used to examine differences in the relative abundances of bacterial genera.ResultsCompared to controls, aggressive cancer patients had statistically significantly lower levels of gut Bifidobacterium, Faecalibacterium, and Collinsella, (all p≤0.05), while they had higher levels of gut Bacteroides (p=0.015). Non-aggressive cancer patients had lower levels of gut Bifidobacterium compared to controls, an association that was approaching statistical significance (p=0.054).ConclusionAggressive-cancer patients showed significantly altered levels of key gut microbes compared to controls. These are preliminary associations, and thus further larger studies are needed to confirm these findings.
Additional Links: PMID-42464944
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@article {pmid42464944,
year = {2026},
author = {Hazan, S and Bao, G and Goudzwaard, A and Ichim, T and Martin, L and Vidal, AC},
title = {Gut Microbiome Alterations in Cancer and Non-cancer Adults: A Cross-Sectional Metagenomic Study.},
journal = {Technology in cancer research & treatment},
volume = {25},
number = {},
pages = {15330338261470516},
doi = {10.1177/15330338261470516},
pmid = {42464944},
issn = {1533-0338},
mesh = {Humans ; Female ; *Metagenomics/methods ; *Gastrointestinal Microbiome/genetics ; Cross-Sectional Studies ; *Neoplasms/microbiology/pathology ; Male ; Middle Aged ; High-Throughput Nucleotide Sequencing ; Adult ; Aged ; *Bacteria/classification/genetics ; Metagenome ; Retrospective Studies ; },
abstract = {IntroductionPrevious studies found associations between cancer and the gut microbiome. Thus, we aimed to investigate the gut microbiome composition in adults with and without cancer to try to identify specific microbes that may be associated with cancer in a cross-sectional, observational, and retrospective study.MethodsStool samples from sixty participants, n=20 controls, n=25 with aggressive cancer, and n=15 with non-aggressive cancer were analyzed using Metagenomic Next Generation Sequencing. Mann-Whitney U test tests were used to examine differences in the relative abundances of bacterial genera.ResultsCompared to controls, aggressive cancer patients had statistically significantly lower levels of gut Bifidobacterium, Faecalibacterium, and Collinsella, (all p≤0.05), while they had higher levels of gut Bacteroides (p=0.015). Non-aggressive cancer patients had lower levels of gut Bifidobacterium compared to controls, an association that was approaching statistical significance (p=0.054).ConclusionAggressive-cancer patients showed significantly altered levels of key gut microbes compared to controls. These are preliminary associations, and thus further larger studies are needed to confirm these findings.},
}
MeSH Terms:
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hide MeSH Terms
Humans
Female
*Metagenomics/methods
*Gastrointestinal Microbiome/genetics
Cross-Sectional Studies
*Neoplasms/microbiology/pathology
Male
Middle Aged
High-Throughput Nucleotide Sequencing
Adult
Aged
*Bacteria/classification/genetics
Metagenome
Retrospective Studies
RevDate: 2026-07-17
Water Deficit Does Not Compromise the Resistance to Insect Herbivores in Plants Associated With Fungal Endophytes Able to Produce Bioactive Alkaloids.
Plant, cell & environment [Epub ahead of print].
Plants growing in nature are exposed to multiple abiotic and biotic stressors that sometimes occur sequentially. We hypothesised that drought will not compromise the resistance levels to herbivores when plants are associated with Epichloë endophytes able to produce bioactive alkaloids. Lolium perenne plants without (nil) and with Epichloë LpTG-3 sp. strain AR37 able (wild type (wt), ∆idtA) and unable (∆idtM) to produce indole diterpene alkaloids were subjected to a drought treatment followed by a challenge with Rhopalosiphum padi aphids at drought recovery. Drought increased the susceptibility to aphids in both nil and ∆idtM-associated plants, whereas it did not affect the aphid resistance in wt-associated plants. Drought increased the aphid resistance in ∆idtD-associated plants, a response that was related to a drought-mediated increase in concentrations of some AR37-derived alkaloids. The negative effects of drought on plants were alleviated through the AR37 symbiosis via host growth promotion associated with increased concentrations of drought protective phytohormones and amino acids (e.g., abscisic acid and proline), and enriched abundance of bacteria belonging to Agrococcus, Chryseobacterium, and Parcubacteria that contain members providing stress protective traits. Our study highlights the key role of endophytes in increasing the performance of plants challenged by abiotic and biotic stressors.
Additional Links: PMID-42464967
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@article {pmid42464967,
year = {2026},
author = {BastÃas, DA and Kumar, S and Prakash, S and Mace, WJ and Morozova, Y and Johnson, RD},
title = {Water Deficit Does Not Compromise the Resistance to Insect Herbivores in Plants Associated With Fungal Endophytes Able to Produce Bioactive Alkaloids.},
journal = {Plant, cell & environment},
volume = {},
number = {},
pages = {},
doi = {10.1111/pce.70756},
pmid = {42464967},
issn = {1365-3040},
support = {//Ministry of Business, Innovation and Employment (MBIE)/ ; },
abstract = {Plants growing in nature are exposed to multiple abiotic and biotic stressors that sometimes occur sequentially. We hypothesised that drought will not compromise the resistance levels to herbivores when plants are associated with Epichloë endophytes able to produce bioactive alkaloids. Lolium perenne plants without (nil) and with Epichloë LpTG-3 sp. strain AR37 able (wild type (wt), ∆idtA) and unable (∆idtM) to produce indole diterpene alkaloids were subjected to a drought treatment followed by a challenge with Rhopalosiphum padi aphids at drought recovery. Drought increased the susceptibility to aphids in both nil and ∆idtM-associated plants, whereas it did not affect the aphid resistance in wt-associated plants. Drought increased the aphid resistance in ∆idtD-associated plants, a response that was related to a drought-mediated increase in concentrations of some AR37-derived alkaloids. The negative effects of drought on plants were alleviated through the AR37 symbiosis via host growth promotion associated with increased concentrations of drought protective phytohormones and amino acids (e.g., abscisic acid and proline), and enriched abundance of bacteria belonging to Agrococcus, Chryseobacterium, and Parcubacteria that contain members providing stress protective traits. Our study highlights the key role of endophytes in increasing the performance of plants challenged by abiotic and biotic stressors.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
Quenching corrinoid-based interactions in a model bacterial coculture.
ISME communications, 6(1):ycag160.
Microbial community structure is driven, in part, by the metabolic interdependencies of resident microbes. Thus, manipulating specific metabolic interactions represents an attractive way to both understand how microbial communities perform complex functions and alter them for therapeutic or environmental effects. However, it is not yet possible to control the availability of those metabolites produced by some members of the community that are required by others. Here, we report the development of a metabolite "quenching" strategy that disrupts a specific metabolic interaction involving corrinoids, the vitamin B12 family of cofactors, by applying a high-affinity corrinoid-binding protein, BtuG, to bacteria engaged in corrinoid cross-feeding. Using a model coculture composed of Sinorhizobium meliloti, a bacterium that produces a corrinoid (cobalamin), and an Escherichia coli strain engineered to be corrinoid-dependent, we demonstrate corrinoid quenching by sequestration of extracellular corrinoid, leading to inhibition of corrinoid-dependent growth. This work establishes a strategy to selectively block microbial interactions that may be more broadly applied to dissecting community structure and function. We expect that applying high-affinity "molecular sponges" to quench nutrient sharing will allow for the identification of key nutrients that structure microbial communities and potentiate precision microbiome manipulation strategies.
Additional Links: PMID-42465057
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@article {pmid42465057,
year = {2026},
author = {Hallberg, ZF and Alvarez-Aponte, ZI and Gaudinier, A and Taga, ME},
title = {Quenching corrinoid-based interactions in a model bacterial coculture.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag160},
pmid = {42465057},
issn = {2730-6151},
abstract = {Microbial community structure is driven, in part, by the metabolic interdependencies of resident microbes. Thus, manipulating specific metabolic interactions represents an attractive way to both understand how microbial communities perform complex functions and alter them for therapeutic or environmental effects. However, it is not yet possible to control the availability of those metabolites produced by some members of the community that are required by others. Here, we report the development of a metabolite "quenching" strategy that disrupts a specific metabolic interaction involving corrinoids, the vitamin B12 family of cofactors, by applying a high-affinity corrinoid-binding protein, BtuG, to bacteria engaged in corrinoid cross-feeding. Using a model coculture composed of Sinorhizobium meliloti, a bacterium that produces a corrinoid (cobalamin), and an Escherichia coli strain engineered to be corrinoid-dependent, we demonstrate corrinoid quenching by sequestration of extracellular corrinoid, leading to inhibition of corrinoid-dependent growth. This work establishes a strategy to selectively block microbial interactions that may be more broadly applied to dissecting community structure and function. We expect that applying high-affinity "molecular sponges" to quench nutrient sharing will allow for the identification of key nutrients that structure microbial communities and potentiate precision microbiome manipulation strategies.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
Coordinated plant and microbial transcriptional responses to oil-sands process-affected water.
ISME communications, 6(1):ycag152.
Constructed wetland treatment systems (CWTSs) are promising options for treating oil-sands process-affected water (OSPW), which contains toxic naphthenic acid fraction compounds (NAFCs). However, the molecular mechanisms underlying NAFCs attenuation by plants and root microbes remain poorly resolved. In our previous mesocosm study, Typha latifolia increased NAFC removal 2.5-fold relative to unplanted controls without reducing plant growth. Here, using RNA from that same experimental system, we applied metatranscriptomics to 40 root samples collected over 60 days to characterize plant and active microbial responses to OSPW exposure. The active root-associated microbial community was dominated by Pseudomonadota, and Burkholderiales remained the most active order, although Flavobacteriaceae (Bacteroidota) activity increased with time when exposed to OSPW. Microbial community composition shifted with both time and water type, and 42 genes with potential roles in NAFC or related organic-compound transformation were differentially expressed in OSPW mesocosms. These responses were dominated by oxidoreductases affiliated mainly with Burkholderiales and Rhizobiales. The host plant also responded strongly to OSPW, up-regulating genes encoding oxidoreductases, transporters, and glycosyltransferases associated with xenobiotic stress and detoxification. Together, these results revealed coordinated plant and microbial transcriptional responses in a system where enhanced NAFC attenuation had already been demonstrated chemically. The observed patterns, however, likely reflect the broader OSPW mixture rather than NAFCs alone.
Additional Links: PMID-42465063
PubMed:
Citation:
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@article {pmid42465063,
year = {2026},
author = {Nweze, JE and Morvan, S and Samad, A and Bergeron, MJ and Degenhardt, D and Tremblay, J and Symonds, K and Muench, DG and Martineau, C and Yergeau, E},
title = {Coordinated plant and microbial transcriptional responses to oil-sands process-affected water.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag152},
pmid = {42465063},
issn = {2730-6151},
abstract = {Constructed wetland treatment systems (CWTSs) are promising options for treating oil-sands process-affected water (OSPW), which contains toxic naphthenic acid fraction compounds (NAFCs). However, the molecular mechanisms underlying NAFCs attenuation by plants and root microbes remain poorly resolved. In our previous mesocosm study, Typha latifolia increased NAFC removal 2.5-fold relative to unplanted controls without reducing plant growth. Here, using RNA from that same experimental system, we applied metatranscriptomics to 40 root samples collected over 60 days to characterize plant and active microbial responses to OSPW exposure. The active root-associated microbial community was dominated by Pseudomonadota, and Burkholderiales remained the most active order, although Flavobacteriaceae (Bacteroidota) activity increased with time when exposed to OSPW. Microbial community composition shifted with both time and water type, and 42 genes with potential roles in NAFC or related organic-compound transformation were differentially expressed in OSPW mesocosms. These responses were dominated by oxidoreductases affiliated mainly with Burkholderiales and Rhizobiales. The host plant also responded strongly to OSPW, up-regulating genes encoding oxidoreductases, transporters, and glycosyltransferases associated with xenobiotic stress and detoxification. Together, these results revealed coordinated plant and microbial transcriptional responses in a system where enhanced NAFC attenuation had already been demonstrated chemically. The observed patterns, however, likely reflect the broader OSPW mixture rather than NAFCs alone.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
Perturbations shift the composition of bacterial DNA carried by virus-like particles in the murine gut microbiome.
bioRxiv : the preprint server for biology pii:2026.07.08.737213.
Horizontal gene transfer (HGT) is a driving force in microbial evolution that allows community members to rapidly evolve to cope with environmental stressors and competition. Despite the importance of HGT for the generation of genetic diversity, little is known about the specific mechanisms or dynamics of transfer in complex communities. Transductomics is a sequencing based technique which identifies potential HGT by bacteriophages (transduction) through sequencing of the transductome - the DNA carried by bacteriophages and other virus-like particles in a sample. We analyzed the murine gut transductome before and after perturbations with antibiotics and Clostridioides difficile infection (CDI). We found that several bacterial families - the Oscillospiraceae, Butyricoccaceae, and Turicibactericeae - disproportionally contributed to the transductome. Some families, like the Butyricicoccaceae, were frequent transducers in both the baseline and perturbed murine gut microbiome while other taxa displayed condition-specific transduction indicating that there may be specific transducing subpopulations or regulatory mechanisms controlling transduction frequency. Additionally, we found a diversity of highly abundant and enriched mobile genetic elements (MGEs) in the transductome including plasmids, integrative conjugative elements, phage satellites and transposons. The detection of MGEs containing conjugative elements suggest that some MGEs may spread through both transduction and conjugation. Overall, our work reveals a complex network of gene exchange occurring through transduction in the gut microbiome.
Additional Links: PMID-42465308
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@article {pmid42465308,
year = {2026},
author = {Maier, JL and Callahan, B and Duerkop, BA and Kleiner, M},
title = {Perturbations shift the composition of bacterial DNA carried by virus-like particles in the murine gut microbiome.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.08.737213},
pmid = {42465308},
issn = {2692-8205},
abstract = {Horizontal gene transfer (HGT) is a driving force in microbial evolution that allows community members to rapidly evolve to cope with environmental stressors and competition. Despite the importance of HGT for the generation of genetic diversity, little is known about the specific mechanisms or dynamics of transfer in complex communities. Transductomics is a sequencing based technique which identifies potential HGT by bacteriophages (transduction) through sequencing of the transductome - the DNA carried by bacteriophages and other virus-like particles in a sample. We analyzed the murine gut transductome before and after perturbations with antibiotics and Clostridioides difficile infection (CDI). We found that several bacterial families - the Oscillospiraceae, Butyricoccaceae, and Turicibactericeae - disproportionally contributed to the transductome. Some families, like the Butyricicoccaceae, were frequent transducers in both the baseline and perturbed murine gut microbiome while other taxa displayed condition-specific transduction indicating that there may be specific transducing subpopulations or regulatory mechanisms controlling transduction frequency. Additionally, we found a diversity of highly abundant and enriched mobile genetic elements (MGEs) in the transductome including plasmids, integrative conjugative elements, phage satellites and transposons. The detection of MGEs containing conjugative elements suggest that some MGEs may spread through both transduction and conjugation. Overall, our work reveals a complex network of gene exchange occurring through transduction in the gut microbiome.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
A family of RRM-1 RNA binding proteins enables cold adaptation and environmental resilience in Bacteroides.
bioRxiv : the preprint server for biology pii:2026.07.07.737135.
UNLABELLED: Bacteria use post-transcriptional regulatory mechanisms to rapidly adjust gene expression during environmental change. In the gut-associated genus Bacteroides, these mechanisms remain poorly defined as these organisms lack canonical RNA chaperones like Hfq and CsrA that coordinate post-transcriptional stress responses in many well-studied model bacteria. Most Bacteroides possess conserved RNA recognition motif-1 (RRM-1) domain-containing RNA-binding proteins (more common in eukaryotes than bacteria) that have been proposed to act as global RNA chaperones. Here, we show that these RNA binding proteins (RBPs) are central to cold stress adaptation. Simultaneous deletion of all rbp genes produces a cold-sensitive growth defect across multiple Bacteroides species, while single deletions do not, revealing conserved functional redundancy. RBP transcripts and proteins accumulate rapidly after temperature downshift, and loss of RBPs extensively reprograms the transcriptome. Cold sensitivity of Bacteroides rbp mutants is not caused by defects in ribosome assembly or rRNA maturation. Instead, we find that in Bacteroides thetaiotaomicron, RBPs act together with BT1884, the sole canonical cold shock protein possessed by this organism. The combined loss of RBPs and BT1884 produces a synthetic severe cold sensitivity phenotype, defining two functionally redundant cold stress systems belonging to unrelated protein families. Strains lacking RBPs show reduced survival under simultaneous cold and oxygen stress, the conditions Bacteroides cells are expected to encounter during host-to-host transmission. Together, these findings establish RRM-1 RBPs as non-canonical cold shock proteins that enable cold adaptation and environmental survival in Bacteroides and suggest how these organisms withstand the stresses of transmission between hosts.
IMPORTANCE: Bacteroides species are among the most abundant and stable members of the human gut microbiome, and they are also among the most readily transmitted between people. Reaching a new host requires surviving conditions outside the gut, including cold and oxygen exposure, yet how these bacteria withstand such stress is not well understood. Most bacteria manage stress using a well-defined set of RNA-binding proteins, but Bacteroides lack these canonical factors. We show that Bacteroides instead rely on a different family of RNA-binding proteins, more typical of eukaryotes than bacteria, to survive cold stress, and that these proteins promote survival under the conditions encountered during transmission. This work identifies a molecular system that allows an abundant and ecologically successful gut bacterium to endure the environmental challenges of moving between hosts.
Additional Links: PMID-42465325
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@article {pmid42465325,
year = {2026},
author = {Lee, H and Basu, A and Vanderpool, CK},
title = {A family of RRM-1 RNA binding proteins enables cold adaptation and environmental resilience in Bacteroides.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.07.737135},
pmid = {42465325},
issn = {2692-8205},
abstract = {UNLABELLED: Bacteria use post-transcriptional regulatory mechanisms to rapidly adjust gene expression during environmental change. In the gut-associated genus Bacteroides, these mechanisms remain poorly defined as these organisms lack canonical RNA chaperones like Hfq and CsrA that coordinate post-transcriptional stress responses in many well-studied model bacteria. Most Bacteroides possess conserved RNA recognition motif-1 (RRM-1) domain-containing RNA-binding proteins (more common in eukaryotes than bacteria) that have been proposed to act as global RNA chaperones. Here, we show that these RNA binding proteins (RBPs) are central to cold stress adaptation. Simultaneous deletion of all rbp genes produces a cold-sensitive growth defect across multiple Bacteroides species, while single deletions do not, revealing conserved functional redundancy. RBP transcripts and proteins accumulate rapidly after temperature downshift, and loss of RBPs extensively reprograms the transcriptome. Cold sensitivity of Bacteroides rbp mutants is not caused by defects in ribosome assembly or rRNA maturation. Instead, we find that in Bacteroides thetaiotaomicron, RBPs act together with BT1884, the sole canonical cold shock protein possessed by this organism. The combined loss of RBPs and BT1884 produces a synthetic severe cold sensitivity phenotype, defining two functionally redundant cold stress systems belonging to unrelated protein families. Strains lacking RBPs show reduced survival under simultaneous cold and oxygen stress, the conditions Bacteroides cells are expected to encounter during host-to-host transmission. Together, these findings establish RRM-1 RBPs as non-canonical cold shock proteins that enable cold adaptation and environmental survival in Bacteroides and suggest how these organisms withstand the stresses of transmission between hosts.
IMPORTANCE: Bacteroides species are among the most abundant and stable members of the human gut microbiome, and they are also among the most readily transmitted between people. Reaching a new host requires surviving conditions outside the gut, including cold and oxygen exposure, yet how these bacteria withstand such stress is not well understood. Most bacteria manage stress using a well-defined set of RNA-binding proteins, but Bacteroides lack these canonical factors. We show that Bacteroides instead rely on a different family of RNA-binding proteins, more typical of eukaryotes than bacteria, to survive cold stress, and that these proteins promote survival under the conditions encountered during transmission. This work identifies a molecular system that allows an abundant and ecologically successful gut bacterium to endure the environmental challenges of moving between hosts.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
Senescence-associated loss of intestinal α1,2-fucose disrupts a modifiable host-microbiome homeostasis axis in people with HIV.
bioRxiv : the preprint server for biology pii:2026.07.09.736798.
BACKGROUND: People with HIV (PWH), despite effective antiretroviral therapy (ART), experience disrupted intestinal homeostasis characterized by microbial dysbiosis and impaired intestinal barrier integrity, which contribute to chronic inflammation and aging-associated comorbidities. However, tractable mechanisms contributing to this dysfunction remain poorly defined.
OBJECTIVE: To determine whether acquired loss of intestinal α1,2-fucose, a host-derived intrinsic prebiotic glycan that supports colonization by short-chain fatty acid (SCFA)-producing bacteria essential for intestinal barrier integrity, contributes to microbiome disruption, impaired epithelial resilience, inflammation, and biological aging in PWH.
DESIGN: Ileal and colonic biopsies, isolated crypts, stool, and blood from PWH on ART and controls underwent multi-omic analyses. Findings were mechanistically interrogated using stool anaerobic fermentation assays and 3D intestinal organoid models of stress-mediated epithelial disruption.
RESULTS: In intestinal tissues, PWH exhibited reduced α1,2-fucosylation and increased senescence-associated expression of the fucose-degrading enzyme α-L-fucosidase. Lower α1,2-fucose tracked with depletion of SCFA-producing bacteria, increased inflammation, and premature biological aging. In anaerobic fermentations, stool from PWH produced fewer SCFAs than controls, whereas supplementation with the human-milk-oligosaccharide-derived α1,2-fucose donor 2'-fucosyllactose restored SCFA production and improved intestinal organoid resilience to stress-mediated disruption.
CONCLUSION: These findings identify acquired loss of intestinal α1,2-fucose as a modifiable host-microbiome mechanism linking epithelial senescence, microbial metabolic dysfunction, impaired barrier resilience, inflammation, and biological aging in treated HIV infection.
SUMMARY BOX: What is already known on this topic: People with HIV on suppressive antiretroviral therapy frequently have persistent intestinal barrier dysfunction, microbial dysbiosis, chronic inflammation, and accelerated biological aging, but the host mechanisms that maintain this disrupted mucosal state remain incompletely defined.What this study adds: This study identifies acquired loss of intestinal α1,2-fucosylation as a feature of treated HIV infection and links this defect to a host fucosidase-high, senescence-enriched mucosal niche, depletion of SCFA-producing bacteria, impaired tight junction-associated barrier signatures, inflammation, and biological aging phenotypes.How this study might affect research, practice or policy: These findings support intestinal glycan ecology as a modifiable host-microbiome axis and provide a rationale for testing α1,2-fucose-replenishing strategies, such as 2'-fucosyllactose, to restore microbial metabolic output and improve epithelial resilience in people with HIV.
Additional Links: PMID-42465415
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@article {pmid42465415,
year = {2026},
author = {Giron, LB and Shaikh, MW and Jungles, TMC and Zhang, L and Engen, PA and Bulut, N and Singh, S and Hasson, JM and Zhang, E and Shankaran, S and Neumann, C and Villanueva, M and Landay, AL and Hope, TJ and Palella, FJ and Corley, MJ and Tateno, H and Hamaker, B and Auslander, N and Redondo, RL and Keshavarzian, A and Abdel-Mohsen, M},
title = {Senescence-associated loss of intestinal α1,2-fucose disrupts a modifiable host-microbiome homeostasis axis in people with HIV.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.09.736798},
pmid = {42465415},
issn = {2692-8205},
abstract = {BACKGROUND: People with HIV (PWH), despite effective antiretroviral therapy (ART), experience disrupted intestinal homeostasis characterized by microbial dysbiosis and impaired intestinal barrier integrity, which contribute to chronic inflammation and aging-associated comorbidities. However, tractable mechanisms contributing to this dysfunction remain poorly defined.
OBJECTIVE: To determine whether acquired loss of intestinal α1,2-fucose, a host-derived intrinsic prebiotic glycan that supports colonization by short-chain fatty acid (SCFA)-producing bacteria essential for intestinal barrier integrity, contributes to microbiome disruption, impaired epithelial resilience, inflammation, and biological aging in PWH.
DESIGN: Ileal and colonic biopsies, isolated crypts, stool, and blood from PWH on ART and controls underwent multi-omic analyses. Findings were mechanistically interrogated using stool anaerobic fermentation assays and 3D intestinal organoid models of stress-mediated epithelial disruption.
RESULTS: In intestinal tissues, PWH exhibited reduced α1,2-fucosylation and increased senescence-associated expression of the fucose-degrading enzyme α-L-fucosidase. Lower α1,2-fucose tracked with depletion of SCFA-producing bacteria, increased inflammation, and premature biological aging. In anaerobic fermentations, stool from PWH produced fewer SCFAs than controls, whereas supplementation with the human-milk-oligosaccharide-derived α1,2-fucose donor 2'-fucosyllactose restored SCFA production and improved intestinal organoid resilience to stress-mediated disruption.
CONCLUSION: These findings identify acquired loss of intestinal α1,2-fucose as a modifiable host-microbiome mechanism linking epithelial senescence, microbial metabolic dysfunction, impaired barrier resilience, inflammation, and biological aging in treated HIV infection.
SUMMARY BOX: What is already known on this topic: People with HIV on suppressive antiretroviral therapy frequently have persistent intestinal barrier dysfunction, microbial dysbiosis, chronic inflammation, and accelerated biological aging, but the host mechanisms that maintain this disrupted mucosal state remain incompletely defined.What this study adds: This study identifies acquired loss of intestinal α1,2-fucosylation as a feature of treated HIV infection and links this defect to a host fucosidase-high, senescence-enriched mucosal niche, depletion of SCFA-producing bacteria, impaired tight junction-associated barrier signatures, inflammation, and biological aging phenotypes.How this study might affect research, practice or policy: These findings support intestinal glycan ecology as a modifiable host-microbiome axis and provide a rationale for testing α1,2-fucose-replenishing strategies, such as 2'-fucosyllactose, to restore microbial metabolic output and improve epithelial resilience in people with HIV.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
High throughput chromatographic ultra-purification of virus-like particles for downstream viromics.
bioRxiv : the preprint server for biology pii:2026.07.09.737491.
Virus-like particles (VLPs) are an abundant component of microbiomes with critical ecological roles such as population control through viral predation and horizontal gene transfer. Studying the collection of viruses in microbiomes (the virome) through metagenomics has provided important insights into the composition and functions of VLPs in different environments. However, the current gold-standard method for VLP purification, CsCl density gradient ultracentrifugation (CsCl), is low throughput, time consuming and suffers from biases which limits the ability to study viromes in larger sample sets and can interfere with data interpretation. Here we present an anion exchange (AEX) chromatography-based approach for the purification of VLPs from microbiome samples that allows for significant increases in throughput and reproducibility while achieving VLP purity levels similar to or higher than CsCl. We used microbiome samples of known composition to first establish and evaluate the AEX approaches and compare them to CsCl. We implemented the AEX approach both for fast performance liquid chromatography (FPLC) and in multi-well plates. We compared the VLPs purified with CsCl and AEX using shotgun metagenomic sequencing and found that AEX performs similarly to or better than CsCl for purification of VLPs. AEX purified VLP-fractions captured significantly more viral DNA compared to CsCl. We also found that both AEX and CsCl were capable of capturing viruses present at extremely low relative abundances (<0.001%). Additionally, we found that DNase digestion and CsCl may bias against filamentous phage morphologies. Finally, we purified VLPs from conventional murine feces using AEX and CsCl. AEX purified murine fecal VLPs had a much higher viral DNA content (85%) than CsCl (41%). While there were some differences in viral contigs assembled from AEX and CsCl VLP metagenomes, these method unique viral contigs made up only small proportions (<8%) of the relative abundance in the VLP metagenomes. AEX, particularly in the multi-well format, enables the ultrapurification of VLPs from tens to hundreds of samples in a single day thus facilitating virome studies with the large sample numbers needed for translational and clinical research.
Additional Links: PMID-42465457
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@article {pmid42465457,
year = {2026},
author = {Maier, J and Deshmukh, N and Kleiner, M},
title = {High throughput chromatographic ultra-purification of virus-like particles for downstream viromics.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.09.737491},
pmid = {42465457},
issn = {2692-8205},
abstract = {Virus-like particles (VLPs) are an abundant component of microbiomes with critical ecological roles such as population control through viral predation and horizontal gene transfer. Studying the collection of viruses in microbiomes (the virome) through metagenomics has provided important insights into the composition and functions of VLPs in different environments. However, the current gold-standard method for VLP purification, CsCl density gradient ultracentrifugation (CsCl), is low throughput, time consuming and suffers from biases which limits the ability to study viromes in larger sample sets and can interfere with data interpretation. Here we present an anion exchange (AEX) chromatography-based approach for the purification of VLPs from microbiome samples that allows for significant increases in throughput and reproducibility while achieving VLP purity levels similar to or higher than CsCl. We used microbiome samples of known composition to first establish and evaluate the AEX approaches and compare them to CsCl. We implemented the AEX approach both for fast performance liquid chromatography (FPLC) and in multi-well plates. We compared the VLPs purified with CsCl and AEX using shotgun metagenomic sequencing and found that AEX performs similarly to or better than CsCl for purification of VLPs. AEX purified VLP-fractions captured significantly more viral DNA compared to CsCl. We also found that both AEX and CsCl were capable of capturing viruses present at extremely low relative abundances (<0.001%). Additionally, we found that DNase digestion and CsCl may bias against filamentous phage morphologies. Finally, we purified VLPs from conventional murine feces using AEX and CsCl. AEX purified murine fecal VLPs had a much higher viral DNA content (85%) than CsCl (41%). While there were some differences in viral contigs assembled from AEX and CsCl VLP metagenomes, these method unique viral contigs made up only small proportions (<8%) of the relative abundance in the VLP metagenomes. AEX, particularly in the multi-well format, enables the ultrapurification of VLPs from tens to hundreds of samples in a single day thus facilitating virome studies with the large sample numbers needed for translational and clinical research.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
Microbiome dysbiosis and its modulation in cancer development, prevention and therapy.
Frontiers in oncology, 16:1852716.
Gut microbiome dysbiosis, a state of microbial imbalance, altered microbial function, and disturbed homeostasis between the gut microbiome and its host, is increasingly recognized as a key contributor to cancer development, progression, and variability in therapeutic response. These microbiome states can facilitate cancer development through chronic inflammation, expansion of microbial genotoxin producers, or disturbances of immune defense mechanisms. In this review, we will discuss current findings on gut microbiome dysbiosis in cancer initiation and progression, emphasizing mechanisms that links dysbiosis to oncogenic transformation and tumor microenvironment remodeling. Furthermore, we will explore microbiome-targeting strategies for cancer prevention and therapeutic support, including dietary modulation, probiotics, prebiotics, and fecal microbiota transplantation. These various microbiome modulations have shown promise in restoring microbial homeostasis, enhancing immunotherapy efficacy, and reducing treatment-associated toxicity. Advances in microbial genomics and metabolomics further enable the identification of biomarkers for predicting cancer risk and therapeutic outcomes. Despite significant progress, translation into clinical settings faces challenges related to interindividual variability, standardization, and mechanistic complexity. Understanding the microbiome-cancer interface provides a platform for personalized, microbiome-informed oncology, paving the way for prevention-driven and precision-guided therapeutics.
Additional Links: PMID-42465573
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@article {pmid42465573,
year = {2026},
author = {Dixit, S and Welker, A and Ortiz, D and Athanasouli, M and Stein-Thoeringer, CK},
title = {Microbiome dysbiosis and its modulation in cancer development, prevention and therapy.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1852716},
pmid = {42465573},
issn = {2234-943X},
abstract = {Gut microbiome dysbiosis, a state of microbial imbalance, altered microbial function, and disturbed homeostasis between the gut microbiome and its host, is increasingly recognized as a key contributor to cancer development, progression, and variability in therapeutic response. These microbiome states can facilitate cancer development through chronic inflammation, expansion of microbial genotoxin producers, or disturbances of immune defense mechanisms. In this review, we will discuss current findings on gut microbiome dysbiosis in cancer initiation and progression, emphasizing mechanisms that links dysbiosis to oncogenic transformation and tumor microenvironment remodeling. Furthermore, we will explore microbiome-targeting strategies for cancer prevention and therapeutic support, including dietary modulation, probiotics, prebiotics, and fecal microbiota transplantation. These various microbiome modulations have shown promise in restoring microbial homeostasis, enhancing immunotherapy efficacy, and reducing treatment-associated toxicity. Advances in microbial genomics and metabolomics further enable the identification of biomarkers for predicting cancer risk and therapeutic outcomes. Despite significant progress, translation into clinical settings faces challenges related to interindividual variability, standardization, and mechanistic complexity. Understanding the microbiome-cancer interface provides a platform for personalized, microbiome-informed oncology, paving the way for prevention-driven and precision-guided therapeutics.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
Association between the subcellular localization of host proteins and gut microbiome and metabolome in metabolic dysfunction-associated steatotic liver disease: a pilot study.
Frontiers in molecular biosciences, 13:1703547.
BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) is estimated to affect 38% of the global population, with limited options for treatment. It could progress to metabolic-associated steatohepatitis (MASH), fibrosis, and hepatocellular carcinoma. Agonists for farnesoid X receptor (FXR), peroxisome proliferation-associated receptors (PPARs), and sirtuin1 (SIRT1) are currently investigated for MASLD treatment. The subcellular localization of those proteins was shown to affect their function and could possibly be affected by different metabolites. Moreover, while those protein targets were found to be affected by the gut microbiome in mice, they have not yet been investigated in humans. Existing evidence independently links the gut microbiome to MASLD onset and demonstrates that host proteins are impacted by the microbiome. Therefore, we aimed at using integrative multi-omics analysis to investigate the interrelationship between the gut microbiome, fecal and serum metabolomes, and those selected protein targets in a cohort of patients with MASLD to identify potential markers differentiating MASLD and MASH.
METHODS: Serum and stool samples were collected from patients with MASLD and healthy controls, while formalin-fixed paraffin-embedded (FFPE) liver biopsies and clinical laboratory tests were obtained from patients only. Expression of the protein targets was analyzed by immunohistochemistry (IHC). Microbiome and metabolome analyses were performed, followed by bioinformatics, correlation, and multivariate and integrated multi-omics analyses.
RESULTS: SIRT1 and FXR subcellular localizations were correlated with multiple bacteria and metabolites, respectively. Three genera (Rothia, Haemophilus, and Acetatifactor) correlated with NAFLD activity score (NAS), and a signature of 20 bacterial genera, 10 fecal and 30 serum metabolites, and 3 host proteins differentiated between MASLD and MASH. Moreover, in silico analysis suggested myristic, lauric, octanoic, and nonanoic acids to putatively affect peroxisome proliferator-activated receptor alpha (PPARA) and FXR, and Coprobacter as an important contributor in our multi-omics model.
CONCLUSION: Our data suggest bacteria and metabolites which potentially affect the subcellular localization, and hence activity, of anti-lipogenic proteins in MASLD patients. We also propose novel discriminatory markers between MASLD and MASH. Our findings form the groundwork for future mechanistic studies of both host and microbial factors possibly contributing to the multifaceted disease outcome and offer potential diagnostic markers.
Additional Links: PMID-42465609
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@article {pmid42465609,
year = {2026},
author = {El Sobky, SA and El-Ekiaby, N and Fawzy, IO and Abdelhamid, AK and Attia, H and Fayed, IH and Badr, Y and Emadeldeen, M and Nagy, A and Negm, M and Negm, MS and Moustafa, A and El-Kassas, M and Farag, MA and Aziz, RK and Abdelaziz, AI},
title = {Association between the subcellular localization of host proteins and gut microbiome and metabolome in metabolic dysfunction-associated steatotic liver disease: a pilot study.},
journal = {Frontiers in molecular biosciences},
volume = {13},
number = {},
pages = {1703547},
pmid = {42465609},
issn = {2296-889X},
abstract = {BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) is estimated to affect 38% of the global population, with limited options for treatment. It could progress to metabolic-associated steatohepatitis (MASH), fibrosis, and hepatocellular carcinoma. Agonists for farnesoid X receptor (FXR), peroxisome proliferation-associated receptors (PPARs), and sirtuin1 (SIRT1) are currently investigated for MASLD treatment. The subcellular localization of those proteins was shown to affect their function and could possibly be affected by different metabolites. Moreover, while those protein targets were found to be affected by the gut microbiome in mice, they have not yet been investigated in humans. Existing evidence independently links the gut microbiome to MASLD onset and demonstrates that host proteins are impacted by the microbiome. Therefore, we aimed at using integrative multi-omics analysis to investigate the interrelationship between the gut microbiome, fecal and serum metabolomes, and those selected protein targets in a cohort of patients with MASLD to identify potential markers differentiating MASLD and MASH.
METHODS: Serum and stool samples were collected from patients with MASLD and healthy controls, while formalin-fixed paraffin-embedded (FFPE) liver biopsies and clinical laboratory tests were obtained from patients only. Expression of the protein targets was analyzed by immunohistochemistry (IHC). Microbiome and metabolome analyses were performed, followed by bioinformatics, correlation, and multivariate and integrated multi-omics analyses.
RESULTS: SIRT1 and FXR subcellular localizations were correlated with multiple bacteria and metabolites, respectively. Three genera (Rothia, Haemophilus, and Acetatifactor) correlated with NAFLD activity score (NAS), and a signature of 20 bacterial genera, 10 fecal and 30 serum metabolites, and 3 host proteins differentiated between MASLD and MASH. Moreover, in silico analysis suggested myristic, lauric, octanoic, and nonanoic acids to putatively affect peroxisome proliferator-activated receptor alpha (PPARA) and FXR, and Coprobacter as an important contributor in our multi-omics model.
CONCLUSION: Our data suggest bacteria and metabolites which potentially affect the subcellular localization, and hence activity, of anti-lipogenic proteins in MASLD patients. We also propose novel discriminatory markers between MASLD and MASH. Our findings form the groundwork for future mechanistic studies of both host and microbial factors possibly contributing to the multifaceted disease outcome and offer potential diagnostic markers.},
}
RevDate: 2026-07-17
From microbes to milestones: Gut bacterial abundances and functional pathways associate with neurodevelopment following preterm birth.
Gut microbiology, 2:None.
The early life gut microbiome has been identified as a potential driver of neurocognitive development. Evidence for this relationship in preterm children, who are at increased risk of both gut microbiome disruptions and neurodevelopmental impairment, is scarce. In a sample of 73 very preterm infants drawn from a prospective birth cohort, we assessed associations between the neonatal gut microbiome and neurodevelopmental outcomes at 9 months and 2 years. The gut microbiome taxonomic and functional profiles were obtained from stool samples collected prior to NICU discharge using shotgun metagenomics. Neurodevelopment was assessed using a battery of outcome measures. We took a consensus-based analytic approach, applying several different methods to investigate microbiome-outcome relationships and focussing on results which were consistently significant across methods. We found the most robust evidence for associations between the abundances of several gut bacterial species and measures related to autistic traits (e.g. Klebsiella spp.), socio-emotional development, including temperament (e.g. Enterobacter cloacae complex, Veillonella parvula), and executive functioning (Clostridium perfringens). The abundances of functional modules involved in gut-brain signalling, particularly those involved in histamine and quinolinic acid metabolism, were associated with outcome measures related to executive functioning and cognitive-behavioural flexibility. This study provides evidence that the neonatal gut microbiome composition may affect longer-term neurodevelopmental profiles following preterm birth, particularly those related to socio-emotional development, autistic traits and executive functioning.
Additional Links: PMID-42465693
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@article {pmid42465693,
year = {2026},
author = {Vaher, K and Kenny, A and Lusarreta Parga, P and Jiménez-Sánchez, L and Turner, H and Smikle, R and Corrigan, A and Cruickshank, H and Rudnicka, M and Fletcher-Watson, S and Bogaert, D and Boardman, JP},
title = {From microbes to milestones: Gut bacterial abundances and functional pathways associate with neurodevelopment following preterm birth.},
journal = {Gut microbiology},
volume = {2},
number = {},
pages = {None},
pmid = {42465693},
issn = {3051-1720},
abstract = {The early life gut microbiome has been identified as a potential driver of neurocognitive development. Evidence for this relationship in preterm children, who are at increased risk of both gut microbiome disruptions and neurodevelopmental impairment, is scarce. In a sample of 73 very preterm infants drawn from a prospective birth cohort, we assessed associations between the neonatal gut microbiome and neurodevelopmental outcomes at 9 months and 2 years. The gut microbiome taxonomic and functional profiles were obtained from stool samples collected prior to NICU discharge using shotgun metagenomics. Neurodevelopment was assessed using a battery of outcome measures. We took a consensus-based analytic approach, applying several different methods to investigate microbiome-outcome relationships and focussing on results which were consistently significant across methods. We found the most robust evidence for associations between the abundances of several gut bacterial species and measures related to autistic traits (e.g. Klebsiella spp.), socio-emotional development, including temperament (e.g. Enterobacter cloacae complex, Veillonella parvula), and executive functioning (Clostridium perfringens). The abundances of functional modules involved in gut-brain signalling, particularly those involved in histamine and quinolinic acid metabolism, were associated with outcome measures related to executive functioning and cognitive-behavioural flexibility. This study provides evidence that the neonatal gut microbiome composition may affect longer-term neurodevelopmental profiles following preterm birth, particularly those related to socio-emotional development, autistic traits and executive functioning.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
The microbiome protects against septic hyperinflammation and bacterial proliferation in a zebrafish model of blood infection with Escherichia coli and mycobacteria.
Frontiers in immunology, 17:1837804.
The microbiome is an important immune regulator, but the mechanisms by which commensal microbes shape systemic host defense during bloodstream infection remain poorly defined and commonly used pre-clinical models have practical, ethical and scientific limitations. Here, we establish a gnotobiotic zebrafish larval model to investigate microbiome-dependent protection against systemic blood infection by Escherichia coli (E. coli) bacteria, an important cause of early onset neonatal sepsis. We also use nontuberculous mycobacteria to infect zebrafish larvae to investigate the contribution of Toll-like receptor 2 (TLR2) in the defense responses. Germ-free (GF) and conventionalized (CONVD) larvae derived from the same clutches were systemically infected with E. coli, revealing that microbiome colonization significantly reduces early mortality. RNAseq revealed a conserved core immune activation program in both GF and CONVD larvae, but the absence of a microbiome was associated with a broader transcriptional response and stronger repression of metabolic pathways, suggesting that commensal microbes buffer infection-induced metabolic suppression. Extending this framework to nontuberculous mycobacteria, we performed systemic infections with fluorescent Mycobacterium marinum and M. avium in tlr2 wild-type and mutant larvae under GF and CONVD conditions. While survival was largely unchanged, imaging-based quantification demonstrated increased bacterial proliferation in tlr2 mutants and in GF larvae, with microbiome-mediated restriction of bacterial burden evident in wild-type but not tlr2-deficient hosts. Together, these data show that microbiome colonization buffers septic outcomes by reshaping systemic inflammatory and metabolic programs and identify TLR2 as a key node linking microbial colonization to effective host defense during nontuberculous mycobacterial infection.
Additional Links: PMID-42465747
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@article {pmid42465747,
year = {2026},
author = {Liu, L and Koch, BEV and Krekels, EHJ and Spaink, HP},
title = {The microbiome protects against septic hyperinflammation and bacterial proliferation in a zebrafish model of blood infection with Escherichia coli and mycobacteria.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1837804},
pmid = {42465747},
issn = {1664-3224},
mesh = {Animals ; Zebrafish/immunology/microbiology ; *Escherichia coli Infections/immunology/microbiology ; Disease Models, Animal ; *Escherichia coli/immunology ; *Microbiota/immunology ; *Mycobacterium Infections, Nontuberculous/immunology/microbiology ; Toll-Like Receptor 2/genetics/metabolism ; Germ-Free Life ; Inflammation/immunology/microbiology ; *Sepsis/microbiology/immunology ; *Bacteremia/immunology/microbiology ; },
abstract = {The microbiome is an important immune regulator, but the mechanisms by which commensal microbes shape systemic host defense during bloodstream infection remain poorly defined and commonly used pre-clinical models have practical, ethical and scientific limitations. Here, we establish a gnotobiotic zebrafish larval model to investigate microbiome-dependent protection against systemic blood infection by Escherichia coli (E. coli) bacteria, an important cause of early onset neonatal sepsis. We also use nontuberculous mycobacteria to infect zebrafish larvae to investigate the contribution of Toll-like receptor 2 (TLR2) in the defense responses. Germ-free (GF) and conventionalized (CONVD) larvae derived from the same clutches were systemically infected with E. coli, revealing that microbiome colonization significantly reduces early mortality. RNAseq revealed a conserved core immune activation program in both GF and CONVD larvae, but the absence of a microbiome was associated with a broader transcriptional response and stronger repression of metabolic pathways, suggesting that commensal microbes buffer infection-induced metabolic suppression. Extending this framework to nontuberculous mycobacteria, we performed systemic infections with fluorescent Mycobacterium marinum and M. avium in tlr2 wild-type and mutant larvae under GF and CONVD conditions. While survival was largely unchanged, imaging-based quantification demonstrated increased bacterial proliferation in tlr2 mutants and in GF larvae, with microbiome-mediated restriction of bacterial burden evident in wild-type but not tlr2-deficient hosts. Together, these data show that microbiome colonization buffers septic outcomes by reshaping systemic inflammatory and metabolic programs and identify TLR2 as a key node linking microbial colonization to effective host defense during nontuberculous mycobacterial infection.},
}
MeSH Terms:
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Animals
Zebrafish/immunology/microbiology
*Escherichia coli Infections/immunology/microbiology
Disease Models, Animal
*Escherichia coli/immunology
*Microbiota/immunology
*Mycobacterium Infections, Nontuberculous/immunology/microbiology
Toll-Like Receptor 2/genetics/metabolism
Germ-Free Life
Inflammation/immunology/microbiology
*Sepsis/microbiology/immunology
*Bacteremia/immunology/microbiology
RevDate: 2026-07-17
CmpDate: 2026-07-17
Effects of cassava polysaccharides on gut microbiome, intestinal barrier and macrophage activation.
Frontiers in immunology, 17:1874777.
CPs possess considerable bioactive potential, yet their underlying immunomodulatory mechanisms remain incompletely elucidated. In the present work, CPCR were extracted from fresh cassava tubers and further separated into five purified polysaccharide fractions (CP1-CP5) with distinct monosaccharide profiles and molecular weights. Systematically investigated the immunomodulatory capacities of CPCR and its purified fractions via in vivo assays using Cy-induced immunosuppressed mice and in vitro tests on RAW264.7 murine macrophages. Multiple readouts were quantified, including gut microbial community structure, fecal SCFAs concentrations, intestinal tight junction protein expression, serum anti-inflammatory cytokine levels, as well as macrophage proliferation, phagocytic activity and inflammatory mediator release. In vivo data demonstrated that CPCR reshaped gut microbiota homeostasis by selectively enriching beneficial commensal genera and families linked to intestinal health, namely Muribaculaceae, Bacteroides, Alloprevotella, and Prevotellaceae. Enrichment of these probiotic taxa boosted intestinal SCFAs production; notably, fecal acetic acid concentration reached 141.0 mg/g following CPCR intervention, significantly exceeding levels measured in both normal control and Cy-induced immunosuppressed groups. Moreover, CPCR robustly upregulated the expression of intestinal barrier proteins ZO-1, occludin and Claudin-1, facilitating the repair and preservation of intestinal epithelial integrity. Serum cytokine profiling revealed prominent elevations in the anti-inflammatory mediators IL-2, IL-4 and IL-10 upon CPCR administration. Structural characterization of isolated subfractions revealed stark compositional disparities: CP1 predominantly consisted of 97% glucose with a molecular weight of 3 kDa, while CP2 contained 31.1% glucose, 20% galactose and 15.2% arabinose with a molecular weight of 62.4 kDa, this represents a preliminary structural characterization of the polysaccharide fractions. The results demonstrated that all CPs fractions could enhance immune cell activity, including phagocytic capacity and anti-inflammatory cytokine secretion. In summary, this study demonstrates that CPs exert immunostimulatory effects through dual pathways: direct activation of macrophage immune function and indirect regulation of gut microbiota-intestinal barrier homeostasis. Our results support the translational potential of CPs as bioactive functional food ingredients for immune regulation.
Additional Links: PMID-42465752
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Citation:
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@article {pmid42465752,
year = {2026},
author = {Yu, H and Yao, Q and Lin, L and Jian, C and Du, P and Zhang, J and Fang, Y and Liu, M and Wang, Q and Zhang, Z},
title = {Effects of cassava polysaccharides on gut microbiome, intestinal barrier and macrophage activation.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1874777},
pmid = {42465752},
issn = {1664-3224},
mesh = {Animals ; *Polysaccharides/pharmacology/isolation & purification/chemistry ; Intestinal Barrier Function/drug effects ; Mice ; *Macrophage Activation/drug effects ; *Gastrointestinal Microbiome/drug effects ; Cytokines/blood ; *Manihot/chemistry ; RAW 264.7 Cells ; Macrophages/immunology/drug effects/metabolism ; Intestinal Mucosa/metabolism/drug effects/immunology ; },
abstract = {CPs possess considerable bioactive potential, yet their underlying immunomodulatory mechanisms remain incompletely elucidated. In the present work, CPCR were extracted from fresh cassava tubers and further separated into five purified polysaccharide fractions (CP1-CP5) with distinct monosaccharide profiles and molecular weights. Systematically investigated the immunomodulatory capacities of CPCR and its purified fractions via in vivo assays using Cy-induced immunosuppressed mice and in vitro tests on RAW264.7 murine macrophages. Multiple readouts were quantified, including gut microbial community structure, fecal SCFAs concentrations, intestinal tight junction protein expression, serum anti-inflammatory cytokine levels, as well as macrophage proliferation, phagocytic activity and inflammatory mediator release. In vivo data demonstrated that CPCR reshaped gut microbiota homeostasis by selectively enriching beneficial commensal genera and families linked to intestinal health, namely Muribaculaceae, Bacteroides, Alloprevotella, and Prevotellaceae. Enrichment of these probiotic taxa boosted intestinal SCFAs production; notably, fecal acetic acid concentration reached 141.0 mg/g following CPCR intervention, significantly exceeding levels measured in both normal control and Cy-induced immunosuppressed groups. Moreover, CPCR robustly upregulated the expression of intestinal barrier proteins ZO-1, occludin and Claudin-1, facilitating the repair and preservation of intestinal epithelial integrity. Serum cytokine profiling revealed prominent elevations in the anti-inflammatory mediators IL-2, IL-4 and IL-10 upon CPCR administration. Structural characterization of isolated subfractions revealed stark compositional disparities: CP1 predominantly consisted of 97% glucose with a molecular weight of 3 kDa, while CP2 contained 31.1% glucose, 20% galactose and 15.2% arabinose with a molecular weight of 62.4 kDa, this represents a preliminary structural characterization of the polysaccharide fractions. The results demonstrated that all CPs fractions could enhance immune cell activity, including phagocytic capacity and anti-inflammatory cytokine secretion. In summary, this study demonstrates that CPs exert immunostimulatory effects through dual pathways: direct activation of macrophage immune function and indirect regulation of gut microbiota-intestinal barrier homeostasis. Our results support the translational potential of CPs as bioactive functional food ingredients for immune regulation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Polysaccharides/pharmacology/isolation & purification/chemistry
Intestinal Barrier Function/drug effects
Mice
*Macrophage Activation/drug effects
*Gastrointestinal Microbiome/drug effects
Cytokines/blood
*Manihot/chemistry
RAW 264.7 Cells
Macrophages/immunology/drug effects/metabolism
Intestinal Mucosa/metabolism/drug effects/immunology
RevDate: 2026-07-17
CmpDate: 2026-07-17
Microbiota-immune-enteric nervous system interactions in functional constipation: a narrative review and hypothesis-generating framework.
Frontiers in immunology, 17:1851825.
Functional constipation (FC), particularly slow-transit constipation (STC), is a heterogeneous disorder of gut-brain interaction that responds poorly to conventional therapies. Accumulating evidence links the microbiota, mucosal immunity, and the enteric nervous system (ENS); their mechanistic integration remains incomplete. In this narrative review, we propose a Trigger-Gateway-Hub-Effector framework as a heuristic and hypothesis-generating model to organize fragmented evidence on microbial-to-immune-neural interactions. Within this framework, dysbiosis-associated microbial metabolites, including short-chain fatty acids, bile acids, methane-related pathways, and lipopolysaccharide, are considered potential upstream "Triggers" that may modulate epithelial and immune homeostasis. "Gateway" processes refer to epithelial barrier vulnerability and mucosal immune changes that may permit microbial or inflammatory signals to affect deeper intestinal compartments. At the "Hub" level, interactions among muscularis macrophages, mast cells, enteric glia cells, and neurons are proposed to integrate these signals and contribute to ENS-adjacent neuroimmune stress. These processes may converge on downstream "Effector" alterations, including neuronal vulnerability, maladaptive plasticity, and disruption of the interstitial cells of Cajal network, particularly in severe or refractory STC. However, there is currently limited direct evidence to support a continuous causal chain linking microbiome-derived signals to dysfunction of the enteroneural system. Many of the proposed mechanisms are inferred from preclinical studies or related gastrointestinal disorders. Therefore, this framework should be interpreted as a testable conceptual model rather than a confirmed pathogenic sequence. We further discuss the translational implications from a systems biology perspective, emphasizing evidence-weighted therapeutic interpretation, mechanism-guided stratification, and integrated microbial-immune-ENS assessment. Future human-centered studies combining multi-omic profiling, spatial tissue analysis, and objective neuromuscular readouts are needed to refine this model and inform precision-oriented therapeutic strategies for FC/STC.
Additional Links: PMID-42465761
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Citation:
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@article {pmid42465761,
year = {2026},
author = {Ge, D and Zhan, Y and Wen, Y and Wu, R and Xu, Q and Ao, Z and Shu, Y and Tang, X},
title = {Microbiota-immune-enteric nervous system interactions in functional constipation: a narrative review and hypothesis-generating framework.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1851825},
pmid = {42465761},
issn = {1664-3224},
mesh = {Humans ; *Enteric Nervous System/immunology/physiopathology ; Animals ; *Gastrointestinal Microbiome/immunology ; *Constipation/immunology/microbiology/physiopathology/metabolism/etiology ; Neuroimmunomodulation ; Dysbiosis/immunology ; },
abstract = {Functional constipation (FC), particularly slow-transit constipation (STC), is a heterogeneous disorder of gut-brain interaction that responds poorly to conventional therapies. Accumulating evidence links the microbiota, mucosal immunity, and the enteric nervous system (ENS); their mechanistic integration remains incomplete. In this narrative review, we propose a Trigger-Gateway-Hub-Effector framework as a heuristic and hypothesis-generating model to organize fragmented evidence on microbial-to-immune-neural interactions. Within this framework, dysbiosis-associated microbial metabolites, including short-chain fatty acids, bile acids, methane-related pathways, and lipopolysaccharide, are considered potential upstream "Triggers" that may modulate epithelial and immune homeostasis. "Gateway" processes refer to epithelial barrier vulnerability and mucosal immune changes that may permit microbial or inflammatory signals to affect deeper intestinal compartments. At the "Hub" level, interactions among muscularis macrophages, mast cells, enteric glia cells, and neurons are proposed to integrate these signals and contribute to ENS-adjacent neuroimmune stress. These processes may converge on downstream "Effector" alterations, including neuronal vulnerability, maladaptive plasticity, and disruption of the interstitial cells of Cajal network, particularly in severe or refractory STC. However, there is currently limited direct evidence to support a continuous causal chain linking microbiome-derived signals to dysfunction of the enteroneural system. Many of the proposed mechanisms are inferred from preclinical studies or related gastrointestinal disorders. Therefore, this framework should be interpreted as a testable conceptual model rather than a confirmed pathogenic sequence. We further discuss the translational implications from a systems biology perspective, emphasizing evidence-weighted therapeutic interpretation, mechanism-guided stratification, and integrated microbial-immune-ENS assessment. Future human-centered studies combining multi-omic profiling, spatial tissue analysis, and objective neuromuscular readouts are needed to refine this model and inform precision-oriented therapeutic strategies for FC/STC.},
}
MeSH Terms:
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Humans
*Enteric Nervous System/immunology/physiopathology
Animals
*Gastrointestinal Microbiome/immunology
*Constipation/immunology/microbiology/physiopathology/metabolism/etiology
Neuroimmunomodulation
Dysbiosis/immunology
RevDate: 2026-07-17
CmpDate: 2026-07-17
Gut-lung axis in radiation-induced lung injury: mechanisms and interventions.
Frontiers in immunology, 17:1806833.
Radiation-induced lung injury (RILI) constrains thoracic radiotherapy dosing and includes acute radiation pneumonitis (RP) and chronic radiation-induced pulmonary fibrosis (RPF). This narrative review explores the gut-lung microbiota axis in RILI, synthesizing evidence from preclinical models, clinical cohorts (N = 52-89), and randomized controlled trials (RCTs). Radiotherapy induces gut dysbiosis, barrier breakdown, and metabolite changes [e.g., short-chain fatty acid (SCFA) and desaminotyrosine (DAT) depletion], promoting inflammation and fibrosis via pathways such as Toll-like receptor 4/nuclear factor kappa B (TLR4/NF-κB), TGF-β/Smad, sphingosine-1-phosphate (S1P)-S1PR, and cGAS-STING in animal studies. Inter-species microbial variations hinder translation, while lung microbiota shifts remain nascent. In non-small cell lung cancer cohorts, lower gut microbiota stability (a marker of dysbiosis) is associated with an increased risk of grade ≥2 RP (multivariable-adjusted models, p < 0.05), with higher baseline Faecalibacterium abundance conferring protection; however, causality remains unproven due to antibiotic confounding. Mechanisms involve lipopolysaccharide (LPS) translocation, interleukin 25 (IL-25)/S1P-driven type 2 innate lymphoid cell (ILC2) migration, regulatory T cell/T helper 17 cell (Treg/Th17) imbalance, and extracellular vesicle (EV) signaling, with biomarkers such as 16S rRNA sequencing and EV-miRNAs (e.g., miR-486-5p). Artificial intelligence models predict RP with 75% accuracy. Phase-specific interventions, such as pre-radiotherapy gut microbiota monitoring, intra-radiotherapy SCFA supplementation, subacute DAT modulation, and RPF-targeted EV therapies, have been explored in preliminary pilot studies [for example, one small study reported approximately 12% FEV1 improvement following fecal microbiota transplantation (FMT)]. Future large-scale, stratified RCTs that properly account for antibiotics, chemotherapy, and immunotherapy are required to establish causality beyond the current largely associative clinical evidence. The integration of immunotherapy and proton therapy in such trials may help clarify gut-lung interactions, including any microbiota-preserving effects of proton therapy; the role of the lung microbiota in fibrosis remains preliminary.
Additional Links: PMID-42465768
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@article {pmid42465768,
year = {2026},
author = {Zhou, P and Jiang, X and Zhang, H and Jiang, S and Zhang, X and Ma, C and Bai, X},
title = {Gut-lung axis in radiation-induced lung injury: mechanisms and interventions.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1806833},
pmid = {42465768},
issn = {1664-3224},
mesh = {Humans ; Animals ; *Gastrointestinal Microbiome/radiation effects/immunology ; *Radiation Pneumonitis/therapy/microbiology/etiology/immunology/metabolism ; *Lung/immunology/microbiology/radiation effects/metabolism ; Dysbiosis ; Radiation Injuries ; },
abstract = {Radiation-induced lung injury (RILI) constrains thoracic radiotherapy dosing and includes acute radiation pneumonitis (RP) and chronic radiation-induced pulmonary fibrosis (RPF). This narrative review explores the gut-lung microbiota axis in RILI, synthesizing evidence from preclinical models, clinical cohorts (N = 52-89), and randomized controlled trials (RCTs). Radiotherapy induces gut dysbiosis, barrier breakdown, and metabolite changes [e.g., short-chain fatty acid (SCFA) and desaminotyrosine (DAT) depletion], promoting inflammation and fibrosis via pathways such as Toll-like receptor 4/nuclear factor kappa B (TLR4/NF-κB), TGF-β/Smad, sphingosine-1-phosphate (S1P)-S1PR, and cGAS-STING in animal studies. Inter-species microbial variations hinder translation, while lung microbiota shifts remain nascent. In non-small cell lung cancer cohorts, lower gut microbiota stability (a marker of dysbiosis) is associated with an increased risk of grade ≥2 RP (multivariable-adjusted models, p < 0.05), with higher baseline Faecalibacterium abundance conferring protection; however, causality remains unproven due to antibiotic confounding. Mechanisms involve lipopolysaccharide (LPS) translocation, interleukin 25 (IL-25)/S1P-driven type 2 innate lymphoid cell (ILC2) migration, regulatory T cell/T helper 17 cell (Treg/Th17) imbalance, and extracellular vesicle (EV) signaling, with biomarkers such as 16S rRNA sequencing and EV-miRNAs (e.g., miR-486-5p). Artificial intelligence models predict RP with 75% accuracy. Phase-specific interventions, such as pre-radiotherapy gut microbiota monitoring, intra-radiotherapy SCFA supplementation, subacute DAT modulation, and RPF-targeted EV therapies, have been explored in preliminary pilot studies [for example, one small study reported approximately 12% FEV1 improvement following fecal microbiota transplantation (FMT)]. Future large-scale, stratified RCTs that properly account for antibiotics, chemotherapy, and immunotherapy are required to establish causality beyond the current largely associative clinical evidence. The integration of immunotherapy and proton therapy in such trials may help clarify gut-lung interactions, including any microbiota-preserving effects of proton therapy; the role of the lung microbiota in fibrosis remains preliminary.},
}
MeSH Terms:
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Humans
Animals
*Gastrointestinal Microbiome/radiation effects/immunology
*Radiation Pneumonitis/therapy/microbiology/etiology/immunology/metabolism
*Lung/immunology/microbiology/radiation effects/metabolism
Dysbiosis
Radiation Injuries
RevDate: 2026-07-17
CmpDate: 2026-07-17
Microbiota in pancreatic cancer: Roles in tumor initiation and progression (Review).
Oncology letters, 32(3):391.
Pancreatic cancer is a highly aggressive malignancy with limited therapeutic options and poor survival outcomes, highlighting the need for an improved understanding of its underlying biology. Advances have positioned the human microbiome as a critical regulator of the initiation and progression of pancreatic cancer. Microbial communities across the oral-gut-tumor axis contribute to tumor initiation through coordinated mechanisms, including the induction of genotoxic stress, chronic inflammation and activation of oncogenic signaling pathways. During tumor progression, microbiota dynamically shape the tumor microenvironment by modulating immune responses, metabolic reprogramming and stromal remodeling. Notably, microbial influences are bidirectional, as tumor-promoting and tumor-suppressive taxa exert opposing effects that converge on shared regulatory pathways within the tumor ecosystem. The present study reviews the current understanding of microbiome involvement in pancreatic cancer, focusing on its mechanistic roles in tumor initiation and progression. Furthermore, the key challenges in the field are discussed, and the emerging opportunities for therapeutic intervention are highlighted. These insights provide a conceptual framework for integrating microbiome research into precision oncology for pancreatic cancer.
Additional Links: PMID-42465857
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@article {pmid42465857,
year = {2026},
author = {Lou, Y and Fan, Y},
title = {Microbiota in pancreatic cancer: Roles in tumor initiation and progression (Review).},
journal = {Oncology letters},
volume = {32},
number = {3},
pages = {391},
pmid = {42465857},
issn = {1792-1082},
abstract = {Pancreatic cancer is a highly aggressive malignancy with limited therapeutic options and poor survival outcomes, highlighting the need for an improved understanding of its underlying biology. Advances have positioned the human microbiome as a critical regulator of the initiation and progression of pancreatic cancer. Microbial communities across the oral-gut-tumor axis contribute to tumor initiation through coordinated mechanisms, including the induction of genotoxic stress, chronic inflammation and activation of oncogenic signaling pathways. During tumor progression, microbiota dynamically shape the tumor microenvironment by modulating immune responses, metabolic reprogramming and stromal remodeling. Notably, microbial influences are bidirectional, as tumor-promoting and tumor-suppressive taxa exert opposing effects that converge on shared regulatory pathways within the tumor ecosystem. The present study reviews the current understanding of microbiome involvement in pancreatic cancer, focusing on its mechanistic roles in tumor initiation and progression. Furthermore, the key challenges in the field are discussed, and the emerging opportunities for therapeutic intervention are highlighted. These insights provide a conceptual framework for integrating microbiome research into precision oncology for pancreatic cancer.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
The effect of dietary fiber based on fermentability and viscosity on the gut microbial metabolites in chronic kidney disease: a systematic review and meta-analysis of experimental and clinical trials.
medRxiv : the preprint server for health sciences pii:2026.07.09.26357677.
BACKGROUND: Chronic kidney disease (CKD) is associated with alterations in the gut microbiome that promote the accumulation of gut-derived uremic solutes and contribute to systemic inflammation, vascular dysfunction, and disease progression. Dietary fiber has emerged as a promising modulator of gut microbial metabolism, yet the influence of fiber physicochemical properties, particularly fermentability and viscosity, on uremic metabolite production in CKD remains poorly understood.
OBJECTIVE: To systematically evaluate the effects of isolated dietary fiber interventions, classified by fermentability and viscosity, on gut microbial metabolites in CKD across experimental rodent models and randomized clinical trials, and to determine whether these fiber properties modify microbial metabolites.
METHODS: A systematic search of PubMed, Embase, CINAHL, and Cochrane Library (through June 2026) identified randomized controlled trials and controlled rodent studies assessing isolated dietary fiber in CKD. Eligible studies reported at least one gut-derived metabolite (i.e., indoxyl sulfate (IS), p-cresyl sulfate (PCS), trimethylamine-N-oxide (TMAO), tryptophan-derived indoles, or short-chain fatty acids (SCFAs)). Random-effects models were used for pooled estimates using weighted mean differences (WMD) for human studies and standardized mean differences (SMD) for animal studies. Subgroup analyses evaluated fiber fermentability, viscosity, intervention dose, duration, and CKD stage. Risk of bias was assessed with ROB-2 and SYRCLE, and evidence certainty with GRADE.
RESULTS: Twenty-eight studies (13 human, 15 animal) met eligibility criteria, comprising 511 participants and 312 animals with CKD. Isolated fiber supplementation, primarily fermentable and non-viscous fibers, reduced IS (human: -0.13 mg/dL; 95% CI: -0.25, -0.01; p = 0.03; animal: -1.99; 95% CI: -3.06, -0.92; p < 0.0001) and pCS (human: -0.23 mg/dL; 95% CI: -0.46, 0.001; p = 0.051; animal: -1.56; 95% CI: -2.08, -1.03; p < 0.0001). SCFAs increased in animal studies, including cecal acetate (2.00, 95% CI: 0.78 to 3.22; p = 0.001) and circulating propionate (1.51, 95% CI: 0.054 to 2.96; p=0.04). There were no dose-dependent effects, but longer interventions (>8 weeks) tended to lower pCS (-0.26 mg/dL, 95% CI: -0.55 to 0.02; p=0.06). Some heterogeneity and low-to-moderate certainty were observed.
CONCLUSION: Isolated dietary fiber reduces major gut-derived uremic solutes in CKD, with fermentability influencing metabolic responsiveness, but with minimal studies on viscous fibers. Larger, longer-duration trials with standardized reporting of total fiber intake and clinical endpoints are needed to guide evidence-based dietary recommendations in CKD.
Additional Links: PMID-42465891
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@article {pmid42465891,
year = {2026},
author = {Mirmohammadali, SN and Carrillo, C and Reed, JB and Kistler, BM and Wilson, HE and Hamaker, B and Moe, SM and Biruete, A},
title = {The effect of dietary fiber based on fermentability and viscosity on the gut microbial metabolites in chronic kidney disease: a systematic review and meta-analysis of experimental and clinical trials.},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.09.26357677},
pmid = {42465891},
abstract = {BACKGROUND: Chronic kidney disease (CKD) is associated with alterations in the gut microbiome that promote the accumulation of gut-derived uremic solutes and contribute to systemic inflammation, vascular dysfunction, and disease progression. Dietary fiber has emerged as a promising modulator of gut microbial metabolism, yet the influence of fiber physicochemical properties, particularly fermentability and viscosity, on uremic metabolite production in CKD remains poorly understood.
OBJECTIVE: To systematically evaluate the effects of isolated dietary fiber interventions, classified by fermentability and viscosity, on gut microbial metabolites in CKD across experimental rodent models and randomized clinical trials, and to determine whether these fiber properties modify microbial metabolites.
METHODS: A systematic search of PubMed, Embase, CINAHL, and Cochrane Library (through June 2026) identified randomized controlled trials and controlled rodent studies assessing isolated dietary fiber in CKD. Eligible studies reported at least one gut-derived metabolite (i.e., indoxyl sulfate (IS), p-cresyl sulfate (PCS), trimethylamine-N-oxide (TMAO), tryptophan-derived indoles, or short-chain fatty acids (SCFAs)). Random-effects models were used for pooled estimates using weighted mean differences (WMD) for human studies and standardized mean differences (SMD) for animal studies. Subgroup analyses evaluated fiber fermentability, viscosity, intervention dose, duration, and CKD stage. Risk of bias was assessed with ROB-2 and SYRCLE, and evidence certainty with GRADE.
RESULTS: Twenty-eight studies (13 human, 15 animal) met eligibility criteria, comprising 511 participants and 312 animals with CKD. Isolated fiber supplementation, primarily fermentable and non-viscous fibers, reduced IS (human: -0.13 mg/dL; 95% CI: -0.25, -0.01; p = 0.03; animal: -1.99; 95% CI: -3.06, -0.92; p < 0.0001) and pCS (human: -0.23 mg/dL; 95% CI: -0.46, 0.001; p = 0.051; animal: -1.56; 95% CI: -2.08, -1.03; p < 0.0001). SCFAs increased in animal studies, including cecal acetate (2.00, 95% CI: 0.78 to 3.22; p = 0.001) and circulating propionate (1.51, 95% CI: 0.054 to 2.96; p=0.04). There were no dose-dependent effects, but longer interventions (>8 weeks) tended to lower pCS (-0.26 mg/dL, 95% CI: -0.55 to 0.02; p=0.06). Some heterogeneity and low-to-moderate certainty were observed.
CONCLUSION: Isolated dietary fiber reduces major gut-derived uremic solutes in CKD, with fermentability influencing metabolic responsiveness, but with minimal studies on viscous fibers. Larger, longer-duration trials with standardized reporting of total fiber intake and clinical endpoints are needed to guide evidence-based dietary recommendations in CKD.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
Unlocking cyanidin-3-glucoside potentials with green technologies: advances in extraction, bioavailability, and stability for therapeutic and non-therapeutic applications.
Frontiers in nutrition, 13:1830948.
Research exploring and coupling green technologies and the multi-functional cyanidin-3-glucoside (C3G) molecule is increasing due to many reasons. Beyond its role in plant defense, emitting several plants' hues, and pollination, the unique C3G's structure supports diverse health benefits (therapeutic) and even photochromic (non-therapeutic) properties. A naturally abundant anthocyanin, carbon-rich C3G molecule is found in pigmented plant parts and is now producible via an engineered E. coli strain; however, its numerous applications suffer from its sensitivity to light, oxygen, enzymes, pH, and heat, and the environmental toll of its conventional extraction has limited real-world use. Green techniques are selected due to their low environmental impact, efficiency, and ability to yield by-products that are capable of withstanding harsh environmental conditions. Recent green innovations such as deep-eutectic solvents (DES) are recovering up to 91% of phenolics with 1.5-3 times higher antioxidant activity, while cyclodextrin encapsulation enables the molecule to boost gut microbiome benefits-promoting good bacterial (Bifidobacterium spp.) growth and suppressing the growth of harmful bacteria (e.g., Clostridium histolyticum) in in vitro, animal, and human trial studies. Coupling sustainable green extraction and delivery methods can boost the therapeutic functions of the C3G molecule through the gut-microbiome-liver-brain-immune system axis and enhance its (non-therapeutic) photochromic and additive benefits through improved molecular stabilization.
Additional Links: PMID-42466143
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@article {pmid42466143,
year = {2026},
author = {Zhu, H and Yu, Y and Akan, OD and Li, B and Egong, EJ and Zhu, M and Bassey, ME and Udofia, OE and Xing, Y and Liu, S},
title = {Unlocking cyanidin-3-glucoside potentials with green technologies: advances in extraction, bioavailability, and stability for therapeutic and non-therapeutic applications.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1830948},
pmid = {42466143},
issn = {2296-861X},
abstract = {Research exploring and coupling green technologies and the multi-functional cyanidin-3-glucoside (C3G) molecule is increasing due to many reasons. Beyond its role in plant defense, emitting several plants' hues, and pollination, the unique C3G's structure supports diverse health benefits (therapeutic) and even photochromic (non-therapeutic) properties. A naturally abundant anthocyanin, carbon-rich C3G molecule is found in pigmented plant parts and is now producible via an engineered E. coli strain; however, its numerous applications suffer from its sensitivity to light, oxygen, enzymes, pH, and heat, and the environmental toll of its conventional extraction has limited real-world use. Green techniques are selected due to their low environmental impact, efficiency, and ability to yield by-products that are capable of withstanding harsh environmental conditions. Recent green innovations such as deep-eutectic solvents (DES) are recovering up to 91% of phenolics with 1.5-3 times higher antioxidant activity, while cyclodextrin encapsulation enables the molecule to boost gut microbiome benefits-promoting good bacterial (Bifidobacterium spp.) growth and suppressing the growth of harmful bacteria (e.g., Clostridium histolyticum) in in vitro, animal, and human trial studies. Coupling sustainable green extraction and delivery methods can boost the therapeutic functions of the C3G molecule through the gut-microbiome-liver-brain-immune system axis and enhance its (non-therapeutic) photochromic and additive benefits through improved molecular stabilization.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
Gut microbiota as modulators of obesity and overweight: a registry-based systematic review of clinical trial evidence.
Frontiers in nutrition, 13:1865785.
BACKGROUND: Background: Obesity is a global epidemic that remains inadequately addressed by healthcare systems. The gut microbiota offers a promising metabolic target, yet systematic reviews of clinical trials on microbiome modulators for obesity are scarce.
METHODS: Using the Trialtrove database (September 16, 2025), we performed a registry-based systematic review with the strategy: "(Disease: Obesity) AND (Mechanism: Microbiome modulator)." We included interventional trials targeting overweight/obese populations with defined microbiome-modulating mechanisms; observational and withdrawn/suspended trials were excluded. Extracted data covered phase, status, intervention type, sponsor, location, and participant characteristics. Descriptive analyses used R software (v4.4.3).
RESULTS: Among 217 included trials, 131 (60%) were completed and 37 (17%) ongoing., Academic institutions led sponsorship (157 trials), followed by commercial (45) and government (14). Trials rose sharply after 2011, peaking at 34 in 2023 (over 80% of Phase IV trials that year). Probiotics dominated (141 trials), followed by synbiotics (21) and FMT (22). China (52) and the US (24) led research. Probiotics prevailed in Phases III/IV, whereas FMT concentrated in Phases II/IV with a higher termination rate.
CONCLUSIONS: This study reveals a rapidly growing yet uneven landscape. Probiotics remain the primary focus, academic institutions the main sponsors, and China/US the core hubs. The field has entered a post-marketing evaluation phase dominated by Phase IV studies. Limitations include reliance on a single database and lack of efficacy data, but the study highlights rapid expansion and heterogeneity in this field. Future research should integrate multiple data sources and quality assessments for more comprehensive evidence.
Additional Links: PMID-42466149
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@article {pmid42466149,
year = {2026},
author = {Jiao, B and Jiang, S},
title = {Gut microbiota as modulators of obesity and overweight: a registry-based systematic review of clinical trial evidence.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1865785},
pmid = {42466149},
issn = {2296-861X},
abstract = {BACKGROUND: Background: Obesity is a global epidemic that remains inadequately addressed by healthcare systems. The gut microbiota offers a promising metabolic target, yet systematic reviews of clinical trials on microbiome modulators for obesity are scarce.
METHODS: Using the Trialtrove database (September 16, 2025), we performed a registry-based systematic review with the strategy: "(Disease: Obesity) AND (Mechanism: Microbiome modulator)." We included interventional trials targeting overweight/obese populations with defined microbiome-modulating mechanisms; observational and withdrawn/suspended trials were excluded. Extracted data covered phase, status, intervention type, sponsor, location, and participant characteristics. Descriptive analyses used R software (v4.4.3).
RESULTS: Among 217 included trials, 131 (60%) were completed and 37 (17%) ongoing., Academic institutions led sponsorship (157 trials), followed by commercial (45) and government (14). Trials rose sharply after 2011, peaking at 34 in 2023 (over 80% of Phase IV trials that year). Probiotics dominated (141 trials), followed by synbiotics (21) and FMT (22). China (52) and the US (24) led research. Probiotics prevailed in Phases III/IV, whereas FMT concentrated in Phases II/IV with a higher termination rate.
CONCLUSIONS: This study reveals a rapidly growing yet uneven landscape. Probiotics remain the primary focus, academic institutions the main sponsors, and China/US the core hubs. The field has entered a post-marketing evaluation phase dominated by Phase IV studies. Limitations include reliance on a single database and lack of efficacy data, but the study highlights rapid expansion and heterogeneity in this field. Future research should integrate multiple data sources and quality assessments for more comprehensive evidence.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
Precision obesity medicine: a translational perspective on epigenetics, the gut microbiome, and AI-assisted multi-omics integration.
Frontiers in genetics, 17:1793503.
Additional Links: PMID-42466301
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@article {pmid42466301,
year = {2026},
author = {Jairoun, AA and Al-Hemyari, SS and Shahwan, M and Al-Ghananeem, AM and Al-Salmi, A and Porntaveetus, T and Alhalaweh, A},
title = {Precision obesity medicine: a translational perspective on epigenetics, the gut microbiome, and AI-assisted multi-omics integration.},
journal = {Frontiers in genetics},
volume = {17},
number = {},
pages = {1793503},
pmid = {42466301},
issn = {1664-8021},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
Metagenomic and Metabolomic Correlates of Immunotherapy Response in Non-Small Cell Lung Cancer.
Research square pii:rs.3.rs-10107631.
Background The gut microbiome may influence cancer treatment response, perhaps by immune system interactions, but studies are limited among non-small cell lung cancer (NSCLC) patients. We investigated associations of the pre-treatment gut microbiome and serum metabolome/lipidome with immune checkpoint inhibitor (ICI) response among patients with stage III-IV NSCLC. Methods We conducted an observational cohort study with fecal and blood collection among 66 patients with stage III-IV NSCLC undergoing ICI therapy, using an updated definition of clinical benefit. Fecal whole genome sequencing, plasma untargeted metabolomics, and serum lipidomics were conducted using liquid chromatography mass spectrometry. Multivariable logistic regression estimated associations of alpha/beta diversity, microbial abundance, metabolites, and lipids with clinical benefit. Microbial taxa, metabolites, lipids, and significant lipids correlations were examined. Results Microbiome composition (beta diversity) differed between participants with and without clinical benefit (P = 0.03). Those with higher relative abundance of Bifidobacterium were less likely (OR per 1-SD = 0.51, 95%CI = 0.25-0.92, P = 0.04) to have clinical benefit. Those with higher Ruminococcus prevalence were more likely (OR = 7.00, 95%CI = 1.80-34.47, P = 0.01) to have clinical benefit. Clinical benefit participants had higher serum concentration of 4-Imidazoleacetate (OR = 6.34, 95%CI = 2.36-22.29, P = 0.001), 6-Bromotryptophan (OR = 3.84, 95%CI = 1.80-10.17, P = 0.002), and lyso-phosphatidylcholines (OR = 4.52, 95%CI = 1.59-17.19, P = 0.01) compared to no clinical benefit, though these findings were not statistically significant after multiple corrections. Conclusions This hypothesis-generating study found Ruminococcus was positively, and Bifidobacterium inversely, associated with ICI response among NSCLC patients. The gut microbiome and related metabolites/lipids were found to be associated with ICI clinical benefit among NSCLC patients. Larger, diverse longitudinal studies are needed to clarify the associations of the microbiome and related metabolites with ICI response among NSCLC patients.
Additional Links: PMID-42466390
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@article {pmid42466390,
year = {2026},
author = {Buro, AW and Gomez, MF and Kim, Y and Ward, NP and Umbarger, M and Ma, L and Vala, A and Hogue, S and Silva, WV and Bailey, A and Pierce, CM and Kim, Y and DeNicola, GM and Byrd, DA and Robinson, LA},
title = {Metagenomic and Metabolomic Correlates of Immunotherapy Response in Non-Small Cell Lung Cancer.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-10107631/v1},
pmid = {42466390},
issn = {2693-5015},
abstract = {Background The gut microbiome may influence cancer treatment response, perhaps by immune system interactions, but studies are limited among non-small cell lung cancer (NSCLC) patients. We investigated associations of the pre-treatment gut microbiome and serum metabolome/lipidome with immune checkpoint inhibitor (ICI) response among patients with stage III-IV NSCLC. Methods We conducted an observational cohort study with fecal and blood collection among 66 patients with stage III-IV NSCLC undergoing ICI therapy, using an updated definition of clinical benefit. Fecal whole genome sequencing, plasma untargeted metabolomics, and serum lipidomics were conducted using liquid chromatography mass spectrometry. Multivariable logistic regression estimated associations of alpha/beta diversity, microbial abundance, metabolites, and lipids with clinical benefit. Microbial taxa, metabolites, lipids, and significant lipids correlations were examined. Results Microbiome composition (beta diversity) differed between participants with and without clinical benefit (P = 0.03). Those with higher relative abundance of Bifidobacterium were less likely (OR per 1-SD = 0.51, 95%CI = 0.25-0.92, P = 0.04) to have clinical benefit. Those with higher Ruminococcus prevalence were more likely (OR = 7.00, 95%CI = 1.80-34.47, P = 0.01) to have clinical benefit. Clinical benefit participants had higher serum concentration of 4-Imidazoleacetate (OR = 6.34, 95%CI = 2.36-22.29, P = 0.001), 6-Bromotryptophan (OR = 3.84, 95%CI = 1.80-10.17, P = 0.002), and lyso-phosphatidylcholines (OR = 4.52, 95%CI = 1.59-17.19, P = 0.01) compared to no clinical benefit, though these findings were not statistically significant after multiple corrections. Conclusions This hypothesis-generating study found Ruminococcus was positively, and Bifidobacterium inversely, associated with ICI response among NSCLC patients. The gut microbiome and related metabolites/lipids were found to be associated with ICI clinical benefit among NSCLC patients. Larger, diverse longitudinal studies are needed to clarify the associations of the microbiome and related metabolites with ICI response among NSCLC patients.},
}
RevDate: 2026-07-17
Beyond Acidification: Microbial Lactate in the Oral Microbiome-Host Axis.
Journal of dental research [Epub ahead of print].
Lactate, the major acidic end-product of carbohydrate metabolism in the oral microbiome, has long been recognized as a key driver of tooth demineralization by lowering the tooth surface pH below the critical threshold for enamel dissolution. Within the framework of the ecological plaque hypothesis, this frequent and prolonged acidification contributes to dysbiosis by favoring acidogenic and aciduric microorganisms. However, accumulating evidence indicates that microbiome-derived lactate plays broader roles in both microbial ecology and host physiology. This review synthesizes current knowledge on the multifaceted functions of lactate within the oral microbiome-host axis. Lactate produced by saccharolytic bacteria, mainly including Streptococcus, Actinomyces, and Lactobacillus, as well as Rothia and Gemella, is extensively used by commensal taxa, including Veillonella, Neisseria, Rothia, and Streptococcus oligofermentans, and is primarily converted into acetate, propionate, and carbon dioxide. These cross-feeding interactions form integral metabolic networks within oral biofilms that are tightly coupled to the production of bioactive molecules, including nitrite, hydrogen peroxide, and hydrogen sulfide, contributing to microbial ecological homeostasis. Nitrite may further enter the systemic circulation and exert physiological effects, such as peripheral vasodilation via nitric oxide production through the nitrate-nitrite-nitric oxide pathway. Furthermore, in addition to directly damaging host cells at high concentrations, lactate may function as a signaling molecule through hydroxycarboxylic acid receptor 1 on host cells, potentially modulating cellular responses by regulating metabolic and signal transduction pathways. Lactate is also transported into cells via monocarboxylate transporters, where it serves as a metabolic substrate for redox regulation and induces epigenetic modifications through histone and non-histone protein lactylation, thereby affecting host cell functions. These multifaceted functions highlight lactate as a metabolic and signaling hub in the oral microbiome-host axis. The modulation of the lactate flux, rather than simply inhibiting microbial lactate production, may offer a new strategy for maintaining and promoting oral and systemic health.
Additional Links: PMID-42466715
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@article {pmid42466715,
year = {2026},
author = {Takahashi, N},
title = {Beyond Acidification: Microbial Lactate in the Oral Microbiome-Host Axis.},
journal = {Journal of dental research},
volume = {},
number = {},
pages = {220345261462879},
doi = {10.1177/00220345261462879},
pmid = {42466715},
issn = {1544-0591},
abstract = {Lactate, the major acidic end-product of carbohydrate metabolism in the oral microbiome, has long been recognized as a key driver of tooth demineralization by lowering the tooth surface pH below the critical threshold for enamel dissolution. Within the framework of the ecological plaque hypothesis, this frequent and prolonged acidification contributes to dysbiosis by favoring acidogenic and aciduric microorganisms. However, accumulating evidence indicates that microbiome-derived lactate plays broader roles in both microbial ecology and host physiology. This review synthesizes current knowledge on the multifaceted functions of lactate within the oral microbiome-host axis. Lactate produced by saccharolytic bacteria, mainly including Streptococcus, Actinomyces, and Lactobacillus, as well as Rothia and Gemella, is extensively used by commensal taxa, including Veillonella, Neisseria, Rothia, and Streptococcus oligofermentans, and is primarily converted into acetate, propionate, and carbon dioxide. These cross-feeding interactions form integral metabolic networks within oral biofilms that are tightly coupled to the production of bioactive molecules, including nitrite, hydrogen peroxide, and hydrogen sulfide, contributing to microbial ecological homeostasis. Nitrite may further enter the systemic circulation and exert physiological effects, such as peripheral vasodilation via nitric oxide production through the nitrate-nitrite-nitric oxide pathway. Furthermore, in addition to directly damaging host cells at high concentrations, lactate may function as a signaling molecule through hydroxycarboxylic acid receptor 1 on host cells, potentially modulating cellular responses by regulating metabolic and signal transduction pathways. Lactate is also transported into cells via monocarboxylate transporters, where it serves as a metabolic substrate for redox regulation and induces epigenetic modifications through histone and non-histone protein lactylation, thereby affecting host cell functions. These multifaceted functions highlight lactate as a metabolic and signaling hub in the oral microbiome-host axis. The modulation of the lactate flux, rather than simply inhibiting microbial lactate production, may offer a new strategy for maintaining and promoting oral and systemic health.},
}
RevDate: 2026-07-17
Wolbachia-centered cytoplasmic axis links elevational mitochondrial DNA turnover with microbiome restructuring.
The ISME journal pii:8736527 [Epub ahead of print].
Mountain gradients act as natural experiments, and elevational mitochondrial DNA clines in insects are often interpreted as signatures of local metabolic adaptation. However, mitochondrial DNA is maternally co-inherited with heritable endosymbionts that can promote cytoplasmic hitchhiking and, when abundant, dominate marker-gene microbiome profiles, complicating inference about environmental forcing. Here we evaluate a symbiont-aware cytoplasmic-axis framework in the tea green leafhopper Empoasca onukii using a densely replicated elevational survey across tea agroecosystems. Across 790 adults from 79 sites spanning 11 to 2750 meters above sea level, we quantified Wolbachia infection prevalence, within-host burden, and strain composition and related these measures to mitochondrial haplotypes, a conservative nuclear reference marker, and whole-insect bacterial community profiles. Wolbachia prevalence, burden, and strain composition varied along elevation, with pronounced strain turnover. Mitochondrial diversity declined and haplotypes homogenized at high elevation, whereas the nuclear reference marker showed weak spatial structure, yielding mitochondrial-nuclear discordance consistent with cytoplasmic hitchhiking and sweep-like mtDNA homogenization. Bacterial community separation was strongest when Wolbachia features were retained but persisted after Wolbachia removal and renormalization, indicating both compositional dominance by Wolbachia and residual restructuring among non-Wolbachia taxa. In a balanced subset, mitochondrial coding variation and host energetic readouts provided observational functional context for the Wolbachia-centered cytoplasmic-axis pattern. Together, these results place Wolbachia at the center of a testable cytoplasmic framework linking elevational mitochondrial turnover with microbiome restructuring, and highlight the broader importance of dominant heritable symbionts.
Additional Links: PMID-42466849
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PubMed:
Citation:
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@article {pmid42466849,
year = {2026},
author = {Zhang, Y and Huang, X and Li, Q and Ruan, Y and Long, Y and Zhang, S and Yang, Y},
title = {Wolbachia-centered cytoplasmic axis links elevational mitochondrial DNA turnover with microbiome restructuring.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag188},
pmid = {42466849},
issn = {1751-7370},
abstract = {Mountain gradients act as natural experiments, and elevational mitochondrial DNA clines in insects are often interpreted as signatures of local metabolic adaptation. However, mitochondrial DNA is maternally co-inherited with heritable endosymbionts that can promote cytoplasmic hitchhiking and, when abundant, dominate marker-gene microbiome profiles, complicating inference about environmental forcing. Here we evaluate a symbiont-aware cytoplasmic-axis framework in the tea green leafhopper Empoasca onukii using a densely replicated elevational survey across tea agroecosystems. Across 790 adults from 79 sites spanning 11 to 2750 meters above sea level, we quantified Wolbachia infection prevalence, within-host burden, and strain composition and related these measures to mitochondrial haplotypes, a conservative nuclear reference marker, and whole-insect bacterial community profiles. Wolbachia prevalence, burden, and strain composition varied along elevation, with pronounced strain turnover. Mitochondrial diversity declined and haplotypes homogenized at high elevation, whereas the nuclear reference marker showed weak spatial structure, yielding mitochondrial-nuclear discordance consistent with cytoplasmic hitchhiking and sweep-like mtDNA homogenization. Bacterial community separation was strongest when Wolbachia features were retained but persisted after Wolbachia removal and renormalization, indicating both compositional dominance by Wolbachia and residual restructuring among non-Wolbachia taxa. In a balanced subset, mitochondrial coding variation and host energetic readouts provided observational functional context for the Wolbachia-centered cytoplasmic-axis pattern. Together, these results place Wolbachia at the center of a testable cytoplasmic framework linking elevational mitochondrial turnover with microbiome restructuring, and highlight the broader importance of dominant heritable symbionts.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
Gut microbiota-nanoparticle interactions in Parkinson's disease: mechanistic insights and therapeutic perspective.
Artificial cells, nanomedicine, and biotechnology, 54(1):321-336.
OBJECTIVE: This review introduces the 'nanomaterial-microbiome-brain interface' as a conceptual framework uniting three systems: gut microbiota, nanoparticles, and neurodegeneration.
MAIN FINDINGS: We synthesize evidence showing that titanium dioxide, silver, and zinc oxide nanoparticles differentially alter microbial composition. These microbial shifts intersect with established gut-brain mechanisms, including short-chain fatty acid production and immune modulation, providing plausible pathways linking nanomaterial exposure to neurological outcomes.
CONCLUSION: We propose the 'nanomaterial-microbiome-brain interface' as a novel conceptual framework with twofold relevance-serving both as a potential contributor to Parkinson's disease pathogenesis through unintentional environmental exposure, and as an underexplored avenue for therapeutic intervention. Critical knowledge gaps persist. Addressing these gaps will require integrated approaches that bridge nanomaterial research, microbiome science, and neurodegeneration studies.
Additional Links: PMID-42466852
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PubMed:
Citation:
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@article {pmid42466852,
year = {2026},
author = {Kafshdooz, L and Safaralizadeh, R},
title = {Gut microbiota-nanoparticle interactions in Parkinson's disease: mechanistic insights and therapeutic perspective.},
journal = {Artificial cells, nanomedicine, and biotechnology},
volume = {54},
number = {1},
pages = {321-336},
doi = {10.1080/21691401.2026.2694921},
pmid = {42466852},
issn = {2169-141X},
mesh = {*Parkinson Disease/microbiology/therapy/metabolism/pathology ; Humans ; *Gastrointestinal Microbiome/drug effects ; Animals ; *Nanoparticles ; *Metal Nanoparticles/chemistry ; },
abstract = {OBJECTIVE: This review introduces the 'nanomaterial-microbiome-brain interface' as a conceptual framework uniting three systems: gut microbiota, nanoparticles, and neurodegeneration.
MAIN FINDINGS: We synthesize evidence showing that titanium dioxide, silver, and zinc oxide nanoparticles differentially alter microbial composition. These microbial shifts intersect with established gut-brain mechanisms, including short-chain fatty acid production and immune modulation, providing plausible pathways linking nanomaterial exposure to neurological outcomes.
CONCLUSION: We propose the 'nanomaterial-microbiome-brain interface' as a novel conceptual framework with twofold relevance-serving both as a potential contributor to Parkinson's disease pathogenesis through unintentional environmental exposure, and as an underexplored avenue for therapeutic intervention. Critical knowledge gaps persist. Addressing these gaps will require integrated approaches that bridge nanomaterial research, microbiome science, and neurodegeneration studies.},
}
MeSH Terms:
show MeSH Terms
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*Parkinson Disease/microbiology/therapy/metabolism/pathology
Humans
*Gastrointestinal Microbiome/drug effects
Animals
*Nanoparticles
*Metal Nanoparticles/chemistry
RevDate: 2026-07-17
The functional structure of foxtail millet rhizoplane microbiome and its association with yield.
Microbiology spectrum [Epub ahead of print].
UNLABELLED: Root-associated microbial communities profoundly influence plant growth and productivity. Although the rhizosphere microbiome has been extensively studied, the functional distinctiveness and host-specific role of the closely adhering rhizoplane microbiota remain unclear. In this study, we performed deep metagenomic sequencing of both the rhizosphere and rhizoplane microbiomes in foxtail millet (Setaria italica). We constructed a comprehensive non-redundant gene catalog, reconstructed 595 metagenome-assembled genomes (MAGs), and analyzed the co-occurrence networks. Our results revealed that the rhizoplane sustains a core microbial network with greater complexity and connectivity than rhizospheres. Metabolically, the rhizoplane microbiome is enriched in the functions underlying host adaptation, including ammonium production and polysaccharide decomposition. Our results showed that the associations between microbial features (taxonomic and functional) and yield were significantly stronger in the rhizoplane than in the rhizosphere. We identified 22 yield-positive MAGs, primarily from Bacillales, harboring genes for plant growth-promoting traits, such as nutrient solubilization and phytohormone synthesis. Collectively, our findings illustrate that the rhizoplane is not only a subset of the rhizosphere but also a critical host-microbe interface and functional hotspot where specialized microbial processes are directly coordinated to enhance plant performance and yield.
IMPORTANCE: Plant roots selectively recruit diverse and beneficial microorganisms from the surrounding soil, assembling a distinctive rhizosphere microbiome. Substantial research, primarily utilizing amplicon sequencing, has elucidated the taxonomic composition of these rhizosphere communities across a wide range of plant species. The functional architecture, assembly processes, and coexistence mechanisms of the rhizoplane microbiome remain poorly understood, and their link to host plant traits is unclear. We elucidate the taxonomic and functional structural disparities between the rhizosphere and rhizoplane microbiomes, thereby clarifying the composition and functional roles of the rhizoplane microbiome, and further examine the association between the rhizoplane microbiome and millet yield. A deeper understanding of root-associated microbial communities may inform the development of effective agricultural probiotics, thereby enhancing sustainable farming practices. Additionally, the candidate biomarkers identified in this work offer potential targets for improving cultivation practices and supporting the long-term agricultural sustainability of foxtail millet.
Additional Links: PMID-42466871
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PubMed:
Citation:
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@article {pmid42466871,
year = {2026},
author = {Jin, C and Chen, Q and Liu, X and Liu, H and Wang, Y},
title = {The functional structure of foxtail millet rhizoplane microbiome and its association with yield.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0070726},
doi = {10.1128/spectrum.00707-26},
pmid = {42466871},
issn = {2165-0497},
abstract = {UNLABELLED: Root-associated microbial communities profoundly influence plant growth and productivity. Although the rhizosphere microbiome has been extensively studied, the functional distinctiveness and host-specific role of the closely adhering rhizoplane microbiota remain unclear. In this study, we performed deep metagenomic sequencing of both the rhizosphere and rhizoplane microbiomes in foxtail millet (Setaria italica). We constructed a comprehensive non-redundant gene catalog, reconstructed 595 metagenome-assembled genomes (MAGs), and analyzed the co-occurrence networks. Our results revealed that the rhizoplane sustains a core microbial network with greater complexity and connectivity than rhizospheres. Metabolically, the rhizoplane microbiome is enriched in the functions underlying host adaptation, including ammonium production and polysaccharide decomposition. Our results showed that the associations between microbial features (taxonomic and functional) and yield were significantly stronger in the rhizoplane than in the rhizosphere. We identified 22 yield-positive MAGs, primarily from Bacillales, harboring genes for plant growth-promoting traits, such as nutrient solubilization and phytohormone synthesis. Collectively, our findings illustrate that the rhizoplane is not only a subset of the rhizosphere but also a critical host-microbe interface and functional hotspot where specialized microbial processes are directly coordinated to enhance plant performance and yield.
IMPORTANCE: Plant roots selectively recruit diverse and beneficial microorganisms from the surrounding soil, assembling a distinctive rhizosphere microbiome. Substantial research, primarily utilizing amplicon sequencing, has elucidated the taxonomic composition of these rhizosphere communities across a wide range of plant species. The functional architecture, assembly processes, and coexistence mechanisms of the rhizoplane microbiome remain poorly understood, and their link to host plant traits is unclear. We elucidate the taxonomic and functional structural disparities between the rhizosphere and rhizoplane microbiomes, thereby clarifying the composition and functional roles of the rhizoplane microbiome, and further examine the association between the rhizoplane microbiome and millet yield. A deeper understanding of root-associated microbial communities may inform the development of effective agricultural probiotics, thereby enhancing sustainable farming practices. Additionally, the candidate biomarkers identified in this work offer potential targets for improving cultivation practices and supporting the long-term agricultural sustainability of foxtail millet.},
}
RevDate: 2026-07-17
Longitudinal changes in the vaginal microbiome associate with spontaneous preterm birth: a focus on stability and specific taxa in a Chinese cohort.
Microbiology spectrum [Epub ahead of print].
Spontaneous preterm birth (sPTB) often results from ascending intra-amniotic infections originating from the vaginal microbiota. This study aimed to characterize vaginal microbial features and identify specific taxa associated with sPTB in a Chinese population. In this prospective cohort study, pregnant women were recruited from Peking Union Medical College Hospital. Vaginal swabs were collected longitudinally at 11-16, 22-28, and 34-37 weeks of gestation. DNA was analyzed using targeted real-time PCR (30 pathogens) and 16S rRNA gene sequencing (V3-V4). Community State Types (CSTs) were defined by enterotype-like clustering. Differential abundance was assessed using MaAsLin3 with Benjamini-Hochberg correction, adjusting for maternal age, BMI, and obstetric history. Among 273 women (26 sPTB, 247 term), no CST was significantly associated with sPTB after multivariable adjustment and false discovery rate (FDR) correction (all q > 0.05). Alpha and beta diversity also showed no significant between-group differences (all q > 0.05). However, longitudinal CST stability was significantly lower in the sPTB group (P < 0.05). Nominally significant associations were observed for Ureaplasma urealyticum (first trimester), Mycoplasma hominis, and Bacteroides fragilis (second trimester), but none survived FDR correction (all q > 0.05). In this Chinese cohort, sPTB was not associated with static CST profiles but with reduced microbial stability over time. Although no single taxon remained significant after correction, several pathogens showed nominal associations, warranting further investigation in larger studies.IMPORTANCEPreterm birth (PTB) is a global maternal and infant health issue affecting approximately 11% of newborns worldwide. In China, the prevalence of PTB was 6.1%. Abnormal vaginal microbiota has been demonstrated to be a risk factor for PTB. Our study is one of the largest studies performed to date to investigate the associations between vaginal microbiome and spontaneous PTB (sPTB) in the Chinese cohort. We found that vaginal microbiome dynamics changes in Community State Types (CSTs) were significantly associated with sPTB. Furthermore, we also found that the microbial risk for sPTB appeared to be the enrichment of specific taxa, suggesting that vaginal dynamics and fine-scale features are important factors to consider in future studies.
Additional Links: PMID-42466879
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PubMed:
Citation:
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@article {pmid42466879,
year = {2026},
author = {Yu, Y and Zhou, J and Zhou, Q and Li, X and Zhang, L and Li, S and Zhu, B and Gao, J and Liu, J},
title = {Longitudinal changes in the vaginal microbiome associate with spontaneous preterm birth: a focus on stability and specific taxa in a Chinese cohort.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0370525},
doi = {10.1128/spectrum.03705-25},
pmid = {42466879},
issn = {2165-0497},
abstract = {Spontaneous preterm birth (sPTB) often results from ascending intra-amniotic infections originating from the vaginal microbiota. This study aimed to characterize vaginal microbial features and identify specific taxa associated with sPTB in a Chinese population. In this prospective cohort study, pregnant women were recruited from Peking Union Medical College Hospital. Vaginal swabs were collected longitudinally at 11-16, 22-28, and 34-37 weeks of gestation. DNA was analyzed using targeted real-time PCR (30 pathogens) and 16S rRNA gene sequencing (V3-V4). Community State Types (CSTs) were defined by enterotype-like clustering. Differential abundance was assessed using MaAsLin3 with Benjamini-Hochberg correction, adjusting for maternal age, BMI, and obstetric history. Among 273 women (26 sPTB, 247 term), no CST was significantly associated with sPTB after multivariable adjustment and false discovery rate (FDR) correction (all q > 0.05). Alpha and beta diversity also showed no significant between-group differences (all q > 0.05). However, longitudinal CST stability was significantly lower in the sPTB group (P < 0.05). Nominally significant associations were observed for Ureaplasma urealyticum (first trimester), Mycoplasma hominis, and Bacteroides fragilis (second trimester), but none survived FDR correction (all q > 0.05). In this Chinese cohort, sPTB was not associated with static CST profiles but with reduced microbial stability over time. Although no single taxon remained significant after correction, several pathogens showed nominal associations, warranting further investigation in larger studies.IMPORTANCEPreterm birth (PTB) is a global maternal and infant health issue affecting approximately 11% of newborns worldwide. In China, the prevalence of PTB was 6.1%. Abnormal vaginal microbiota has been demonstrated to be a risk factor for PTB. Our study is one of the largest studies performed to date to investigate the associations between vaginal microbiome and spontaneous PTB (sPTB) in the Chinese cohort. We found that vaginal microbiome dynamics changes in Community State Types (CSTs) were significantly associated with sPTB. Furthermore, we also found that the microbial risk for sPTB appeared to be the enrichment of specific taxa, suggesting that vaginal dynamics and fine-scale features are important factors to consider in future studies.},
}
RevDate: 2026-07-17
16S rRNA gene V4 amplicon sequence data from Acropora pulchra tissue microbiome samples from Madura Island, Indonesia.
Microbiology resource announcements [Epub ahead of print].
We report 16S rRNA gene V4 amplicon sequence data from five Acropora pulchra tissue microbiome samples collected from Madura Island, Indonesia, in September 2020. Raw reads are generated on the Illumina NovaSeq 6000 platform, and processed operational taxonomic unit-based files are publicly available for future coral microbiome studies.
Additional Links: PMID-42467015
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PubMed:
Citation:
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@article {pmid42467015,
year = {2026},
author = {Alina, DN and Pasaribu, B and Maqbul, I and Sari, QW and Rachmawati, R},
title = {16S rRNA gene V4 amplicon sequence data from Acropora pulchra tissue microbiome samples from Madura Island, Indonesia.},
journal = {Microbiology resource announcements},
volume = {},
number = {},
pages = {e0055226},
doi = {10.1128/mra.00552-26},
pmid = {42467015},
issn = {2576-098X},
abstract = {We report 16S rRNA gene V4 amplicon sequence data from five Acropora pulchra tissue microbiome samples collected from Madura Island, Indonesia, in September 2020. Raw reads are generated on the Illumina NovaSeq 6000 platform, and processed operational taxonomic unit-based files are publicly available for future coral microbiome studies.},
}
RevDate: 2026-07-17
Complete genome sequencing and assembly of two Novosphingobium spp. isolated from the phyllosphere of Actinidia chinensis (kiwifruit).
Microbiology resource announcements [Epub ahead of print].
Two Novosphingobium strains designated as TK46 and TK71 were isolated from kiwifruit leaves (Actinidia chinensis var. chinensis 'Zesy002,' commonly known as Gold3) in Te Kaha, New Zealand. We report their complete genome sequences, providing valuable resources for understanding their ecology and potential applications in plant-associated microbial research.
Additional Links: PMID-42467016
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PubMed:
Citation:
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@article {pmid42467016,
year = {2026},
author = {Idelchik, P and Summers, MC and Gerth, ML},
title = {Complete genome sequencing and assembly of two Novosphingobium spp. isolated from the phyllosphere of Actinidia chinensis (kiwifruit).},
journal = {Microbiology resource announcements},
volume = {},
number = {},
pages = {e0025726},
doi = {10.1128/mra.00257-26},
pmid = {42467016},
issn = {2576-098X},
abstract = {Two Novosphingobium strains designated as TK46 and TK71 were isolated from kiwifruit leaves (Actinidia chinensis var. chinensis 'Zesy002,' commonly known as Gold3) in Te Kaha, New Zealand. We report their complete genome sequences, providing valuable resources for understanding their ecology and potential applications in plant-associated microbial research.},
}
RevDate: 2026-07-17
Balancing act of cytokines in controlling the severity of Clostridioides difficile infection.
Infection and immunity [Epub ahead of print].
The severity of Clostridioides difficile infection is dictated by a complex interplay of various host cell types and inflammatory mediators responding to the pathogen and surrounding microbiome. An effective immune response must carefully balance controlling C. difficile-mediated pathology and systemic dissemination of opportunistic bacteria while avoiding collateral immunopathology. In addition, a successful immune response must also promote restorative mechanisms to repair toxin-induced disruptions to the intestinal barrier. Here, we review the immune response to C. difficile infection with a specific focus on the role of innate immune-induced cytokines.
Additional Links: PMID-42467062
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PubMed:
Citation:
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@article {pmid42467062,
year = {2026},
author = {Mears, KS and Abt, MC},
title = {Balancing act of cytokines in controlling the severity of Clostridioides difficile infection.},
journal = {Infection and immunity},
volume = {},
number = {},
pages = {e0055125},
doi = {10.1128/iai.00551-25},
pmid = {42467062},
issn = {1098-5522},
abstract = {The severity of Clostridioides difficile infection is dictated by a complex interplay of various host cell types and inflammatory mediators responding to the pathogen and surrounding microbiome. An effective immune response must carefully balance controlling C. difficile-mediated pathology and systemic dissemination of opportunistic bacteria while avoiding collateral immunopathology. In addition, a successful immune response must also promote restorative mechanisms to repair toxin-induced disruptions to the intestinal barrier. Here, we review the immune response to C. difficile infection with a specific focus on the role of innate immune-induced cytokines.},
}
RevDate: 2026-07-17
CmpDate: 2026-07-17
Neoadjuvant therapies for clear cell renal cell carcinoma: review of current evidence and future applications.
World journal of urology, 44(1):.
PURPOSE: Neoadjuvant systemic therapy for clear cell renal cell carcinoma (ccRCC) aim to improve oncological and survival outcomes in patients with high-risk disease. This review evaluates contemporary evidence for neoadjuvant and perioperative systemic therapies in ccRCC, with a focus on localised high-risk disease, venous tumour thrombus and metastatic or cytoreductive settings.
METHODS: A review of the literature was performed using PubMed, Embase and Web of Science from database inception to February 2026. Eligible studies included randomised controlled trials, prospective and retrospective clinical studies, and translational research evaluating neoadjuvant therapies in RCC. Evidence was synthesised by therapeutic class, with emphasis on prospective trials and clinically relevant outcomes.
RESULTS: Neoadjuvant TKIs demonstrate mild to moderate tumour shrinkage and reduction in tumour thrombus burden, with a resultant improvement in operative complexity and an increase in the number of patients eligible for surgical intervention. ICI monotherapy has shown limited efficacy in early-phase studies. However, combination ICI-TKI regimens report higher objective response rates on interval imaging, with tumour downstaging and encouraging early disease-free survival results. Perioperative complication rates appear acceptable across studies, with no consistent increase in surgical morbidity. However, discordance between radiological and pathological responses remains a limitation. Translational studies further highlight the potential role of immune profiling, genomic biomarkers, microbiome modulation and theranostic approaches, although prospective validation remains lacking.
CONCLUSION: Neoadjuvant therapy in ccRCC is feasible and demonstrates promising early efficacy, particularly with combination regimens. However, current evidence is limited by heterogeneity and lack of long-term outcomes. Larger prospective trials incorporating translational endpoints are required to define optimal treatment strategies and establish survival benefit.
Additional Links: PMID-42467100
PubMed:
Citation:
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@article {pmid42467100,
year = {2026},
author = {McMaster, T and McVeigh, N and Chen, DC and Al-Khanaty, A and Sandhu, K and Carll, J and Woon, DT and Murphy, DG and Lawrentschuck, N and Au, L and Ali, M and Siva, S and Perera, M},
title = {Neoadjuvant therapies for clear cell renal cell carcinoma: review of current evidence and future applications.},
journal = {World journal of urology},
volume = {44},
number = {1},
pages = {},
pmid = {42467100},
issn = {1433-8726},
mesh = {Humans ; *Carcinoma, Renal Cell/therapy/secondary ; *Kidney Neoplasms/therapy/pathology/drug therapy ; *Neoadjuvant Therapy ; },
abstract = {PURPOSE: Neoadjuvant systemic therapy for clear cell renal cell carcinoma (ccRCC) aim to improve oncological and survival outcomes in patients with high-risk disease. This review evaluates contemporary evidence for neoadjuvant and perioperative systemic therapies in ccRCC, with a focus on localised high-risk disease, venous tumour thrombus and metastatic or cytoreductive settings.
METHODS: A review of the literature was performed using PubMed, Embase and Web of Science from database inception to February 2026. Eligible studies included randomised controlled trials, prospective and retrospective clinical studies, and translational research evaluating neoadjuvant therapies in RCC. Evidence was synthesised by therapeutic class, with emphasis on prospective trials and clinically relevant outcomes.
RESULTS: Neoadjuvant TKIs demonstrate mild to moderate tumour shrinkage and reduction in tumour thrombus burden, with a resultant improvement in operative complexity and an increase in the number of patients eligible for surgical intervention. ICI monotherapy has shown limited efficacy in early-phase studies. However, combination ICI-TKI regimens report higher objective response rates on interval imaging, with tumour downstaging and encouraging early disease-free survival results. Perioperative complication rates appear acceptable across studies, with no consistent increase in surgical morbidity. However, discordance between radiological and pathological responses remains a limitation. Translational studies further highlight the potential role of immune profiling, genomic biomarkers, microbiome modulation and theranostic approaches, although prospective validation remains lacking.
CONCLUSION: Neoadjuvant therapy in ccRCC is feasible and demonstrates promising early efficacy, particularly with combination regimens. However, current evidence is limited by heterogeneity and lack of long-term outcomes. Larger prospective trials incorporating translational endpoints are required to define optimal treatment strategies and establish survival benefit.},
}
MeSH Terms:
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Humans
*Carcinoma, Renal Cell/therapy/secondary
*Kidney Neoplasms/therapy/pathology/drug therapy
*Neoadjuvant Therapy
RevDate: 2026-07-17
CmpDate: 2026-07-17
Stenotrophomonas maltophilia in a Rhipicephalus linnaei tick cell culture: detection, antibiotic resistance and multi-locus sequence typing.
Antonie van Leeuwenhoek, 119(8):.
Ticks harbour diverse microbial communities, but opportunistic and environmentally associated bacteria within these systems remain poorly understood. During attempts to establish primary cell cultures from surface-sterilized embryos of the dog tick Rhipicephalus linnaei, we detected the presence of Stenotrophomonas maltophilia, a multidrug-resistant environmental bacterium and emerging opportunistic pathogen. Microscopic examination of Giemsa-stained smears showed abundant extracellular rod-shaped bacteria closely associated with degenerating tick cells, with no evidence of intracellular infection. Molecular identification based on 16S and 23S rRNA gene sequencing confirmed the bacteria as S. maltophilia, and antibiotic susceptibility testing revealed resistance to amoxicillin-clavulanic acid, imipenem, cefoxitin, and nitrofurantoin, but susceptibility to meropenem. Multi-locus sequence typing (MLST) identified the isolate as sequence type 948 (ST948), which is a single-locus variant of ST408 and a double-locus variant of ST144, both of which are representatives of environmental and clinical S. maltophilia strains from diverse geographic origins. These findings provide the first evidence of S. maltophilia occurring in a tick-derived cell culture system and highlight the need to consider opportunistic bacteria when interpreting tick microbiome and cell culture-based studies, particularly those involving veterinary-relevant tick species.
Additional Links: PMID-42467116
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@article {pmid42467116,
year = {2026},
author = {Husin, NA and Loong, SK and Lee, HY and Sahimin, N and Yap, PC and Khoo, JJ and Darby, A and Bell-Sakyi, L and Makepeace, BL and Low, VL},
title = {Stenotrophomonas maltophilia in a Rhipicephalus linnaei tick cell culture: detection, antibiotic resistance and multi-locus sequence typing.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {8},
pages = {},
pmid = {42467116},
issn = {1572-9699},
support = {MO002-2019 & TIDREC-2023//Ministry of Higher Education, Malaysia/ ; 223743/Z/21/Z/WT_/Wellcome Trust/United Kingdom ; },
mesh = {Animals ; *Rhipicephalus/microbiology ; *Stenotrophomonas maltophilia/genetics/drug effects/isolation & purification/classification ; Anti-Bacterial Agents/pharmacology ; RNA, Ribosomal, 16S/genetics ; Multilocus Sequence Typing ; Microbial Sensitivity Tests ; Phylogeny ; *Drug Resistance, Bacterial ; DNA, Bacterial/genetics ; RNA, Ribosomal, 23S/genetics ; },
abstract = {Ticks harbour diverse microbial communities, but opportunistic and environmentally associated bacteria within these systems remain poorly understood. During attempts to establish primary cell cultures from surface-sterilized embryos of the dog tick Rhipicephalus linnaei, we detected the presence of Stenotrophomonas maltophilia, a multidrug-resistant environmental bacterium and emerging opportunistic pathogen. Microscopic examination of Giemsa-stained smears showed abundant extracellular rod-shaped bacteria closely associated with degenerating tick cells, with no evidence of intracellular infection. Molecular identification based on 16S and 23S rRNA gene sequencing confirmed the bacteria as S. maltophilia, and antibiotic susceptibility testing revealed resistance to amoxicillin-clavulanic acid, imipenem, cefoxitin, and nitrofurantoin, but susceptibility to meropenem. Multi-locus sequence typing (MLST) identified the isolate as sequence type 948 (ST948), which is a single-locus variant of ST408 and a double-locus variant of ST144, both of which are representatives of environmental and clinical S. maltophilia strains from diverse geographic origins. These findings provide the first evidence of S. maltophilia occurring in a tick-derived cell culture system and highlight the need to consider opportunistic bacteria when interpreting tick microbiome and cell culture-based studies, particularly those involving veterinary-relevant tick species.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Rhipicephalus/microbiology
*Stenotrophomonas maltophilia/genetics/drug effects/isolation & purification/classification
Anti-Bacterial Agents/pharmacology
RNA, Ribosomal, 16S/genetics
Multilocus Sequence Typing
Microbial Sensitivity Tests
Phylogeny
*Drug Resistance, Bacterial
DNA, Bacterial/genetics
RNA, Ribosomal, 23S/genetics
RevDate: 2026-07-17
CmpDate: 2026-07-17
Microplastics, the gut microbiome and ageing: mechanisms and intervention strategies.
Environmental geochemistry and health, 48(11):.
As a pervasive global environmental concern, micro- and nanoplastic (MNPs) pollution leads to widespread systemic human exposure via three main routes: oral ingestion, inhalation, and dermal absorption. Accumulating evidence demonstrates that MNPs are strongly associated with ageing and age-related pathologies, including cardiovascular and neurodegenerative disorders. Meanwhile, the gut microbiome, an intensely studied regulatory mediator, plays a critical role in modulating human ageing. This review systematically summarizes the routes of human exposure to MNPs and their mechanistic links to human ageing. It delineates the interplay among MNPs, the gut microbiome and human ageing, and elucidates how the MNPs-gut microbiome Axis drives oxidative stress, chronic inflammation, cellular senescence, and mitochondrial dysfunction, disrupts epigenetic modulation, and activates core ageing-related pathways such as TLR4/NF-κB, ultimately exacerbating systemic inflammation and organ dysfunction. Furthermore, this review proposes multi-pronged intervention strategies, providing a scientific basis for mitigating MNPs pollution and its associated health risks, and offering novel theoretical insights for the development of anti-ageing interventions.
Additional Links: PMID-42467131
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@article {pmid42467131,
year = {2026},
author = {Li, Z and Li, Y and Yurong, T and Guojun, W},
title = {Microplastics, the gut microbiome and ageing: mechanisms and intervention strategies.},
journal = {Environmental geochemistry and health},
volume = {48},
number = {11},
pages = {},
pmid = {42467131},
issn = {1573-2983},
mesh = {Humans ; *Aging/drug effects ; *Gastrointestinal Microbiome/drug effects ; *Microplastics/toxicity ; Environmental Exposure ; Oxidative Stress/drug effects ; Animals ; *Environmental Pollutants/toxicity ; Inflammation ; },
abstract = {As a pervasive global environmental concern, micro- and nanoplastic (MNPs) pollution leads to widespread systemic human exposure via three main routes: oral ingestion, inhalation, and dermal absorption. Accumulating evidence demonstrates that MNPs are strongly associated with ageing and age-related pathologies, including cardiovascular and neurodegenerative disorders. Meanwhile, the gut microbiome, an intensely studied regulatory mediator, plays a critical role in modulating human ageing. This review systematically summarizes the routes of human exposure to MNPs and their mechanistic links to human ageing. It delineates the interplay among MNPs, the gut microbiome and human ageing, and elucidates how the MNPs-gut microbiome Axis drives oxidative stress, chronic inflammation, cellular senescence, and mitochondrial dysfunction, disrupts epigenetic modulation, and activates core ageing-related pathways such as TLR4/NF-κB, ultimately exacerbating systemic inflammation and organ dysfunction. Furthermore, this review proposes multi-pronged intervention strategies, providing a scientific basis for mitigating MNPs pollution and its associated health risks, and offering novel theoretical insights for the development of anti-ageing interventions.},
}
MeSH Terms:
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Humans
*Aging/drug effects
*Gastrointestinal Microbiome/drug effects
*Microplastics/toxicity
Environmental Exposure
Oxidative Stress/drug effects
Animals
*Environmental Pollutants/toxicity
Inflammation
RevDate: 2026-07-17
CmpDate: 2026-07-17
A comparative analysis of gut microbiome in dogs using short- and long-reads of 16S rRNA sequences reveals workflow-dependent biases.
Veterinary research communications, 50(5):.
Short-read Illumina sequencing of hypervariable regions of the 16S rRNA gene and long-read Oxford Nanopore Technologies (ONT) sequencing of the full-length 16S gene are increasingly used to profile microbial communities. However, differences in sequencing chemistry, read length, and taxonomic assignment methods raise concerns about the comparability of microbiome profiles and their impact on biological interpretation. Faecal samples from two groups of healthy dogs, 8 young (32 < age < 59 months) and 8 old (age > 109 months), were analysed. Taxonomic relative abundances obtained from Illumina and ONT sequencing were compared after nomenclature harmonisation. Agreement between workflows was assessed using Bland-Altman analysis on log2-transformed relative abundances. Although the mean bias at the genus level was small (0.229), limits of agreement indicated poor interchangeability between workflows. When restricted to taxa detected by both workflows, variability decreased but a larger negative bias emerged, suggesting abundance-dependent discrepancies. The effects of sequencing workflow on biologically relevant signals related to host age were evaluated by computing alpha and beta diversity metrics independently within each workflow. Alpha diversity differed between workflows, with ONT yielding higher Shannon diversity and richness values than Illumina. Beta diversity analyses indicated significant (p < 0.05) age-related shifts in community composition only in ONT, with differences in variance explained and effect sizes. Workflow comparisons revealed taxon-specific differences at phylum, family, and genus levels, affecting both moderately and highly abundant taxa. These findings indicate that sequencing workflow choice impacts microbiome profiling and downstream interpretation, underscoring the need for care in cross-workflow comparisons.
Additional Links: PMID-42467133
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@article {pmid42467133,
year = {2026},
author = {Polacchini, G and Stefanon, B and Mongillo, P and Licastro, D},
title = {A comparative analysis of gut microbiome in dogs using short- and long-reads of 16S rRNA sequences reveals workflow-dependent biases.},
journal = {Veterinary research communications},
volume = {50},
number = {5},
pages = {},
pmid = {42467133},
issn = {1573-7446},
mesh = {Animals ; Dogs/microbiology ; *RNA, Ribosomal, 16S/genetics/analysis ; *Gastrointestinal Microbiome/genetics ; Feces/microbiology ; *Bacteria/classification/genetics ; Workflow ; Sequence Analysis, DNA/veterinary ; },
abstract = {Short-read Illumina sequencing of hypervariable regions of the 16S rRNA gene and long-read Oxford Nanopore Technologies (ONT) sequencing of the full-length 16S gene are increasingly used to profile microbial communities. However, differences in sequencing chemistry, read length, and taxonomic assignment methods raise concerns about the comparability of microbiome profiles and their impact on biological interpretation. Faecal samples from two groups of healthy dogs, 8 young (32 < age < 59 months) and 8 old (age > 109 months), were analysed. Taxonomic relative abundances obtained from Illumina and ONT sequencing were compared after nomenclature harmonisation. Agreement between workflows was assessed using Bland-Altman analysis on log2-transformed relative abundances. Although the mean bias at the genus level was small (0.229), limits of agreement indicated poor interchangeability between workflows. When restricted to taxa detected by both workflows, variability decreased but a larger negative bias emerged, suggesting abundance-dependent discrepancies. The effects of sequencing workflow on biologically relevant signals related to host age were evaluated by computing alpha and beta diversity metrics independently within each workflow. Alpha diversity differed between workflows, with ONT yielding higher Shannon diversity and richness values than Illumina. Beta diversity analyses indicated significant (p < 0.05) age-related shifts in community composition only in ONT, with differences in variance explained and effect sizes. Workflow comparisons revealed taxon-specific differences at phylum, family, and genus levels, affecting both moderately and highly abundant taxa. These findings indicate that sequencing workflow choice impacts microbiome profiling and downstream interpretation, underscoring the need for care in cross-workflow comparisons.},
}
MeSH Terms:
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Animals
Dogs/microbiology
*RNA, Ribosomal, 16S/genetics/analysis
*Gastrointestinal Microbiome/genetics
Feces/microbiology
*Bacteria/classification/genetics
Workflow
Sequence Analysis, DNA/veterinary
RevDate: 2026-07-17
CmpDate: 2026-07-17
Advancements in the study of gut microbiome in disease diagnosis.
Antonie van Leeuwenhoek, 119(8):.
This review summarizes disease-associated changes in gut microbial composition and evaluates the diagnostic performance of models constructed with different machine-learning algorithms. The review seeks to answer questions related to the relationship between the human gut microbiome and disease progression, how different machine learning algorithms affect disease diagnosis using gut microbiome data, and how disease-specific microbial communities impact diagnostic models. Multiple studies report that gut microbiome dysbiosis is commonly observed in many diseases, though patterns vary between conditions and cohorts. Large-scale computational analyses are increasingly applied to identify microbial signatures and to build diagnostic models; however, model performance often depends on data source, preprocessing and choice of algorithm. Overall, evidence indicates disease-associated shifts in gut microbial composition, and that diagnostic model accuracy is sensitive to cohort, sequencing and modeling choices. While certain taxa recur across studies for some diseases, heterogeneity between cohorts limits immediate clinical translation; thus, harmonized study designs and external validation are required. Future work should prioritize reproducible multi-cohort analyses, transparent reporting (e.g., PRISMA for reviews) and prospective validation before clinical deployment.
Additional Links: PMID-42467286
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@article {pmid42467286,
year = {2026},
author = {Liu, K and Huang, Z and Liu, Q},
title = {Advancements in the study of gut microbiome in disease diagnosis.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {8},
pages = {},
pmid = {42467286},
issn = {1572-9699},
mesh = {Humans ; *Gastrointestinal Microbiome ; Machine Learning ; Dysbiosis/microbiology/diagnosis ; Algorithms ; },
abstract = {This review summarizes disease-associated changes in gut microbial composition and evaluates the diagnostic performance of models constructed with different machine-learning algorithms. The review seeks to answer questions related to the relationship between the human gut microbiome and disease progression, how different machine learning algorithms affect disease diagnosis using gut microbiome data, and how disease-specific microbial communities impact diagnostic models. Multiple studies report that gut microbiome dysbiosis is commonly observed in many diseases, though patterns vary between conditions and cohorts. Large-scale computational analyses are increasingly applied to identify microbial signatures and to build diagnostic models; however, model performance often depends on data source, preprocessing and choice of algorithm. Overall, evidence indicates disease-associated shifts in gut microbial composition, and that diagnostic model accuracy is sensitive to cohort, sequencing and modeling choices. While certain taxa recur across studies for some diseases, heterogeneity between cohorts limits immediate clinical translation; thus, harmonized study designs and external validation are required. Future work should prioritize reproducible multi-cohort analyses, transparent reporting (e.g., PRISMA for reviews) and prospective validation before clinical deployment.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome
Machine Learning
Dysbiosis/microbiology/diagnosis
Algorithms
RevDate: 2026-07-17
Ethylene-REF6 regulatory module enables endophyte-mediated thermotolerance of plant growth and reproduction.
Cell reports, 45(7):117688 pii:S2211-1247(26)00766-7 [Epub ahead of print].
Global warming affects plant growth and yield, posing a major threat to global food security. Male sexual reproduction is the most sensitive stage for plant yield under elevated temperature (eT). We show here that under eT conditions, plant growth and male reproduction depend on the ethylene-mediated activity of the histone demethylase REF6. Although eT-compromised plant performance of wild-type plants can be fortified by treatment with the ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC), ref6 mutant plants are insensitive to ACC, showing that ethylene-dependent eT-induced genes depend on REF6 histone demethylase activity. Sexual reproduction and yield, including pollen viability and germination, are strongly compromised in ethylene and ref6 mutants under eT conditions. Intriguingly, we demonstrate that the bacterial endophyte Enterobacter sp. SA187 deploys ethylene-mediated REF6 to protect plant growth and reproduction to eT. These results show that microbiome-assisted approaches can help to ensure food safety under changing climate conditions.
Additional Links: PMID-42467534
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PubMed:
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@article {pmid42467534,
year = {2026},
author = {Fatima, A and Shekhawat, K and Alidrissi, L and Alzayed, W and Farooq, HU and Nagarajan, AP and Gutierrez-Marcos, J and Hirt, H},
title = {Ethylene-REF6 regulatory module enables endophyte-mediated thermotolerance of plant growth and reproduction.},
journal = {Cell reports},
volume = {45},
number = {7},
pages = {117688},
doi = {10.1016/j.celrep.2026.117688},
pmid = {42467534},
issn = {2211-1247},
abstract = {Global warming affects plant growth and yield, posing a major threat to global food security. Male sexual reproduction is the most sensitive stage for plant yield under elevated temperature (eT). We show here that under eT conditions, plant growth and male reproduction depend on the ethylene-mediated activity of the histone demethylase REF6. Although eT-compromised plant performance of wild-type plants can be fortified by treatment with the ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC), ref6 mutant plants are insensitive to ACC, showing that ethylene-dependent eT-induced genes depend on REF6 histone demethylase activity. Sexual reproduction and yield, including pollen viability and germination, are strongly compromised in ethylene and ref6 mutants under eT conditions. Intriguingly, we demonstrate that the bacterial endophyte Enterobacter sp. SA187 deploys ethylene-mediated REF6 to protect plant growth and reproduction to eT. These results show that microbiome-assisted approaches can help to ensure food safety under changing climate conditions.},
}
RevDate: 2026-07-17
24-Epibrassinolide is associated with shifts in rhizosphere microbial assembly and arsenic speciation in rice-cultivated paddy soil.
Journal of environmental management, 414:130468 pii:S0301-4797(26)01928-6 [Epub ahead of print].
Arsenic (As) contamination in paddy soils poses a significant environmental challenge due to its high mobility and potential uptake by rice. Although rhizosphere processes strongly regulate As transformation, the potential role of exogenous phytohormones in modulating these processes remains insufficiently understood. This study investigated the effects of 24-epibrassinolide (EBL) on rhizosphere properties, microbial communities, and As speciation in a rice-cultivated microcosm under different As contamination levels and soil conditions. EBL application significantly altered rhizosphere environmental conditions, increasing soil redox potential (Eh) by 7-20 mV and enhancing soil organic carbon availability. Under high As stress (50 mg kg[-1]), EBL shifted bacterial-community composition, increasing the relative abundance of Proteobacteria by up to 167.6% while decreasing Firmicutes by up to 80.4%. These changes were accompanied by significant increases in soil enzyme activities and alterations in As speciation. In natural soils, the highest EBL treatment reduced the proportion of As(III) by approximately 15% and increased As(V) by approximately 14% relative to the untreated control. Multivariate analyses revealed significant associations among microbial-community composition, soil physicochemical properties, enzyme activities, and As speciation. Overall, the results suggest that EBL may influence As behavior in paddy soils by modifying rhizosphere environmental conditions and biological processes. This study provides new insights into phytohormone-mediated regulation of arsenic dynamics and highlights the potential of EBL as a management strategy for reducing As mobility during early rice growth stages.
Additional Links: PMID-42468124
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PubMed:
Citation:
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@article {pmid42468124,
year = {2026},
author = {Xiao, L and Xu, X and Liang, Y and Yang, D and Wang, G and Liu, H and Motelica-Heino, M},
title = {24-Epibrassinolide is associated with shifts in rhizosphere microbial assembly and arsenic speciation in rice-cultivated paddy soil.},
journal = {Journal of environmental management},
volume = {414},
number = {},
pages = {130468},
doi = {10.1016/j.jenvman.2026.130468},
pmid = {42468124},
issn = {1095-8630},
abstract = {Arsenic (As) contamination in paddy soils poses a significant environmental challenge due to its high mobility and potential uptake by rice. Although rhizosphere processes strongly regulate As transformation, the potential role of exogenous phytohormones in modulating these processes remains insufficiently understood. This study investigated the effects of 24-epibrassinolide (EBL) on rhizosphere properties, microbial communities, and As speciation in a rice-cultivated microcosm under different As contamination levels and soil conditions. EBL application significantly altered rhizosphere environmental conditions, increasing soil redox potential (Eh) by 7-20 mV and enhancing soil organic carbon availability. Under high As stress (50 mg kg[-1]), EBL shifted bacterial-community composition, increasing the relative abundance of Proteobacteria by up to 167.6% while decreasing Firmicutes by up to 80.4%. These changes were accompanied by significant increases in soil enzyme activities and alterations in As speciation. In natural soils, the highest EBL treatment reduced the proportion of As(III) by approximately 15% and increased As(V) by approximately 14% relative to the untreated control. Multivariate analyses revealed significant associations among microbial-community composition, soil physicochemical properties, enzyme activities, and As speciation. Overall, the results suggest that EBL may influence As behavior in paddy soils by modifying rhizosphere environmental conditions and biological processes. This study provides new insights into phytohormone-mediated regulation of arsenic dynamics and highlights the potential of EBL as a management strategy for reducing As mobility during early rice growth stages.},
}
RevDate: 2026-07-17
Plant-microbe interactions between Trichoderma and Brassica vegetables: Biostimulatory activity, biological control and molecular perspectives.
Microbiological research, 312:128637 pii:S0944-5013(26)00201-6 [Epub ahead of print].
Brassica crops are among the most economically important vegetable and oilseed plants worldwide, providing food and industrial resources. However, most Brassica species show limited or absent associations with arbuscular mycorrhizal fungi (AMF), restricting the use of mycorrhiza-based microbial inputs and emphasizing the need for alternative beneficial microorganisms. In this context, fungi of the genus Trichoderma have emerged as versatile plant-associated microbes with potential for sustainable agriculture. This review synthesizes current knowledge on Trichoderma-Brassica interactions, integrating evidence from plant physiology, fungal ecology, molecular signaling, and agronomic applications. The review first outlines the biological and agronomic relevance of Brassica crops, including their taxonomic diversity, global distribution, and production of bioactive metabolites. It then examines the ecological and biotechnological importance of Trichoderma, highlighting diversity, mechanisms of action, and use as a biological control agent and plant growth-promoting fungus. Particular emphasis is placed on the molecular and physiological processes underlying Trichoderma-Brassica interactions, such as root colonization strategies, modulation of plant defense pathways, nutrient mobilization, and enhanced tolerance to abiotic stresses. Finally, the review discusses challenges for the deployment of Trichoderma-based bioinoculants, including strain specificity, formulation constraints, and consistency under field conditions. Overall, advancing our understanding of Trichoderma-Brassica interactions offers opportunities to design microbial strategies to improve crop productivity, resilience, and sustainability in the context of climate change and environmentally responsible agriculture.
Additional Links: PMID-42468405
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Citation:
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@article {pmid42468405,
year = {2026},
author = {Eugui, D and Velasco, P and Poveda, J},
title = {Plant-microbe interactions between Trichoderma and Brassica vegetables: Biostimulatory activity, biological control and molecular perspectives.},
journal = {Microbiological research},
volume = {312},
number = {},
pages = {128637},
doi = {10.1016/j.micres.2026.128637},
pmid = {42468405},
issn = {1618-0623},
abstract = {Brassica crops are among the most economically important vegetable and oilseed plants worldwide, providing food and industrial resources. However, most Brassica species show limited or absent associations with arbuscular mycorrhizal fungi (AMF), restricting the use of mycorrhiza-based microbial inputs and emphasizing the need for alternative beneficial microorganisms. In this context, fungi of the genus Trichoderma have emerged as versatile plant-associated microbes with potential for sustainable agriculture. This review synthesizes current knowledge on Trichoderma-Brassica interactions, integrating evidence from plant physiology, fungal ecology, molecular signaling, and agronomic applications. The review first outlines the biological and agronomic relevance of Brassica crops, including their taxonomic diversity, global distribution, and production of bioactive metabolites. It then examines the ecological and biotechnological importance of Trichoderma, highlighting diversity, mechanisms of action, and use as a biological control agent and plant growth-promoting fungus. Particular emphasis is placed on the molecular and physiological processes underlying Trichoderma-Brassica interactions, such as root colonization strategies, modulation of plant defense pathways, nutrient mobilization, and enhanced tolerance to abiotic stresses. Finally, the review discusses challenges for the deployment of Trichoderma-based bioinoculants, including strain specificity, formulation constraints, and consistency under field conditions. Overall, advancing our understanding of Trichoderma-Brassica interactions offers opportunities to design microbial strategies to improve crop productivity, resilience, and sustainability in the context of climate change and environmentally responsible agriculture.},
}
RevDate: 2026-07-17
Synthesis, separation and absolute configuration of all chiral compounds of the equol pathway with evaluation of commercial samples.
Food chemistry, 525(Pt 2):150336 pii:S0308-8146(26)02496-9 [Epub ahead of print].
Daidzein, an isoflavone found in legumes, can undergo a series of enzymatic reductions to become equol. Equol has more potent bioactivity than daidzein. Not all humans have the necessary enzymes within the gut microbiome to convert daidzein to equol, thus missing out on health benefits like chemoprophylaxis and menopausal symptom relief. The intermediates between daidzein and equol are dihydrodaidzein and tetrahydrodaidzein, which are chiral like equol. An achiral HPLC method is presented that separates daidzein and its metabolites including O-desmethylangolensin, a molecule produced by individuals that cannot make equol. Chiral separation methods for all entities in the daidzein to equol pathway are presented including the absolute configuration of these analytes as determined using vibrational circular dichroism. This is the first instance of direct absolute configuration assignment of these molecules. Three commercially available equol supplements were analyzed using the developed methods and discrepancies between the label claims and results are discussed.
Additional Links: PMID-42468417
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@article {pmid42468417,
year = {2026},
author = {Razo-Smith, A and Parveen, N and Dhaubhadel, U and Lovely, CJ and Nafie, J and Armstrong, DW},
title = {Synthesis, separation and absolute configuration of all chiral compounds of the equol pathway with evaluation of commercial samples.},
journal = {Food chemistry},
volume = {525},
number = {Pt 2},
pages = {150336},
doi = {10.1016/j.foodchem.2026.150336},
pmid = {42468417},
issn = {1873-7072},
abstract = {Daidzein, an isoflavone found in legumes, can undergo a series of enzymatic reductions to become equol. Equol has more potent bioactivity than daidzein. Not all humans have the necessary enzymes within the gut microbiome to convert daidzein to equol, thus missing out on health benefits like chemoprophylaxis and menopausal symptom relief. The intermediates between daidzein and equol are dihydrodaidzein and tetrahydrodaidzein, which are chiral like equol. An achiral HPLC method is presented that separates daidzein and its metabolites including O-desmethylangolensin, a molecule produced by individuals that cannot make equol. Chiral separation methods for all entities in the daidzein to equol pathway are presented including the absolute configuration of these analytes as determined using vibrational circular dichroism. This is the first instance of direct absolute configuration assignment of these molecules. Three commercially available equol supplements were analyzed using the developed methods and discrepancies between the label claims and results are discussed.},
}
RevDate: 2026-07-17
The enteric nervous system: A neuroimmune conductor regulating intestinal homeostasis and inflammation.
Molecular immunology, 197:23-33 pii:S0161-5890(26)00165-3 [Epub ahead of print].
The gastrointestinal tract is densely innervated by the enteric nervous system (ENS), a complex neural network that regulates intestinal physiology. Emerging advances highlight the essential contributions of ENS to immune homeostasis and inflammatory responses within the gut. This review synthesizes current understanding of the interactions between the intrinsic enteric neurons and various intestinal immune cells, epithelium cells and the microbiome. We also discuss recent technological developments that enhance our ability to dissect the immunomodulatory functions of enteric neurons. Elucidating these complex communication pathways is critical for advancing our understanding of gut function and mucosal inflammation, and for developing novel therapeutic strategies for gastrointestinal disorders.
Additional Links: PMID-42468437
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@article {pmid42468437,
year = {2026},
author = {Wang, Y and Xu, H},
title = {The enteric nervous system: A neuroimmune conductor regulating intestinal homeostasis and inflammation.},
journal = {Molecular immunology},
volume = {197},
number = {},
pages = {23-33},
doi = {10.1016/j.molimm.2026.07.004},
pmid = {42468437},
issn = {1872-9142},
abstract = {The gastrointestinal tract is densely innervated by the enteric nervous system (ENS), a complex neural network that regulates intestinal physiology. Emerging advances highlight the essential contributions of ENS to immune homeostasis and inflammatory responses within the gut. This review synthesizes current understanding of the interactions between the intrinsic enteric neurons and various intestinal immune cells, epithelium cells and the microbiome. We also discuss recent technological developments that enhance our ability to dissect the immunomodulatory functions of enteric neurons. Elucidating these complex communication pathways is critical for advancing our understanding of gut function and mucosal inflammation, and for developing novel therapeutic strategies for gastrointestinal disorders.},
}
RevDate: 2026-07-17
Editorial overview: Integrating Evolutionary, Ecological, and Technological Frontiers in a Rapidly Changing World.
Resistance in pest species is no longer confined to classical genetic mechanisms or agricultural landscapes; instead, it emerges from a multilayered interplay of ecology, behavior, microbiomes, dispersal networks, and human-built environments. Across the manuscripts in this issue, a unifying picture emerges: urbanization and indoor environments act as powerful evolutionary arenas, shaping how pests invade, persist, and adapt to chemical, biological, and environmental pressures. Recent work on indoor pests, including cockroaches, bed bugs, and rodents, reveals how monitoring technologies, behavioral ecology, and microbe-mediated processes influence early detection and resistance management. Studies of long-distance dispersal in mosquitoes demonstrate how human transport networks accelerate the spread of adaptive alleles, including insecticide resistance, while creating spatial mosaics of selection within cities. Research on invasive termites, social wasps, and ants highlights how bridgehead effects, supercoloniality, and urban adaptation interact with microbial symbionts to shape invasion success and resistance trajectories. Meanwhile, emerging insights into microbiome-mediated detoxification show that resistance can arise not only from host genomes but also from microbial metabolism, epigenetic modulation, and environmentally structured microbial communities. Together, these contributions illustrate that pest resistance is an inherently cross-scale phenomenon, from genes and symbionts to cities and global trade routes. By integrating perspectives from molecular biology, invasion ecology, urban entomology, and microbial symbiosis, this issue reframes resistance as a dynamic, multi-dimensional process shaped by human behavior and built environments. Understanding these shared mechanisms is essential for predicting future resistance threats and designing sustainable, evolution-informed management strategies across indoor, urban, and global contexts.
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@article {pmid42468573,
year = {2026},
author = {Booth, W and Veera Singham, G},
title = {Editorial overview: Integrating Evolutionary, Ecological, and Technological Frontiers in a Rapidly Changing World.},
journal = {Current opinion in insect science},
volume = {},
number = {},
pages = {101580},
doi = {10.1016/j.cois.2026.101580},
pmid = {42468573},
issn = {2214-5753},
abstract = {Resistance in pest species is no longer confined to classical genetic mechanisms or agricultural landscapes; instead, it emerges from a multilayered interplay of ecology, behavior, microbiomes, dispersal networks, and human-built environments. Across the manuscripts in this issue, a unifying picture emerges: urbanization and indoor environments act as powerful evolutionary arenas, shaping how pests invade, persist, and adapt to chemical, biological, and environmental pressures. Recent work on indoor pests, including cockroaches, bed bugs, and rodents, reveals how monitoring technologies, behavioral ecology, and microbe-mediated processes influence early detection and resistance management. Studies of long-distance dispersal in mosquitoes demonstrate how human transport networks accelerate the spread of adaptive alleles, including insecticide resistance, while creating spatial mosaics of selection within cities. Research on invasive termites, social wasps, and ants highlights how bridgehead effects, supercoloniality, and urban adaptation interact with microbial symbionts to shape invasion success and resistance trajectories. Meanwhile, emerging insights into microbiome-mediated detoxification show that resistance can arise not only from host genomes but also from microbial metabolism, epigenetic modulation, and environmentally structured microbial communities. Together, these contributions illustrate that pest resistance is an inherently cross-scale phenomenon, from genes and symbionts to cities and global trade routes. By integrating perspectives from molecular biology, invasion ecology, urban entomology, and microbial symbiosis, this issue reframes resistance as a dynamic, multi-dimensional process shaped by human behavior and built environments. Understanding these shared mechanisms is essential for predicting future resistance threats and designing sustainable, evolution-informed management strategies across indoor, urban, and global contexts.},
}
RevDate: 2026-07-17
Gut microbiota alterations are associated with uterine immune homeostasis via microbiota-metabolite interactions.
Journal of advanced research pii:S2090-1232(26)00587-4 [Epub ahead of print].
INTRODUCTION: Uterine inflammation is a major cause of infertility and is commonly associated with local bacterial infection. However, the association between gut microbiota and uterine immune homeostasis remains incompletely understood.
OBJECTIVES: This study aimed to examine the association between gut microbiota dysbiosis and uterine inflammation, and to identify microbiota-associated factors linked to host immune responses.
METHODS: An antibiotic-induced dysbiosis mouse model was established, followed by fecal microbiota transplantation (FMT), microbial supplementation, metabolite intervention, and acute E. coli challenge to assess inflammation-related outcomes. Uterine inflammation, barrier integrity, and immune responses were evaluated. Gut microbiota and fecal metabolites were profiled by 16S rRNA sequencing and untargeted metabolomics, respectively.
RESULTS: Gut microbiota dysbiosis was associated with increased uterine inflammation, as indicated by elevated cytokine levels, immune cell infiltration, and impaired epithelial barrier integrity, whereas FMT partially reversed these changes. Taxonomic analysis showed a marked reduction in Prevotellaceae abundance during dysbiosis, which increased following microbial reconstitution. Supplementation with Prevotella copri was associated with reduced uterine inflammation and improved barrier integrity in dysbiotic mice. Integrated microbiome-metabolome analysis revealed that allopregnanolone was strongly associated with Prevotellaceae abundance. Dysbiosis was accompanied by reduced allopregnanolone levels, which increased after FMT. Exogenous administration of allopregnanolone was associated with reduced inflammatory markers and improved epithelial barrier integrity. Importantly, gut microbiota dysbiosis was associated with increased susceptibility to E. coli-induced uterine inflammation, whereas FMT, Prevotella copri, and allopregnanolone were associated with attenuation of infection-related inflammatory responses and tissue injury.
CONCLUSION: Together, these findings support a microbiota-metabolite-host interaction pattern in which Prevotella copri, together with the host-associated metabolite allopregnanolone, is associated with uterine immune homeostasis. While these results provide functional insights, further studies are required to elucidate the mechanisms linking gut microbiota to uterine inflammation.
Additional Links: PMID-42468804
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@article {pmid42468804,
year = {2026},
author = {Gong, Z and Wang, Y and Mao, W and Gao, R and Bao, W and Dai, J and Dong, Y and Mu, Z and Fu, Y and Hu, X and Zhang, S and Liu, B},
title = {Gut microbiota alterations are associated with uterine immune homeostasis via microbiota-metabolite interactions.},
journal = {Journal of advanced research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jare.2026.07.043},
pmid = {42468804},
issn = {2090-1224},
abstract = {INTRODUCTION: Uterine inflammation is a major cause of infertility and is commonly associated with local bacterial infection. However, the association between gut microbiota and uterine immune homeostasis remains incompletely understood.
OBJECTIVES: This study aimed to examine the association between gut microbiota dysbiosis and uterine inflammation, and to identify microbiota-associated factors linked to host immune responses.
METHODS: An antibiotic-induced dysbiosis mouse model was established, followed by fecal microbiota transplantation (FMT), microbial supplementation, metabolite intervention, and acute E. coli challenge to assess inflammation-related outcomes. Uterine inflammation, barrier integrity, and immune responses were evaluated. Gut microbiota and fecal metabolites were profiled by 16S rRNA sequencing and untargeted metabolomics, respectively.
RESULTS: Gut microbiota dysbiosis was associated with increased uterine inflammation, as indicated by elevated cytokine levels, immune cell infiltration, and impaired epithelial barrier integrity, whereas FMT partially reversed these changes. Taxonomic analysis showed a marked reduction in Prevotellaceae abundance during dysbiosis, which increased following microbial reconstitution. Supplementation with Prevotella copri was associated with reduced uterine inflammation and improved barrier integrity in dysbiotic mice. Integrated microbiome-metabolome analysis revealed that allopregnanolone was strongly associated with Prevotellaceae abundance. Dysbiosis was accompanied by reduced allopregnanolone levels, which increased after FMT. Exogenous administration of allopregnanolone was associated with reduced inflammatory markers and improved epithelial barrier integrity. Importantly, gut microbiota dysbiosis was associated with increased susceptibility to E. coli-induced uterine inflammation, whereas FMT, Prevotella copri, and allopregnanolone were associated with attenuation of infection-related inflammatory responses and tissue injury.
CONCLUSION: Together, these findings support a microbiota-metabolite-host interaction pattern in which Prevotella copri, together with the host-associated metabolite allopregnanolone, is associated with uterine immune homeostasis. While these results provide functional insights, further studies are required to elucidate the mechanisms linking gut microbiota to uterine inflammation.},
}
RevDate: 2026-07-17
Source- and solubility-specific choline, gut microbiota, and dyslipidemia risk: TMAO-associated and non-TMAO-associated patterns in a prospective cohort study.
The American journal of clinical nutrition pii:S0002-9165(26)00249-2 [Epub ahead of print].
BACKGROUND: Dietary choline, a major precursor of the gut microbial metabolite trimethylamine N-oxide (TMAO), is implicated in dyslipidemia risk, however, source- and form-specific associations and interactions with gut microbiota remain unclear.
OBJECTIVE: To examine longitudinal associations of source- and form-specific dietary choline with plasma TMAO and dyslipidemia, and to identify gut microbiota interactions.
METHODS: Using data from the China Health and Nutrition Survey (2018-2023), dietary intake was assessed via three consecutive 24-h recalls in this prospective cohort study. Two-level generalized linear mixed-effects models were applied in 4828 adults (mean age 55.9 ± 12.6 years, 56.6% women) to assess choline-dyslipidemia associations. Choline-TMAO and TMAO-dyslipidemia analyses were conducted in 1091 participants free of dyslipidemia at baseline. Among 7169 adults with gut microbiome data, LASSO and logistic regression identified lipid-associated gut genera, TMAO relationships were examined in a subset of 693 participants.
RESULTS: Higher intakes of total (Q4 vs. Q1: OR = 1.261; 95% CI: 1.007, 1.580), red meat-derived (OR = 1.75; 95% CI: 1.196, 2.568), and lipid-soluble choline (OR = 1.304; 95% CI: 1.047, 1.624) were associated with higher risk of elevated LDL-C, while vegetable-derived choline was inversely associated. Egg-derived and lipid-soluble choline were positively associated with plasma TMAO, which was prospectively associated with 5-year incident dyslipidemia (Q4 vs. Q1: OR = 1.620; 95% CI: 1.047, 2.509), elevated LDL-C (Q3 vs Q1: OR = 2.478; 95% CI: 1.187, 5.174), and hypertriglyceridemia (Q4 vs. Q1: OR = 1.829; 95% CI: 1.028, 3.225). Three TMAO-associated genera were identified: Lachnospiraceae and Phascolarctobacterium as pro-risk taxa, and Turicibacter as protective. The adverse LDL-C association of egg-derived choline was observed exclusively in Phascolarctobacterium-enriched individuals.
CONCLUSIONS: Dietary choline source and solubility differentially associated with dyslipidemia risk through TMAO-associated and non-TMAO-associated patterns, with gut microbiota as key modulators.
Additional Links: PMID-42468829
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PubMed:
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@article {pmid42468829,
year = {2026},
author = {Zhang, X and Jia, X and Zhang, J and Guan, F and Wei, Y and Du, S and Du, W and Huang, F and Ouyang, Y and Li, L and Bai, J and Su, C and Wang, H and Zhang, B},
title = {Source- and solubility-specific choline, gut microbiota, and dyslipidemia risk: TMAO-associated and non-TMAO-associated patterns in a prospective cohort study.},
journal = {The American journal of clinical nutrition},
volume = {},
number = {},
pages = {101440},
doi = {10.1016/j.ajcnut.2026.101440},
pmid = {42468829},
issn = {1938-3207},
abstract = {BACKGROUND: Dietary choline, a major precursor of the gut microbial metabolite trimethylamine N-oxide (TMAO), is implicated in dyslipidemia risk, however, source- and form-specific associations and interactions with gut microbiota remain unclear.
OBJECTIVE: To examine longitudinal associations of source- and form-specific dietary choline with plasma TMAO and dyslipidemia, and to identify gut microbiota interactions.
METHODS: Using data from the China Health and Nutrition Survey (2018-2023), dietary intake was assessed via three consecutive 24-h recalls in this prospective cohort study. Two-level generalized linear mixed-effects models were applied in 4828 adults (mean age 55.9 ± 12.6 years, 56.6% women) to assess choline-dyslipidemia associations. Choline-TMAO and TMAO-dyslipidemia analyses were conducted in 1091 participants free of dyslipidemia at baseline. Among 7169 adults with gut microbiome data, LASSO and logistic regression identified lipid-associated gut genera, TMAO relationships were examined in a subset of 693 participants.
RESULTS: Higher intakes of total (Q4 vs. Q1: OR = 1.261; 95% CI: 1.007, 1.580), red meat-derived (OR = 1.75; 95% CI: 1.196, 2.568), and lipid-soluble choline (OR = 1.304; 95% CI: 1.047, 1.624) were associated with higher risk of elevated LDL-C, while vegetable-derived choline was inversely associated. Egg-derived and lipid-soluble choline were positively associated with plasma TMAO, which was prospectively associated with 5-year incident dyslipidemia (Q4 vs. Q1: OR = 1.620; 95% CI: 1.047, 2.509), elevated LDL-C (Q3 vs Q1: OR = 2.478; 95% CI: 1.187, 5.174), and hypertriglyceridemia (Q4 vs. Q1: OR = 1.829; 95% CI: 1.028, 3.225). Three TMAO-associated genera were identified: Lachnospiraceae and Phascolarctobacterium as pro-risk taxa, and Turicibacter as protective. The adverse LDL-C association of egg-derived choline was observed exclusively in Phascolarctobacterium-enriched individuals.
CONCLUSIONS: Dietary choline source and solubility differentially associated with dyslipidemia risk through TMAO-associated and non-TMAO-associated patterns, with gut microbiota as key modulators.},
}
RevDate: 2026-07-17
Viral Infections in Stocker Cattle and Their Implications for Bovine Respiratory Disease.
The Veterinary clinics of North America. Food animal practice pii:S0749-0720(26)00029-0 [Epub ahead of print].
Bovine respiratory disease complex (BRDC) remains a leading cause of morbidity and economic loss in stocker cattle, particularly during the transition from weaning to feedlot placement. Virus-induced changes promote microbiome imbalance and facilitate secondary bacterial infections, leading to bronchopneumonia. The high transmissibility of these viruses, with basic reproduction numbers ranging from approximately 3 to 36, contributes to rapid spread under feedlot conditions. This article reviews the epidemiology, pathogenesis, transmission, diagnosis, and control of major viral pathogens associated with BRDC and highlights the importance of integrated management strategies, including stress reduction, biosecurity, vaccination, and early diagnostics, for effective disease control.
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@article {pmid42469078,
year = {2026},
author = {Rajput, M and Chase, CCL},
title = {Viral Infections in Stocker Cattle and Their Implications for Bovine Respiratory Disease.},
journal = {The Veterinary clinics of North America. Food animal practice},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cvfa.2026.04.006},
pmid = {42469078},
issn = {1558-4240},
abstract = {Bovine respiratory disease complex (BRDC) remains a leading cause of morbidity and economic loss in stocker cattle, particularly during the transition from weaning to feedlot placement. Virus-induced changes promote microbiome imbalance and facilitate secondary bacterial infections, leading to bronchopneumonia. The high transmissibility of these viruses, with basic reproduction numbers ranging from approximately 3 to 36, contributes to rapid spread under feedlot conditions. This article reviews the epidemiology, pathogenesis, transmission, diagnosis, and control of major viral pathogens associated with BRDC and highlights the importance of integrated management strategies, including stress reduction, biosecurity, vaccination, and early diagnostics, for effective disease control.},
}
RevDate: 2026-07-17
Alternative to invasive bronchoscopy: validating tracheal aspirates for microbiome profiling in intensive care unit pneumonia patients.
Scientific reports pii:10.1038/s41598-026-60691-8 [Epub ahead of print].
Pneumonia causes significant mortality in intensive care unit (ICU) patients, yet traditional culture-based pathogen detection lacks sufficient sensitivity. While bronchoalveolar lavage fluid (BAL) provides optimal diagnostic yield, bronchoscopy is often contraindicated in critically ill patients. This study compares the respiratory microbiome profiles of paired tracheal aspirate (ETA) and BAL samples from pneumonia patients in a tertiary hospital ICU (n=23, November 2019-September 2022). Using 16S rRNA next-generation sequencing, we analyzed microbial diversity (Shannon Index), taxonomic composition, and differential abundance (edgeR). Results showed comparable diversity indices and microbial communities between ETA and BAL samples, with ETA successfully capturing key pneumonia-related microbial signatures. These findings validate ETA as a reliable, less invasive alternative to BAL for respiratory microbiome analysis in critically ill patients, establishing the groundwork for future clinical applications.
Additional Links: PMID-42469295
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@article {pmid42469295,
year = {2026},
author = {Govindasamy, P and Cho, JY and Yang, J and Yang, B and Kim, SH and Lee, KM and Choe, KH and Lee, OJ and Kim, EG and Mathee, K and Narasimhan, G and Shin, YM},
title = {Alternative to invasive bronchoscopy: validating tracheal aspirates for microbiome profiling in intensive care unit pneumonia patients.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-60691-8},
pmid = {42469295},
issn = {2045-2322},
abstract = {Pneumonia causes significant mortality in intensive care unit (ICU) patients, yet traditional culture-based pathogen detection lacks sufficient sensitivity. While bronchoalveolar lavage fluid (BAL) provides optimal diagnostic yield, bronchoscopy is often contraindicated in critically ill patients. This study compares the respiratory microbiome profiles of paired tracheal aspirate (ETA) and BAL samples from pneumonia patients in a tertiary hospital ICU (n=23, November 2019-September 2022). Using 16S rRNA next-generation sequencing, we analyzed microbial diversity (Shannon Index), taxonomic composition, and differential abundance (edgeR). Results showed comparable diversity indices and microbial communities between ETA and BAL samples, with ETA successfully capturing key pneumonia-related microbial signatures. These findings validate ETA as a reliable, less invasive alternative to BAL for respiratory microbiome analysis in critically ill patients, establishing the groundwork for future clinical applications.},
}
RevDate: 2026-07-17
Shotgun Metagenomics Reveals Skin Microbiome Composition and Function in Infant Atopic Disease.
Allergy [Epub ahead of print].
BACKGROUND: Atopic dermatitis (AD), food sensitization (FS), and food allergy (FA) frequently co-occur in infancy, but the factors underlying distinct atopic phenotypes remain unclear. Although FLG null mutations are major genetic risk factors for AD, they explain only part of disease heritability, suggesting a potential role for the skin microbiome. This study examined how early-life skin microbiome composition and its interaction with host genetics contribute to distinct atopic phenotypes in infancy.
METHODS: We analyzed > 1000 skin swabs from 429 infants in the VITALITY cohort using deep shotgun metagenomic sequencing at 2-3 months (pre-diagnosis) and 12 months (post-diagnosis). Differential abundance, strain-level, and microbial genome-wide association analyses were performed to identify taxonomic and functional features associated with AD, FS, FA, their co-occurrence, and FLG mutation status.
RESULTS: Within AD, microbial signatures differed by co-occurring FA or FS. At 12 months, Staphylococcus epidermidis was enriched in infants with AD alone, whereas infants with AD and FA showed decreased Staphylococcus hominis and Lactococcus species, and increased Dermacoccus nishinomiyaensis and Malassezia slooffiae. At 2-3 months, early skin dysbiosis characterized by enrichment of Staphylococcus species was associated with later development of AD with FS or FA, but not AD alone. Among infants with AD, FLG mutation carriers showed additional microbial shifts, including reduced Streptococcus species and increased M. slooffiae. Strain-level analyses revealed mother-infant sharing of AD-associated taxa, and microbial genome-wide association analyses identified species-specific genes linked to AD severity.
CONCLUSIONS: Infant atopic phenotypes are associated with distinct, phenotype-specific skin microbiome features that emerge before and after disease onset, highlighting the microbiome as a potential target for early risk stratification.
Additional Links: PMID-42469597
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PubMed:
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@article {pmid42469597,
year = {2026},
author = {Shen, Z and Eckert, JK and Saffery, R and Allen, KJ and Walsh, A and , and Deming, C and Chen, Q and Laky, K and Li, JM and Chatman, L and , and Kong, HH and Perrett, KP and Segre, JA and Frischmeyer-Guerrerio, PA},
title = {Shotgun Metagenomics Reveals Skin Microbiome Composition and Function in Infant Atopic Disease.},
journal = {Allergy},
volume = {},
number = {},
pages = {},
doi = {10.1111/all.70449},
pmid = {42469597},
issn = {1398-9995},
support = {AR084058/NH/NIH HHS/United States ; UM1AI109565/NH/NIH HHS/United States ; APP1146913//National Health and Medical Research Council/ ; GNT2008911//National Health and Medical Research Council/ ; 26-PBII-T1-04//WSU Office of Research/ ; },
abstract = {BACKGROUND: Atopic dermatitis (AD), food sensitization (FS), and food allergy (FA) frequently co-occur in infancy, but the factors underlying distinct atopic phenotypes remain unclear. Although FLG null mutations are major genetic risk factors for AD, they explain only part of disease heritability, suggesting a potential role for the skin microbiome. This study examined how early-life skin microbiome composition and its interaction with host genetics contribute to distinct atopic phenotypes in infancy.
METHODS: We analyzed > 1000 skin swabs from 429 infants in the VITALITY cohort using deep shotgun metagenomic sequencing at 2-3 months (pre-diagnosis) and 12 months (post-diagnosis). Differential abundance, strain-level, and microbial genome-wide association analyses were performed to identify taxonomic and functional features associated with AD, FS, FA, their co-occurrence, and FLG mutation status.
RESULTS: Within AD, microbial signatures differed by co-occurring FA or FS. At 12 months, Staphylococcus epidermidis was enriched in infants with AD alone, whereas infants with AD and FA showed decreased Staphylococcus hominis and Lactococcus species, and increased Dermacoccus nishinomiyaensis and Malassezia slooffiae. At 2-3 months, early skin dysbiosis characterized by enrichment of Staphylococcus species was associated with later development of AD with FS or FA, but not AD alone. Among infants with AD, FLG mutation carriers showed additional microbial shifts, including reduced Streptococcus species and increased M. slooffiae. Strain-level analyses revealed mother-infant sharing of AD-associated taxa, and microbial genome-wide association analyses identified species-specific genes linked to AD severity.
CONCLUSIONS: Infant atopic phenotypes are associated with distinct, phenotype-specific skin microbiome features that emerge before and after disease onset, highlighting the microbiome as a potential target for early risk stratification.},
}
RevDate: 2023-10-17
CmpDate: 2021-08-10
Bowel preparation in colorectal surgery: the day of reckoning is here.
The British journal of surgery, 108(4):340-341.
Before the use of mechanical bowel preparation is either eliminated or subjected to a clinical trial, its scientific premise should be reconsidered, and consensus of its redesign discussed by a panel of experts including surgeons, infectious disease specialists, microbiome scientists, and clinical trialists.
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@article {pmid33793758,
year = {2021},
author = {Alverdy, JC},
title = {Bowel preparation in colorectal surgery: the day of reckoning is here.},
journal = {The British journal of surgery},
volume = {108},
number = {4},
pages = {340-341},
pmid = {33793758},
issn = {1365-2168},
support = {R01 GM062344/GM/NIGMS NIH HHS/United States ; },
mesh = {Antibiotic Prophylaxis/methods ; Colon/*surgery ; Humans ; *Preoperative Care/methods ; Rectum/*surgery ; Venous Thromboembolism/prevention & control ; },
abstract = {Before the use of mechanical bowel preparation is either eliminated or subjected to a clinical trial, its scientific premise should be reconsidered, and consensus of its redesign discussed by a panel of experts including surgeons, infectious disease specialists, microbiome scientists, and clinical trialists.},
}
MeSH Terms:
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Antibiotic Prophylaxis/methods
Colon/*surgery
Humans
*Preoperative Care/methods
Rectum/*surgery
Venous Thromboembolism/prevention & control
RevDate: 2026-07-15
Joint contributions of host genetics and heritable gut microbiota to semen quality variation in Duroc boars.
NPJ biofilms and microbiomes pii:10.1038/s41522-026-01073-w [Epub ahead of print].
Host genetics and gut microbiota jointly influence host phenotypes. To investigate the genetic and microbial factors affecting boar semen quality, we analyzed whole-genome resequencing and fecal 16S rRNA sequencing data from 1128 Duroc boars. Gut microbiota profiling showed that Firmicutes, Bacteroidetes, and Proteobacteria were dominant phyla, while farm type, herd type, strain, and age significantly affected microbial composition. Genome-wide association analysis identified 32 significant SNPs associated with semen traits, and microbiome-wide association analysis detected 251 genus-level associations. Variance component analysis indicated that host genetics, gut microbiota, and their interactions contributed substantially to semen quality variation. Heritability analysis identified 73 heritable genera, and microbial GWAS further detected 242 SNPs associated with 18 heritable genera. Mendelian randomization analysis further supported a significant association between the heritable genus Intestinibacter and sperm motility. Notably, overlapping genomic regions on chromosome 10 were associated with both Intestinibacter abundance and sperm motility, suggesting that host genetic variation may influence semen quality directly or indirectly through modulation of heritable gut microbiota. These findings provide new insights into host genetics-microbiota interactions underlying boar semen quality.
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PubMed:
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@article {pmid42457696,
year = {2026},
author = {Guo, L and Meng, X and Zhang, Q and Tan, J and Sun, H and Jiang, S and Wei, H and Peng, J},
title = {Joint contributions of host genetics and heritable gut microbiota to semen quality variation in Duroc boars.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-01073-w},
pmid = {42457696},
issn = {2055-5008},
support = {CARS-35//Agriculture Research System of China/ ; 32430099//National Science and Technology Major Project/ ; 2662023DKPY002//Fundamental Research Funds for the Central Universities/ ; },
abstract = {Host genetics and gut microbiota jointly influence host phenotypes. To investigate the genetic and microbial factors affecting boar semen quality, we analyzed whole-genome resequencing and fecal 16S rRNA sequencing data from 1128 Duroc boars. Gut microbiota profiling showed that Firmicutes, Bacteroidetes, and Proteobacteria were dominant phyla, while farm type, herd type, strain, and age significantly affected microbial composition. Genome-wide association analysis identified 32 significant SNPs associated with semen traits, and microbiome-wide association analysis detected 251 genus-level associations. Variance component analysis indicated that host genetics, gut microbiota, and their interactions contributed substantially to semen quality variation. Heritability analysis identified 73 heritable genera, and microbial GWAS further detected 242 SNPs associated with 18 heritable genera. Mendelian randomization analysis further supported a significant association between the heritable genus Intestinibacter and sperm motility. Notably, overlapping genomic regions on chromosome 10 were associated with both Intestinibacter abundance and sperm motility, suggesting that host genetic variation may influence semen quality directly or indirectly through modulation of heritable gut microbiota. These findings provide new insights into host genetics-microbiota interactions underlying boar semen quality.},
}
RevDate: 2026-07-15
Effect of post-weaning glutamine and/or liquid milk replacer supplementation on pig growth and intestinal development.
Scientific reports pii:10.1038/s41598-026-60788-0 [Epub ahead of print].
This study aimed to determine the effect of supplemental liquid milk replacer and/or 1% L-glutamine on intestinal function and growth in weaned pigs. Pigs (12 pens/treatment, each with 10 pigs) were assigned to one of 4 treatments from day (D) 0-10 post-weaning (pw): (1) control diet; dry pelleted starter diet only; (2) control diet plus supplemental liquid milk replacer; (3) control diet with dietary inclusion of 1% L-glutamine and (4) control diet with dietary inclusion of 1% L-glutamine plus supplemental liquid milk replacer with dietary inclusion of 1% L-glutamine. Pig weight and feed disappearance were recorded at intervals up to slaughter at ~ 120 kg. At D7 pw, 40 pigs (n = 10/treatment) were euthanised and intestinal tissues collected for histology and gene expression analyses. Liquid milk replacer supplementation increased average daily feed intake and average daily gain from D0-D10 pw and D20-D47 pw and body weight up to slaughter. It also increased villus height in the small intestine, decreased expression of pro-inflammatory cytokines (IL17, IL18, IL22) in the jejunum and increased faecal abundance of Rikenellaceae RC9 and Oscillaspiraceae UCG-002 at D11 pw. In conclusion, while glutamine supplementation did not affect pig growth or intestinal integrity, milk replacer increased feed intake and improved intestinal health and lifetime growth in pigs.
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@article {pmid42457777,
year = {2026},
author = {Arnaud, EA and Gardiner, GE and Vasa, SR and Cormican, P and Ryan, MT and O' Doherty, JV and Sweeney, T and Lawlor, PG},
title = {Effect of post-weaning glutamine and/or liquid milk replacer supplementation on pig growth and intestinal development.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-60788-0},
pmid = {42457777},
issn = {2045-2322},
support = {2019R518//The Irish Department of Agriculture, Food and the Marine/ ; 2019R518//The Irish Department of Agriculture, Food and the Marine/ ; 2019R518//The Irish Department of Agriculture, Food and the Marine/ ; 2019R518//The Irish Department of Agriculture, Food and the Marine/ ; 2019R518//The Irish Department of Agriculture, Food and the Marine/ ; 2019R518//The Irish Department of Agriculture, Food and the Marine/ ; 2019R518//The Irish Department of Agriculture, Food and the Marine/ ; 2019R518//The Irish Department of Agriculture, Food and the Marine/ ; 2019221//Teagasc Walsh Scholarship/ ; },
abstract = {This study aimed to determine the effect of supplemental liquid milk replacer and/or 1% L-glutamine on intestinal function and growth in weaned pigs. Pigs (12 pens/treatment, each with 10 pigs) were assigned to one of 4 treatments from day (D) 0-10 post-weaning (pw): (1) control diet; dry pelleted starter diet only; (2) control diet plus supplemental liquid milk replacer; (3) control diet with dietary inclusion of 1% L-glutamine and (4) control diet with dietary inclusion of 1% L-glutamine plus supplemental liquid milk replacer with dietary inclusion of 1% L-glutamine. Pig weight and feed disappearance were recorded at intervals up to slaughter at ~ 120 kg. At D7 pw, 40 pigs (n = 10/treatment) were euthanised and intestinal tissues collected for histology and gene expression analyses. Liquid milk replacer supplementation increased average daily feed intake and average daily gain from D0-D10 pw and D20-D47 pw and body weight up to slaughter. It also increased villus height in the small intestine, decreased expression of pro-inflammatory cytokines (IL17, IL18, IL22) in the jejunum and increased faecal abundance of Rikenellaceae RC9 and Oscillaspiraceae UCG-002 at D11 pw. In conclusion, while glutamine supplementation did not affect pig growth or intestinal integrity, milk replacer increased feed intake and improved intestinal health and lifetime growth in pigs.},
}
RevDate: 2026-07-15
Supplementation with long-chain polyunsaturated fatty acids to extremely preterm infants associates with development of the intestinal microbiota.
Pediatric research [Epub ahead of print].
BACKGROUND: Supplementation with arachidonic acid (AA) and docosahexaenoic acid (DHA) to extremely preterm infants reduces the risk of severe retinopathy of prematurity (ROP). The main aim of this study was to explore the involvement of AA:DHA supplementation in the developing gut microbiome, and its possible contribution to the ROP-protective effect. Secondly, additional covariates for microbiome maturation were evaluated.
METHODS: Longitudinal gut microbiome profiles and bacterial gene pathways were characterised using shot-gun metagenomics in 75 extremely preterm infants who participated in a randomized clinical trial on AA:DHA supplementation. Serum protein levels quantified using proximity extension assays were merged with the microbiome data.
RESULTS: AA:DHA supplementation was linked to an increase in relative abundance of Citrobacter koseri and associated with changes in proteins and metabolic pathways. Occurrence of severe ROP was associated with microbiome alpha diversity (Shannon and Evenness) and beta diversity (Bray-Curtis). Additionally, study centre and gestational age at birth impacted the microbiome composition.
CONCLUSION: We conclude that AA:DHA supplementation impacts the microbiome. However, the current study could not determine the causality between the supplementation, microbiome and ROP-decrease. Nonetheless, these findings highlight the complex interplay between external interventions, including nutritional supplements, and the gut microbiome development in extremely preterm infants.
IMPACT: Longitudinal gut microbiome profiles, bacterial gene pathways and serum protein expressions were determined using shotgun metagenomics and proximity extension assays in 75 extremely preterm infants included in a multicentre randomized clinical trial investigating enteral fatty acid supplementation. Dynamic shifts in microbiome and pathway composition were seen from birth to 34 weeks gestational age. Arachidonic acid (AA) and docosahexaenoic acid (DHA) supplementation was linked to an increase in relative abundance of Citrobacter koseri and associated with changes in proteins and metabolic pathways. However, the causality between the supplementation, microbiome, and ROP-decrease could not be determined.
Additional Links: PMID-42457990
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@article {pmid42457990,
year = {2026},
author = {Danielsson, H and Portlock, T and Hellström, A and Nilsson, A and Sävman, K and Wackernagel, D and Hansen-Pupp, I and Ley, D and Shoaie, S and Uhlén, M and Brusselaers, N and Elfvin, A},
title = {Supplementation with long-chain polyunsaturated fatty acids to extremely preterm infants associates with development of the intestinal microbiota.},
journal = {Pediatric research},
volume = {},
number = {},
pages = {},
pmid = {42457990},
issn = {1530-0447},
abstract = {BACKGROUND: Supplementation with arachidonic acid (AA) and docosahexaenoic acid (DHA) to extremely preterm infants reduces the risk of severe retinopathy of prematurity (ROP). The main aim of this study was to explore the involvement of AA:DHA supplementation in the developing gut microbiome, and its possible contribution to the ROP-protective effect. Secondly, additional covariates for microbiome maturation were evaluated.
METHODS: Longitudinal gut microbiome profiles and bacterial gene pathways were characterised using shot-gun metagenomics in 75 extremely preterm infants who participated in a randomized clinical trial on AA:DHA supplementation. Serum protein levels quantified using proximity extension assays were merged with the microbiome data.
RESULTS: AA:DHA supplementation was linked to an increase in relative abundance of Citrobacter koseri and associated with changes in proteins and metabolic pathways. Occurrence of severe ROP was associated with microbiome alpha diversity (Shannon and Evenness) and beta diversity (Bray-Curtis). Additionally, study centre and gestational age at birth impacted the microbiome composition.
CONCLUSION: We conclude that AA:DHA supplementation impacts the microbiome. However, the current study could not determine the causality between the supplementation, microbiome and ROP-decrease. Nonetheless, these findings highlight the complex interplay between external interventions, including nutritional supplements, and the gut microbiome development in extremely preterm infants.
IMPACT: Longitudinal gut microbiome profiles, bacterial gene pathways and serum protein expressions were determined using shotgun metagenomics and proximity extension assays in 75 extremely preterm infants included in a multicentre randomized clinical trial investigating enteral fatty acid supplementation. Dynamic shifts in microbiome and pathway composition were seen from birth to 34 weeks gestational age. Arachidonic acid (AA) and docosahexaenoic acid (DHA) supplementation was linked to an increase in relative abundance of Citrobacter koseri and associated with changes in proteins and metabolic pathways. However, the causality between the supplementation, microbiome, and ROP-decrease could not be determined.},
}
RevDate: 2026-07-15
CmpDate: 2026-07-16
Human colostrum as a probiotic reservoir: a genomic insights into potential probiotic traits.
Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology], 57(1):.
Human colostrum is rich in a variety of nutrients and beneficial bacteria known to benefit host health. Whole genome sequencing was performed to explore the probiotic potential of six bacterial strains isolated from human colostrum, i.e., Staphylococcus haemolyticus, Micrococcus luteus, Micrococcus lylae, Staphylococcus warneri, and Bacillus altitudinis. The genome was completely annotated and characterized by various bioinformatics tools and databases, including RAST, eggNOG, KEGG, CAZy, antiSMASH, and BAGEL. The analysis showed the existence of essential probiotic-associated genes involved in adhesion, resistance to osmotic stress, synthesis of exopolysaccharide (EPS), tolerance to acid and bile, and synthesis of antibacterial drugs. Moreover, the genomes revealed the functional capacity of these isolates, encoding various stress response genes, protective elements, bacteriocins, and secondary metabolites. These results confirm the potential of human colostrum bacteria as promising probiotic agents.
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@article {pmid42458189,
year = {2026},
author = {Raval, K and Nimbalkar, S and Hanumanthraju, A and Shekh, S and Kunjadiya, A and Dalwadi, P and Pujara, R and Patel, D and Joshi, C},
title = {Human colostrum as a probiotic reservoir: a genomic insights into potential probiotic traits.},
journal = {Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]},
volume = {57},
number = {1},
pages = {},
pmid = {42458189},
issn = {1678-4405},
mesh = {Humans ; *Probiotics/isolation & purification ; *Colostrum/microbiology ; Genome, Bacterial ; *Bacteria/isolation & purification/genetics/classification ; Female ; Whole Genome Sequencing ; },
abstract = {Human colostrum is rich in a variety of nutrients and beneficial bacteria known to benefit host health. Whole genome sequencing was performed to explore the probiotic potential of six bacterial strains isolated from human colostrum, i.e., Staphylococcus haemolyticus, Micrococcus luteus, Micrococcus lylae, Staphylococcus warneri, and Bacillus altitudinis. The genome was completely annotated and characterized by various bioinformatics tools and databases, including RAST, eggNOG, KEGG, CAZy, antiSMASH, and BAGEL. The analysis showed the existence of essential probiotic-associated genes involved in adhesion, resistance to osmotic stress, synthesis of exopolysaccharide (EPS), tolerance to acid and bile, and synthesis of antibacterial drugs. Moreover, the genomes revealed the functional capacity of these isolates, encoding various stress response genes, protective elements, bacteriocins, and secondary metabolites. These results confirm the potential of human colostrum bacteria as promising probiotic agents.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Probiotics/isolation & purification
*Colostrum/microbiology
Genome, Bacterial
*Bacteria/isolation & purification/genetics/classification
Female
Whole Genome Sequencing
RevDate: 2026-07-15
Influence of urban wastewaters and rainfall runoffs on community composition and function of river biofilms: a focus on nanoplastics.
Environmental science and pollution research international [Epub ahead of print].
Biofilms are critical mediators of contaminant fate in aquatic environments, acting as sites for the accumulation and potential degradation of plastic materials amongst other contaminants. However, the ecological impacts of urban pollution on freshwater biofilm composition and function remain poorly understood. In this study, we examined how anthropogenic contamination, including nanoplastics, alters biofilm communities in the Saint-Lawrence River (Québec, Canada). To test this, freshwater mussels and bare terracotta tiles for biofilm colonization were placed together in cages at three sites along the Saint-Lawrence River: a combined sewers and street runoffs site, a site downstream of a large city (2 million inhabitants), and a site 8 km downstream of a municipal effluent dispersion plume. The experiment involved two replicate cages per site and a 3-month exposure period. Biofilms were harvested at the end of the experiment to determine the levels of plastic-related contaminants (plastic nanoparticles), functional activity (esterase activity, lipids, oxidative stress, and plastic biodegradation capacity), and community composition by 16S rRNA sequencing. In parallel, the digestive gland of mussels was sampled to assess the microbiome's capacity to degrade plastics, oxidative stress, and heterotrophic bacterial load from undsinfected wastewaters. The data revealed that biofilms from the rainfall overflow site were most contaminated with nanoplastics, while those from the municipal effluent dispersion plume contained significantly more lipids. Biofilms from the overflow site also exhibited increased esterase activity and biodegradation index compared to the other sites. However, no signs of oxidative stress were observed in biofilms from the overflow site compared to those of the municipal effluent plume site. Microbial community composition showed only a marginal shift among sites (PERMANOVA, F = 1.69, p = 0.066), while differences in community dispersion were highly significant (PERMDISP, p < 0.001), reflecting increased heterogeneity at urban-impacted locations. Thus, urban pollution did not uniformly impair biofilm communities; instead, it resulted in site-specific ecological responses, including elevated oxidative stress at the municipal effluent plume site and substantial community heterogeneity and instability at the overflow site. Additionally, microbial taxonomic analysis of biofilms revealed an increased presence of bacterial species typically associated with the plastisphere and known to degrade plastics in aquatic environments. In mussels, the biodegradation index and bacterial load were significantly increased at the overflow and downstream effluent sites, respectively. In conclusion, both mussels and biofilms may represent critical compartments in plastic pollution dynamics in urban environments as evidenced by their increased capacity to degrade plastics.
Additional Links: PMID-42458202
PubMed:
Citation:
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@article {pmid42458202,
year = {2026},
author = {André, C and Taranu, ZE and Gagné, F},
title = {Influence of urban wastewaters and rainfall runoffs on community composition and function of river biofilms: a focus on nanoplastics.},
journal = {Environmental science and pollution research international},
volume = {},
number = {},
pages = {},
pmid = {42458202},
issn = {1614-7499},
abstract = {Biofilms are critical mediators of contaminant fate in aquatic environments, acting as sites for the accumulation and potential degradation of plastic materials amongst other contaminants. However, the ecological impacts of urban pollution on freshwater biofilm composition and function remain poorly understood. In this study, we examined how anthropogenic contamination, including nanoplastics, alters biofilm communities in the Saint-Lawrence River (Québec, Canada). To test this, freshwater mussels and bare terracotta tiles for biofilm colonization were placed together in cages at three sites along the Saint-Lawrence River: a combined sewers and street runoffs site, a site downstream of a large city (2 million inhabitants), and a site 8 km downstream of a municipal effluent dispersion plume. The experiment involved two replicate cages per site and a 3-month exposure period. Biofilms were harvested at the end of the experiment to determine the levels of plastic-related contaminants (plastic nanoparticles), functional activity (esterase activity, lipids, oxidative stress, and plastic biodegradation capacity), and community composition by 16S rRNA sequencing. In parallel, the digestive gland of mussels was sampled to assess the microbiome's capacity to degrade plastics, oxidative stress, and heterotrophic bacterial load from undsinfected wastewaters. The data revealed that biofilms from the rainfall overflow site were most contaminated with nanoplastics, while those from the municipal effluent dispersion plume contained significantly more lipids. Biofilms from the overflow site also exhibited increased esterase activity and biodegradation index compared to the other sites. However, no signs of oxidative stress were observed in biofilms from the overflow site compared to those of the municipal effluent plume site. Microbial community composition showed only a marginal shift among sites (PERMANOVA, F = 1.69, p = 0.066), while differences in community dispersion were highly significant (PERMDISP, p < 0.001), reflecting increased heterogeneity at urban-impacted locations. Thus, urban pollution did not uniformly impair biofilm communities; instead, it resulted in site-specific ecological responses, including elevated oxidative stress at the municipal effluent plume site and substantial community heterogeneity and instability at the overflow site. Additionally, microbial taxonomic analysis of biofilms revealed an increased presence of bacterial species typically associated with the plastisphere and known to degrade plastics in aquatic environments. In mussels, the biodegradation index and bacterial load were significantly increased at the overflow and downstream effluent sites, respectively. In conclusion, both mussels and biofilms may represent critical compartments in plastic pollution dynamics in urban environments as evidenced by their increased capacity to degrade plastics.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
Enhancing the understanding of environmental microbiomes through topic modeling: a quantitative and qualitative analysis.
Environmental microbiome, 21(1):.
BACKGROUND: Understanding ecosystem dynamics is essential for assessing ecosystem health, yet remains challenging due to complex biotic and abiotic interactions. Microbial communities are valuable indicators of environmental change, but the high dimensionality of microbiome data requires advanced analytical methods. This study explores the use of topic modeling (TM), an unsupervised machine learning approach initially designed for text analysis, to analyze microbiome data from the dynamic Warnow Estuary on the southern Baltic Sea coast.
RESULTS: We applied TM to estuarine microbiome data and compared its performance to traditional dimensionality reduction methods, Principal Component Analysis (PCA) and Principal Coordinate Analysis (PCoA). Quantitative results indicate that TM performs comparably to conventional approaches in preserving ecological and functional information, and in certain aspects even superior. In addition, we show qualitatively that Non-Negative Matrix Factorization (NNMF), a TM method, captures latent patterns in the data providing an interpretable perspective on the microbiome. In this exploratory framework, NNMF suggested five distinct sub-communities within the estuary that appear to follow a seasonal succession influenced by freshwater inflow. These sub-communities were associated with specific ranges of salinity and temperature and showed distinct taxonomic profiles, with shared characteristics across the estuarine system.
CONCLUSIONS: Our findings suggest that TM is a useful tool for exploring complex environmental microbiome datasets, offering a complementary perspective that can provide additional ecological insights. TM's ability to highlight coherent microbial community patterns indicates its promise for supporting environmental monitoring and informing targeted ecosystem management in dynamic habitats, though further studies are needed to fully assess its applicability.
Additional Links: PMID-42458608
PubMed:
Citation:
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@article {pmid42458608,
year = {2026},
author = {Kujat, AS and Hassenrück, C and Lüdtke, S and Labrenz, M and Sperlea, T},
title = {Enhancing the understanding of environmental microbiomes through topic modeling: a quantitative and qualitative analysis.},
journal = {Environmental microbiome},
volume = {21},
number = {1},
pages = {},
pmid = {42458608},
issn = {2524-6372},
abstract = {BACKGROUND: Understanding ecosystem dynamics is essential for assessing ecosystem health, yet remains challenging due to complex biotic and abiotic interactions. Microbial communities are valuable indicators of environmental change, but the high dimensionality of microbiome data requires advanced analytical methods. This study explores the use of topic modeling (TM), an unsupervised machine learning approach initially designed for text analysis, to analyze microbiome data from the dynamic Warnow Estuary on the southern Baltic Sea coast.
RESULTS: We applied TM to estuarine microbiome data and compared its performance to traditional dimensionality reduction methods, Principal Component Analysis (PCA) and Principal Coordinate Analysis (PCoA). Quantitative results indicate that TM performs comparably to conventional approaches in preserving ecological and functional information, and in certain aspects even superior. In addition, we show qualitatively that Non-Negative Matrix Factorization (NNMF), a TM method, captures latent patterns in the data providing an interpretable perspective on the microbiome. In this exploratory framework, NNMF suggested five distinct sub-communities within the estuary that appear to follow a seasonal succession influenced by freshwater inflow. These sub-communities were associated with specific ranges of salinity and temperature and showed distinct taxonomic profiles, with shared characteristics across the estuarine system.
CONCLUSIONS: Our findings suggest that TM is a useful tool for exploring complex environmental microbiome datasets, offering a complementary perspective that can provide additional ecological insights. TM's ability to highlight coherent microbial community patterns indicates its promise for supporting environmental monitoring and informing targeted ecosystem management in dynamic habitats, though further studies are needed to fully assess its applicability.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
Multi-omic modelling of body mass index response to a dietary weight loss intervention.
Gut microbes, 18(1):2696645.
Obesity is a multifactorial condition, and there is wide heterogeneity in responses to weight loss interventions. Although it remains challenging, modeling responses to weight loss interventions can help tailor treatments, increase weight loss success, or improve our understanding of underlying pathophysiology. We leveraged multi-omic (genetics; gut microbiota: taxonomy, inferred gene pathways and metabolite dynamics; blood metabolomics) and clinical data (e.g., lipids, blood glucose) from a 12-month behavioral weight loss trial of adults (n = 150) with overweight/obesity, to forecast longitudinal body mass index (BMI) and BMI change (ΔBMI) using Mixed Effects Random Forests (MERF) and GLMM-Lasso. Across modeling approaches and outcomes, routinely available clinical variables and blood metabolomics consistently improved prediction over basic demographics, and metabolomics added value beyond clinical information. Across models, the combined omic risk score most improved models of longitudinal BMI trajectories, explaining 20.5-26.0% marginal variance (R[2]m), whereas metabolomic risk scores most improved BMI change prediction (R[2]m = 52.9-59.3%). Gut microbial taxonomy and inferred gene pathways offered modest but significant gains for some models and outcomes, while metabolite dynamics consistently failed to enhance performance. The most important features in the models included insulin, glycoprotein acetyls, lipoprotein sizes, and certain amino acids, aligning with known inflammatory and metabolic mechanisms. These findings support that select blood-based biomarkers correlate with individual responses to weight loss efforts.
Additional Links: PMID-42458730
Publisher:
PubMed:
Citation:
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@article {pmid42458730,
year = {2026},
author = {Yeo, EN and Scadden, AW and Caterer, ZT and Sutton, KJ and Konigsberg, IR and Cole, JB and Litkowski, EM and Pan, Z and Lozupone, CA and Ostendorf, DM and MacLean, PS and Melanson, EL and Bessesen, DH and Borengasser, SJ and Lange, EM and Catenacci, VA and Stanislawski, MA},
title = {Multi-omic modelling of body mass index response to a dietary weight loss intervention.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2696645},
doi = {10.1080/19490976.2026.2696645},
pmid = {42458730},
issn = {1949-0984},
mesh = {Humans ; Multiomics ; *Body Mass Index ; *Obesity/diet therapy/metabolism ; *Weight Loss ; Female ; Male ; Adult ; Metabolomics ; Gastrointestinal Microbiome ; Middle Aged ; *Overweight/diet therapy ; },
abstract = {Obesity is a multifactorial condition, and there is wide heterogeneity in responses to weight loss interventions. Although it remains challenging, modeling responses to weight loss interventions can help tailor treatments, increase weight loss success, or improve our understanding of underlying pathophysiology. We leveraged multi-omic (genetics; gut microbiota: taxonomy, inferred gene pathways and metabolite dynamics; blood metabolomics) and clinical data (e.g., lipids, blood glucose) from a 12-month behavioral weight loss trial of adults (n = 150) with overweight/obesity, to forecast longitudinal body mass index (BMI) and BMI change (ΔBMI) using Mixed Effects Random Forests (MERF) and GLMM-Lasso. Across modeling approaches and outcomes, routinely available clinical variables and blood metabolomics consistently improved prediction over basic demographics, and metabolomics added value beyond clinical information. Across models, the combined omic risk score most improved models of longitudinal BMI trajectories, explaining 20.5-26.0% marginal variance (R[2]m), whereas metabolomic risk scores most improved BMI change prediction (R[2]m = 52.9-59.3%). Gut microbial taxonomy and inferred gene pathways offered modest but significant gains for some models and outcomes, while metabolite dynamics consistently failed to enhance performance. The most important features in the models included insulin, glycoprotein acetyls, lipoprotein sizes, and certain amino acids, aligning with known inflammatory and metabolic mechanisms. These findings support that select blood-based biomarkers correlate with individual responses to weight loss efforts.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Multiomics
*Body Mass Index
*Obesity/diet therapy/metabolism
*Weight Loss
Female
Male
Adult
Metabolomics
Gastrointestinal Microbiome
Middle Aged
*Overweight/diet therapy
RevDate: 2026-07-16
CmpDate: 2026-07-16
Longitudinal modelling of microbiome subcommunities reveals parity-dependent dynamics during pregnancy and postpartum.
Gut microbes, 18(1):2690907.
BACKGROUND: Dysregulation of maternal adaptations to pregnancy due to high pre-pregnancy BMI (pBMI) is associated with worsened health outcomes for mothers and children. The role of the gut microbiome in these adaptations remains unclear.
METHODS: Stool samples were collected from pregnant participants (n = 52) enrolled in the Be Healthy in Pregnancy study (NCT01689961) during first, second, and third trimesters, and 6-months postpartum, along with samples from their infants at 6 months of age. Following 16S rRNA gene sequencing, we implemented time-aligned LDA (TALDA) using a time-weighted sampling strategy with exponentially decaying weights to construct time-proximal cohorts, applied LDA to each cohort independently, and aligned resulting topics using the alto R package. Infant samples were analyzed using standard LDA.
RESULTS: Seven distinct subcommunities were identified, one of which represented perineal contamination and was excluded from further analysis. Remaining subcommunities had distinct taxonomic definitions which remained stable throughout pregnancy (mean cross-cohort stability 0.899) while subcommunity proportions within individuals varied. Multiparous individuals showed greater shifts in subcommunity proportions during early pregnancy, while primiparous individuals displayed progressively increasing shifts with the largest changes during the transition from pregnancy to postpartum. High pBMI was associated with reduced microbiome remodelling, particularly among multiparous individuals. In exploratory analyses, maternal SCFA-producing subcommunity abundance at late pregnancy was positively associated with infant Bifidobacterium-dominated subcommunity proportions at 6 months, while pBMI > 25 was independently associated with lower infant Bifidobacterium.
CONCLUSION: TALDA effectively distinguished between stable subcommunity definitions and dynamic subcommunity proportions, revealing that the microbiome maintains functional organization while subcommunity proportional contributions shift over the course of pregnancy and postpartum. These maternal dynamics may have intergenerational consequences through their influence on infant gut colonization. This work demonstrates that maternal factors modify microbiome trajectories and supports the existence of an ecological memory of pregnancy history within the maternal gut microbiome.
Additional Links: PMID-42458733
Publisher:
PubMed:
Citation:
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@article {pmid42458733,
year = {2026},
author = {Kennedy, KM and Fernando, S and Atkinson, SA and Surette, MG and Jeganathan, P and Sloboda, DM},
title = {Longitudinal modelling of microbiome subcommunities reveals parity-dependent dynamics during pregnancy and postpartum.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2690907},
doi = {10.1080/19490976.2026.2690907},
pmid = {42458733},
issn = {1949-0984},
mesh = {Adult ; Female ; Humans ; Infant ; Pregnancy ; *Bacteria/classification/genetics/isolation & purification ; Feces/microbiology ; *Gastrointestinal Microbiome ; Longitudinal Studies ; *Parity ; *Postpartum Period ; RNA, Ribosomal, 16S/genetics ; Randomized Controlled Trials as Topic ; },
abstract = {BACKGROUND: Dysregulation of maternal adaptations to pregnancy due to high pre-pregnancy BMI (pBMI) is associated with worsened health outcomes for mothers and children. The role of the gut microbiome in these adaptations remains unclear.
METHODS: Stool samples were collected from pregnant participants (n = 52) enrolled in the Be Healthy in Pregnancy study (NCT01689961) during first, second, and third trimesters, and 6-months postpartum, along with samples from their infants at 6 months of age. Following 16S rRNA gene sequencing, we implemented time-aligned LDA (TALDA) using a time-weighted sampling strategy with exponentially decaying weights to construct time-proximal cohorts, applied LDA to each cohort independently, and aligned resulting topics using the alto R package. Infant samples were analyzed using standard LDA.
RESULTS: Seven distinct subcommunities were identified, one of which represented perineal contamination and was excluded from further analysis. Remaining subcommunities had distinct taxonomic definitions which remained stable throughout pregnancy (mean cross-cohort stability 0.899) while subcommunity proportions within individuals varied. Multiparous individuals showed greater shifts in subcommunity proportions during early pregnancy, while primiparous individuals displayed progressively increasing shifts with the largest changes during the transition from pregnancy to postpartum. High pBMI was associated with reduced microbiome remodelling, particularly among multiparous individuals. In exploratory analyses, maternal SCFA-producing subcommunity abundance at late pregnancy was positively associated with infant Bifidobacterium-dominated subcommunity proportions at 6 months, while pBMI > 25 was independently associated with lower infant Bifidobacterium.
CONCLUSION: TALDA effectively distinguished between stable subcommunity definitions and dynamic subcommunity proportions, revealing that the microbiome maintains functional organization while subcommunity proportional contributions shift over the course of pregnancy and postpartum. These maternal dynamics may have intergenerational consequences through their influence on infant gut colonization. This work demonstrates that maternal factors modify microbiome trajectories and supports the existence of an ecological memory of pregnancy history within the maternal gut microbiome.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Adult
Female
Humans
Infant
Pregnancy
*Bacteria/classification/genetics/isolation & purification
Feces/microbiology
*Gastrointestinal Microbiome
Longitudinal Studies
*Parity
*Postpartum Period
RNA, Ribosomal, 16S/genetics
Randomized Controlled Trials as Topic
RevDate: 2026-07-16
Gut-Brain Axis Mechanisms and Microbiome Abnormalities in Autism Spectrum Disorder and Therapeutic Implications.
Current neuropharmacology pii:CN-EPUB-156955 [Epub ahead of print].
ASD has been associated with alterations of the microbiota-gut-brain axis, a bidirectional system that links gut microbiota to neural, endocrine, and immune pathways. Multi-omics studies indicate that most of the ASD affected individuals have lower levels of beneficial taxa, including Bifidobacterium, Lactobacillus gemelhinis, Faecalibacterium prausnitzii, and Roseburia species, and also enrichment with potentially pathogenic strains. Dysbiosis likely affects SCFA, especially butyrate, production. Butyrate acts via GPR41 and GPR43, which maintain the gut barrier and reduce inflammation. Lower butyrate and receptor activity can weaken the barrier, leading to systemic and neuroinflammation implicated in ASD. Effects of the microbiota on neurotransmission also seem pertinent, with alteration in tryptophan metabolism being able to affect central nervous system serotonin availability, and imbalance in GABA glutamate signaling potentially playing a role in excitatory inhibitory dysregulation. Immune crosstalk is paramount in these processes, as micro-bial products and SCFAs are able to influence microglial activity and brain-derived neurotrophic factor signaling with consequent impacts on synaptic plasticity and behavior. This narrative review synthesises societal momentum with current understanding and treatment approaches related to the microbiome of ASD. Probiotics, prebiotics, precision nutrition, and faecal microbiota transplanta-tion (FMT) have reported promising evidence of symptom reduction and, in some studies, behavior. Evidence is still mixed because of strain variation, dosing, delivery protocols, and follow-up. We delineate priorities for randomized, adequately powered experiments that incorporate longitudinal multi-omics, immune phenotyping, and standardized neurobehavioral assessments, while taking into account developmental timing and individual variation. Collectively, the current evidence suggests the gut-brain axis as a potential contributor to ASD biology and a potential target of therapy. Customized plans to rehabilitate SCFA production, enhance barrier function, and normalize neuro-immune and neurotransmitter pathways may augment current practice. Establishing causality and determining which patients benefit from which interventions when are the essential next steps.
Additional Links: PMID-42458949
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PubMed:
Citation:
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@article {pmid42458949,
year = {2026},
author = {Khan, H and Wang, YM and Iftikhar, I and Arif, B and Khan, B and Kiyani, MM and Al-Hussain, F and Bashir, S and Li, HT},
title = {Gut-Brain Axis Mechanisms and Microbiome Abnormalities in Autism Spectrum Disorder and Therapeutic Implications.},
journal = {Current neuropharmacology},
volume = {},
number = {},
pages = {},
doi = {10.2174/011570159X423517260330192710},
pmid = {42458949},
issn = {1875-6190},
abstract = {ASD has been associated with alterations of the microbiota-gut-brain axis, a bidirectional system that links gut microbiota to neural, endocrine, and immune pathways. Multi-omics studies indicate that most of the ASD affected individuals have lower levels of beneficial taxa, including Bifidobacterium, Lactobacillus gemelhinis, Faecalibacterium prausnitzii, and Roseburia species, and also enrichment with potentially pathogenic strains. Dysbiosis likely affects SCFA, especially butyrate, production. Butyrate acts via GPR41 and GPR43, which maintain the gut barrier and reduce inflammation. Lower butyrate and receptor activity can weaken the barrier, leading to systemic and neuroinflammation implicated in ASD. Effects of the microbiota on neurotransmission also seem pertinent, with alteration in tryptophan metabolism being able to affect central nervous system serotonin availability, and imbalance in GABA glutamate signaling potentially playing a role in excitatory inhibitory dysregulation. Immune crosstalk is paramount in these processes, as micro-bial products and SCFAs are able to influence microglial activity and brain-derived neurotrophic factor signaling with consequent impacts on synaptic plasticity and behavior. This narrative review synthesises societal momentum with current understanding and treatment approaches related to the microbiome of ASD. Probiotics, prebiotics, precision nutrition, and faecal microbiota transplanta-tion (FMT) have reported promising evidence of symptom reduction and, in some studies, behavior. Evidence is still mixed because of strain variation, dosing, delivery protocols, and follow-up. We delineate priorities for randomized, adequately powered experiments that incorporate longitudinal multi-omics, immune phenotyping, and standardized neurobehavioral assessments, while taking into account developmental timing and individual variation. Collectively, the current evidence suggests the gut-brain axis as a potential contributor to ASD biology and a potential target of therapy. Customized plans to rehabilitate SCFA production, enhance barrier function, and normalize neuro-immune and neurotransmitter pathways may augment current practice. Establishing causality and determining which patients benefit from which interventions when are the essential next steps.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
Ecological restructuring of the nonbacterial fecal microbiome in obesity across human cohorts.
Gut microbes, 18(1):2701446.
Obesity is a complex metabolic disorder increasingly linked to alterations in the gut microbiome. While most research has focused on bacterial communities, the contribution of nonbacterial components including viruses, archaea, and eukaryotic microorganisms remains insufficiently characterized. Here, we performed a multicohort analysis to investigate the role of the nonbacterial gut microbiome in obesity across three independent human cohorts. Using compositional analyses adjusted for key covariates and network based approaches, we identified consistent multikingdom alterations associated with obesity. Individuals without obesity showed a reproducible enrichment of methanogenic archaea, particularly Methanobrevibacter smithii and Methanobrevibacter millerae, whereas individuals with obesity were characterized by increased abundance of bacteriophages from the class Caudoviricetes. In an elderly cohort, eukaryotic taxa such as Blastocystis spp. were additionally associated with the without obesity group. These patterns were largely consistent across cohorts and robust to sex stratification. Beyond taxonomic differences, ecological network analyses revealed substantial reorganization of microbial interactions in obesity. The identity and composition of hub taxa differed significantly between obesity and without obesity networks across all cohorts, indicating a shift in the taxa occupying central ecological roles. Notably, these differences were observed even when similar microbial kingdoms were represented, underscoring the importance of species-level resolution. Collectively, our findings demonstrate that obesity is associated with coordinated compositional and ecological alterations across the nonbacterial gut microbiome. This multikingdom perspective expands current understanding of microbiome dysbiosis in metabolic disease and highlights the archaeome and virome as potential contributors to host metabolic health.
Additional Links: PMID-42458961
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PubMed:
Citation:
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@article {pmid42458961,
year = {2026},
author = {Gallardo-Nuell, L and Rosell-DÃaz, M and Garre-Olmo, J and Puig, J and Ramos, R and Pons, J and Pérez-Brocal, V and Moya, A and Mayneris-Perxachs, J and Fernández-Real, JM},
title = {Ecological restructuring of the nonbacterial fecal microbiome in obesity across human cohorts.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2701446},
doi = {10.1080/19490976.2026.2701446},
pmid = {42458961},
issn = {1949-0984},
mesh = {Humans ; *Obesity/microbiology ; *Feces/microbiology ; Male ; Cohort Studies ; *Gastrointestinal Microbiome ; Female ; Bacteria/classification/isolation & purification/genetics ; Archaea/classification/isolation & purification/genetics ; Aged ; },
abstract = {Obesity is a complex metabolic disorder increasingly linked to alterations in the gut microbiome. While most research has focused on bacterial communities, the contribution of nonbacterial components including viruses, archaea, and eukaryotic microorganisms remains insufficiently characterized. Here, we performed a multicohort analysis to investigate the role of the nonbacterial gut microbiome in obesity across three independent human cohorts. Using compositional analyses adjusted for key covariates and network based approaches, we identified consistent multikingdom alterations associated with obesity. Individuals without obesity showed a reproducible enrichment of methanogenic archaea, particularly Methanobrevibacter smithii and Methanobrevibacter millerae, whereas individuals with obesity were characterized by increased abundance of bacteriophages from the class Caudoviricetes. In an elderly cohort, eukaryotic taxa such as Blastocystis spp. were additionally associated with the without obesity group. These patterns were largely consistent across cohorts and robust to sex stratification. Beyond taxonomic differences, ecological network analyses revealed substantial reorganization of microbial interactions in obesity. The identity and composition of hub taxa differed significantly between obesity and without obesity networks across all cohorts, indicating a shift in the taxa occupying central ecological roles. Notably, these differences were observed even when similar microbial kingdoms were represented, underscoring the importance of species-level resolution. Collectively, our findings demonstrate that obesity is associated with coordinated compositional and ecological alterations across the nonbacterial gut microbiome. This multikingdom perspective expands current understanding of microbiome dysbiosis in metabolic disease and highlights the archaeome and virome as potential contributors to host metabolic health.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Obesity/microbiology
*Feces/microbiology
Male
Cohort Studies
*Gastrointestinal Microbiome
Female
Bacteria/classification/isolation & purification/genetics
Archaea/classification/isolation & purification/genetics
Aged
RevDate: 2026-07-16
Bacteria Colonization is Associated with Inflammation-Antigen Presentation Imbalance in Myeloid Cells and Tumor Microenvironment Features in Melanoma.
Immunological investigations [Epub ahead of print].
BACKGROUND: Intracellular microbes have been detected in multiple tumors, but their impact on the tumor microenvironment of melanoma and immune regulation remains unclear.
METHODS: We applied single-cell host-microbe interaction analysis to single cell RNA sequencing data from 42 melanoma samples to characterize host-microbe interactions. Multiple functional annotation approaches were integrated to assess immune and tumor cell transcriptional states associated with bacteria colonization.
RESULTS: Intracellular bacteria, particularly human-colonizing bacteria were associated with distinct transcriptional alterations in the tumor immune microenvironment, characterized by increased inflammation and reduced antigen presentation signatures in myeloid cells, along with enhanced innate immune-related transcriptional patterns, whereas adaptive T cell-related immune signatures were reduced. Tumor cells also exhibited transcriptional alterations, including increased metabolic activity and extracellular matrix remodeling pathways. At the bulk transcriptomic level, colonizing bacteria-associated chronic inflammatory features were correlated with increased CD8+ T cell infiltration and improved overall survival, while also showing a potential association with responses to immunotherapy.
CONCLUSIONS: Intracellular colonizing bacteria were associated with inflammation-antigen presentation imbalance in melanoma tumor microenvironment.
Additional Links: PMID-42458994
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PubMed:
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@article {pmid42458994,
year = {2026},
author = {Gong, Z and Guo, W and Zhang, Z and Du, H and Wu, X and Tu, J},
title = {Bacteria Colonization is Associated with Inflammation-Antigen Presentation Imbalance in Myeloid Cells and Tumor Microenvironment Features in Melanoma.},
journal = {Immunological investigations},
volume = {},
number = {},
pages = {1-25},
doi = {10.1080/08820139.2026.2702079},
pmid = {42458994},
issn = {1532-4311},
abstract = {BACKGROUND: Intracellular microbes have been detected in multiple tumors, but their impact on the tumor microenvironment of melanoma and immune regulation remains unclear.
METHODS: We applied single-cell host-microbe interaction analysis to single cell RNA sequencing data from 42 melanoma samples to characterize host-microbe interactions. Multiple functional annotation approaches were integrated to assess immune and tumor cell transcriptional states associated with bacteria colonization.
RESULTS: Intracellular bacteria, particularly human-colonizing bacteria were associated with distinct transcriptional alterations in the tumor immune microenvironment, characterized by increased inflammation and reduced antigen presentation signatures in myeloid cells, along with enhanced innate immune-related transcriptional patterns, whereas adaptive T cell-related immune signatures were reduced. Tumor cells also exhibited transcriptional alterations, including increased metabolic activity and extracellular matrix remodeling pathways. At the bulk transcriptomic level, colonizing bacteria-associated chronic inflammatory features were correlated with increased CD8+ T cell infiltration and improved overall survival, while also showing a potential association with responses to immunotherapy.
CONCLUSIONS: Intracellular colonizing bacteria were associated with inflammation-antigen presentation imbalance in melanoma tumor microenvironment.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
Immunometabolic Dysregulation in Preeclampsia: Emerging Roles of Inflammation, Insulin Resistance, Uric Acid, and the Gut Microbiome.
Mediators of inflammation, 2026(1):e7890624.
Preeclampsia is a major cause of maternal and perinatal morbidity around the world. It is increasingly recognized as a disorder of systemic immunometabolic dysregulation rather than isolated placental dysfunction. Increasing evidence links chronic inflammation, insulin resistance, and changes in uric acid metabolism to the initiation and progression of preeclampsia. In addition, emerging evidence indicates that maternal gut dysbiosis is an upstream regulator of systemic immune and metabolic dysfunction via the gut-systemic-decidual axis. This review synthesizes current mechanistic, clinical, and translational evidence on the interplay between immune activation, metabolic dysfunction, and uric acid biology in relation to preeclampsia, highlighting emerging biomarkers and therapeutic implications. A narrative review was performed of experimental, epidemiological, and clinical studies found in peer-reviewed journals. The review focused on pathways involving innate and adaptive immune activation, inflammation, insulin signaling abnormalities, endothelial dysfunction, and how uric acid affects placental and vascular biology. Preeclampsia shows increased activation of the innate immune system, a shift toward Th1/Th17 responses, vascular inflammation, and impaired immune tolerance. These immune disturbances combine with pregnancy-associated insulin resistance, exacerbating oxidative stress and endothelial dysfunction, thereby reducing oxygen supply to the placenta. Elevated levels of serum uric acid (SUA), previously regarded as merely a marker of disease severity, are now thought to actively promote inflammasome activation, inhibit nitric oxide (NO), and disrupt trophoblast function. Together, these interconnected pathways form self-reinforcing immunometabolic feedback loops that sustain vascular damage and drive the progression of the disease. Recent studies indicate that changes in the composition of maternal gut microbiota and their metabolites, such as short-chain fatty acids (SCFAs) and endotoxins, can lead to systemic inflammation, endothelial dysfunction, and reduced immune tolerance. Immunometabolic dysregulation provides a comprehensive framework for understanding the pathogenesis of preeclampsia. Integrating inflammatory pathways, insulin resistance, serum uric acid, and alterations in the gut, systemic, and decidual microbiomes may improve risk stratification and facilitate the development of targeted preventive strategies. Nevertheless, well-designed longitudinal and interventional studies are needed to validate these associations, establish causal relationships, and translate emerging evidence into effective prevention and management approaches across diverse populations.
Additional Links: PMID-42459061
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@article {pmid42459061,
year = {2026},
author = {Ali, N},
title = {Immunometabolic Dysregulation in Preeclampsia: Emerging Roles of Inflammation, Insulin Resistance, Uric Acid, and the Gut Microbiome.},
journal = {Mediators of inflammation},
volume = {2026},
number = {1},
pages = {e7890624},
pmid = {42459061},
issn = {1466-1861},
mesh = {Humans ; Female ; *Pre-Eclampsia/metabolism/immunology ; *Uric Acid/metabolism/blood ; *Insulin Resistance/physiology ; Pregnancy ; *Inflammation/metabolism/immunology ; *Gastrointestinal Microbiome/physiology ; Animals ; },
abstract = {Preeclampsia is a major cause of maternal and perinatal morbidity around the world. It is increasingly recognized as a disorder of systemic immunometabolic dysregulation rather than isolated placental dysfunction. Increasing evidence links chronic inflammation, insulin resistance, and changes in uric acid metabolism to the initiation and progression of preeclampsia. In addition, emerging evidence indicates that maternal gut dysbiosis is an upstream regulator of systemic immune and metabolic dysfunction via the gut-systemic-decidual axis. This review synthesizes current mechanistic, clinical, and translational evidence on the interplay between immune activation, metabolic dysfunction, and uric acid biology in relation to preeclampsia, highlighting emerging biomarkers and therapeutic implications. A narrative review was performed of experimental, epidemiological, and clinical studies found in peer-reviewed journals. The review focused on pathways involving innate and adaptive immune activation, inflammation, insulin signaling abnormalities, endothelial dysfunction, and how uric acid affects placental and vascular biology. Preeclampsia shows increased activation of the innate immune system, a shift toward Th1/Th17 responses, vascular inflammation, and impaired immune tolerance. These immune disturbances combine with pregnancy-associated insulin resistance, exacerbating oxidative stress and endothelial dysfunction, thereby reducing oxygen supply to the placenta. Elevated levels of serum uric acid (SUA), previously regarded as merely a marker of disease severity, are now thought to actively promote inflammasome activation, inhibit nitric oxide (NO), and disrupt trophoblast function. Together, these interconnected pathways form self-reinforcing immunometabolic feedback loops that sustain vascular damage and drive the progression of the disease. Recent studies indicate that changes in the composition of maternal gut microbiota and their metabolites, such as short-chain fatty acids (SCFAs) and endotoxins, can lead to systemic inflammation, endothelial dysfunction, and reduced immune tolerance. Immunometabolic dysregulation provides a comprehensive framework for understanding the pathogenesis of preeclampsia. Integrating inflammatory pathways, insulin resistance, serum uric acid, and alterations in the gut, systemic, and decidual microbiomes may improve risk stratification and facilitate the development of targeted preventive strategies. Nevertheless, well-designed longitudinal and interventional studies are needed to validate these associations, establish causal relationships, and translate emerging evidence into effective prevention and management approaches across diverse populations.},
}
MeSH Terms:
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Humans
Female
*Pre-Eclampsia/metabolism/immunology
*Uric Acid/metabolism/blood
*Insulin Resistance/physiology
Pregnancy
*Inflammation/metabolism/immunology
*Gastrointestinal Microbiome/physiology
Animals
RevDate: 2026-07-16
Individualized Biochemical Profiling in Drug Design: Integrating MultiOmics, Nanotechnology, and Machine Learning.
Current pharmaceutical biotechnology pii:CPB-EPUB-156968 [Epub ahead of print].
The introduction of individualized biochemical profiles is allowing to revolutionize modern medicinal chemistry by providing more comprehensive data for the development of drugs, their refinement and clinical application. Conventional methods frequently underestimate inter-individual variability, resulting in inferior efficacy or adverse reactions. This new approach highlights the importance of personalized biochemical signatures in moulding pharmacokinetics and pharmacodynamics of drug candidates in accordance with the genomic variations, epigenetic alterations, and interaction of the host with its microbiome. The said parameters influence the absorption, distribution, metabolism, and excretion (ADME), forcing a re-evaluating the classical drug designing model. Individualized biochemical profiling will be fuelled by the combined impact of pharmacogenomics, high-throughput screening, and quantitative structure-activity relationship (QSAR) models, enabling the improvement of drug candidates better suited to an individual's metabolic and enzymatic ranges. This approach will notably help in predicting druginduced liver injury (DILI) and other organ-specific toxicities, allowing improved safety with novel treatments before clinical trials. In addition, individualized biochemical data can also enhance the accuracy of nanocarrier-based drug delivery systems by combining enzyme and receptor expression patterns, resulting in better tissue targeting and fewer off-target effects. This narrative review was conducted through a structured search of peer-reviewed literature from leading scientific databases, with emphasis on recent and translationally relevant studies. The article aims to explore how the amalgamation of these three fields (metabolomics, targeted nanotechnology, and machine learning) has the potential to reshape clinical interventions and allow researchers to refine drug reactions at the individual level.
Additional Links: PMID-42459088
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@article {pmid42459088,
year = {2026},
author = {Ahmad, R and Siddiqui, S and Habib, S and Moinuddin, and Kashif Zaidi, S},
title = {Individualized Biochemical Profiling in Drug Design: Integrating MultiOmics, Nanotechnology, and Machine Learning.},
journal = {Current pharmaceutical biotechnology},
volume = {},
number = {},
pages = {},
doi = {10.2174/0113892010481219260630203205},
pmid = {42459088},
issn = {1873-4316},
abstract = {The introduction of individualized biochemical profiles is allowing to revolutionize modern medicinal chemistry by providing more comprehensive data for the development of drugs, their refinement and clinical application. Conventional methods frequently underestimate inter-individual variability, resulting in inferior efficacy or adverse reactions. This new approach highlights the importance of personalized biochemical signatures in moulding pharmacokinetics and pharmacodynamics of drug candidates in accordance with the genomic variations, epigenetic alterations, and interaction of the host with its microbiome. The said parameters influence the absorption, distribution, metabolism, and excretion (ADME), forcing a re-evaluating the classical drug designing model. Individualized biochemical profiling will be fuelled by the combined impact of pharmacogenomics, high-throughput screening, and quantitative structure-activity relationship (QSAR) models, enabling the improvement of drug candidates better suited to an individual's metabolic and enzymatic ranges. This approach will notably help in predicting druginduced liver injury (DILI) and other organ-specific toxicities, allowing improved safety with novel treatments before clinical trials. In addition, individualized biochemical data can also enhance the accuracy of nanocarrier-based drug delivery systems by combining enzyme and receptor expression patterns, resulting in better tissue targeting and fewer off-target effects. This narrative review was conducted through a structured search of peer-reviewed literature from leading scientific databases, with emphasis on recent and translationally relevant studies. The article aims to explore how the amalgamation of these three fields (metabolomics, targeted nanotechnology, and machine learning) has the potential to reshape clinical interventions and allow researchers to refine drug reactions at the individual level.},
}
RevDate: 2026-07-16
Bridging periodontitis and clonal hematopoiesis: implications for solid tumor metastasis, clinical trial design, and microbiome dynamics. Comment on: "Ligature-induced periodontitis promotes Dnmt3aR878H-driven clonal hematopoiesis".
Haematologica [Epub ahead of print].
Not available.
Additional Links: PMID-42459134
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@article {pmid42459134,
year = {2026},
author = {Cheng, C and Wu, X},
title = {Bridging periodontitis and clonal hematopoiesis: implications for solid tumor metastasis, clinical trial design, and microbiome dynamics. Comment on: "Ligature-induced periodontitis promotes Dnmt3aR878H-driven clonal hematopoiesis".},
journal = {Haematologica},
volume = {},
number = {},
pages = {},
doi = {10.3324/haematol.2026.301567},
pmid = {42459134},
issn = {1592-8721},
abstract = {Not available.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
Precision nutrition in Asian populations: a Multi-omics review of mechanisms, biomarkers, and implementation pathways.
Journal of nutritional science, 15:e59.
The rapid expansion of omics technologies has created new opportunities to understand inter-individual variations in metabolic responses to diet. Such advances are particularly relevant for Asian populations, which exhibit distinct metabolic characteristics, including increased visceral adiposity, reduced β-cell reserves, and heightened susceptibility to type 2 diabetes at lower BMI levels, compared to Western populations. This review synthesizes the current evidence on metabolomic and genomic biomarkers associated with metabolic health in Asians and outlines the mechanistic pathways through which diet influences these biomarkers. Metabolomic signatures, such as lysophosphatidylcholines, micronutrient-derived metabolites, amino acid profiles, and oxidative stress indicators, have demonstrated strong potential for the early detection of metabolic dysfunction. In addition, carbohydrate-related markers of glycemic excursions, microbiome-derived metabolites, and diet-responsive fatty acid profiles may help capture the heterogeneity in postprandial regulation and diet responsiveness. Genetic variants enriched in Asian populations, including TMEM182- and NPC1L1-related polymorphisms, further modulate lipid metabolism, adipogenesis, and glycemic regulation. We also highlighted β-cell and nutrient-handling loci (e.g. KCNQ1, TCF7L2, SLC30A8, FUT2/6, BCMO1, and FADS1/2) as mechanistic anchors for biologically stratified dietary personalization. We discuss nutrient-metabolite interactions - particularly those involving dietary fibre and legumes - within culturally patterned Asian diets and highlight culturally consistent dietary strategies supported by multi-omics evidence. Finally, we propose a translational framework for implementing precision nutrition in Asia, emphasizing analytical standardization, clinician training, digital health integration, and equity considerations. Together, these insights underscore the potential of multi-omics approaches to inform individualized dietary recommendations and improve metabolic health across diverse Asian populations.
Additional Links: PMID-42459212
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@article {pmid42459212,
year = {2026},
author = {Kim, M},
title = {Precision nutrition in Asian populations: a Multi-omics review of mechanisms, biomarkers, and implementation pathways.},
journal = {Journal of nutritional science},
volume = {15},
number = {},
pages = {e59},
pmid = {42459212},
issn = {2048-6790},
mesh = {Humans ; Biomarkers/metabolism ; Multiomics ; *Asian People/genetics ; *Diet ; Metabolomics ; *Precision Medicine ; Diabetes Mellitus, Type 2 ; },
abstract = {The rapid expansion of omics technologies has created new opportunities to understand inter-individual variations in metabolic responses to diet. Such advances are particularly relevant for Asian populations, which exhibit distinct metabolic characteristics, including increased visceral adiposity, reduced β-cell reserves, and heightened susceptibility to type 2 diabetes at lower BMI levels, compared to Western populations. This review synthesizes the current evidence on metabolomic and genomic biomarkers associated with metabolic health in Asians and outlines the mechanistic pathways through which diet influences these biomarkers. Metabolomic signatures, such as lysophosphatidylcholines, micronutrient-derived metabolites, amino acid profiles, and oxidative stress indicators, have demonstrated strong potential for the early detection of metabolic dysfunction. In addition, carbohydrate-related markers of glycemic excursions, microbiome-derived metabolites, and diet-responsive fatty acid profiles may help capture the heterogeneity in postprandial regulation and diet responsiveness. Genetic variants enriched in Asian populations, including TMEM182- and NPC1L1-related polymorphisms, further modulate lipid metabolism, adipogenesis, and glycemic regulation. We also highlighted β-cell and nutrient-handling loci (e.g. KCNQ1, TCF7L2, SLC30A8, FUT2/6, BCMO1, and FADS1/2) as mechanistic anchors for biologically stratified dietary personalization. We discuss nutrient-metabolite interactions - particularly those involving dietary fibre and legumes - within culturally patterned Asian diets and highlight culturally consistent dietary strategies supported by multi-omics evidence. Finally, we propose a translational framework for implementing precision nutrition in Asia, emphasizing analytical standardization, clinician training, digital health integration, and equity considerations. Together, these insights underscore the potential of multi-omics approaches to inform individualized dietary recommendations and improve metabolic health across diverse Asian populations.},
}
MeSH Terms:
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Humans
Biomarkers/metabolism
Multiomics
*Asian People/genetics
*Diet
Metabolomics
*Precision Medicine
Diabetes Mellitus, Type 2
RevDate: 2026-07-16
CmpDate: 2026-07-16
Scalp microbiome in male androgenetic alopecia: 16S rRNA sequencing-based clinical characterization, mouse model validation, and effects on hair follicle cells.
Frontiers in cellular and infection microbiology, 16:1878609.
INTRODUCTION: Persistent microinflammation in androgenetic alopecia (AGA) may contribute to hair follicle miniaturization, but whether scalp microbial dysbiosis serves as its trigger remains unclear. This study integrated clinical samples, an animal model, and in vitro experiments to investigate the scalp microbiome in AGA.
METHODS: Scalp microbial samples were collected from four regions (frontal, vertex, temporal, occipital) of 12 AGA patients and 12 healthy controls (96 samples in total) and analyzed by 16S rRNA gene sequencing. An AGA mouse model was established using testosterone propionate to evaluate histopathology and skin microbiota. The effects of Staphylococcus epidermidis-derived phenol-soluble modulins PSMγ and PSMδ on human dermal papilla cell (HDPC) proliferation were assessed, and the effect of PSMδ on cell migration was also examined.
RESULTS: AGA patients exhibited elevated overall scalp microbial richness and diversity, with a marked decrease in Staphylococcus abundance that was most pronounced in the frontal and vertex regions. The mouse model also displayed significant restructuring of the skin microbiota; however, Staphylococcus showed marked enrichment-a direction opposite to that in humans. Together, these findings indicate that aberrant Staphylococcus abundance serves as a sensitive bio-indicator of the AGA pathological state. PSMδ significantly promoted HDPC proliferation in a time- and concentration-dependent manner, demonstrating a wider effective concentration window and milder action, and it also significantly enhanced cell migration.
DISCUSSION: The dysregulation of Staphylococcus abundance is a key feature of scalp microbial dysbiosis in AGA. PSMδ possesses dual potential in modulating hair follicle cell activity and maintaining microecological homeostasis, providing new insights for microbiome-targeted interventions in AGA.
Additional Links: PMID-42459334
PubMed:
Citation:
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@article {pmid42459334,
year = {2026},
author = {Zhang, L and Qin, M and Li, D and Wang, K and Wang, T and Zhou, Y and Yao, X and Tian, Y and Pang, M},
title = {Scalp microbiome in male androgenetic alopecia: 16S rRNA sequencing-based clinical characterization, mouse model validation, and effects on hair follicle cells.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1878609},
pmid = {42459334},
issn = {2235-2988},
mesh = {Animals ; Male ; RNA, Ribosomal, 16S/genetics ; Humans ; *Alopecia/microbiology/pathology ; Disease Models, Animal ; Mice ; *Hair Follicle/microbiology/pathology/cytology ; Skin Microbiome ; *Scalp/microbiology/pathology ; Adult ; *Microbiota ; Cell Proliferation/drug effects ; Cell Movement ; Dysbiosis/microbiology ; },
abstract = {INTRODUCTION: Persistent microinflammation in androgenetic alopecia (AGA) may contribute to hair follicle miniaturization, but whether scalp microbial dysbiosis serves as its trigger remains unclear. This study integrated clinical samples, an animal model, and in vitro experiments to investigate the scalp microbiome in AGA.
METHODS: Scalp microbial samples were collected from four regions (frontal, vertex, temporal, occipital) of 12 AGA patients and 12 healthy controls (96 samples in total) and analyzed by 16S rRNA gene sequencing. An AGA mouse model was established using testosterone propionate to evaluate histopathology and skin microbiota. The effects of Staphylococcus epidermidis-derived phenol-soluble modulins PSMγ and PSMδ on human dermal papilla cell (HDPC) proliferation were assessed, and the effect of PSMδ on cell migration was also examined.
RESULTS: AGA patients exhibited elevated overall scalp microbial richness and diversity, with a marked decrease in Staphylococcus abundance that was most pronounced in the frontal and vertex regions. The mouse model also displayed significant restructuring of the skin microbiota; however, Staphylococcus showed marked enrichment-a direction opposite to that in humans. Together, these findings indicate that aberrant Staphylococcus abundance serves as a sensitive bio-indicator of the AGA pathological state. PSMδ significantly promoted HDPC proliferation in a time- and concentration-dependent manner, demonstrating a wider effective concentration window and milder action, and it also significantly enhanced cell migration.
DISCUSSION: The dysregulation of Staphylococcus abundance is a key feature of scalp microbial dysbiosis in AGA. PSMδ possesses dual potential in modulating hair follicle cell activity and maintaining microecological homeostasis, providing new insights for microbiome-targeted interventions in AGA.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Male
RNA, Ribosomal, 16S/genetics
Humans
*Alopecia/microbiology/pathology
Disease Models, Animal
Mice
*Hair Follicle/microbiology/pathology/cytology
Skin Microbiome
*Scalp/microbiology/pathology
Adult
*Microbiota
Cell Proliferation/drug effects
Cell Movement
Dysbiosis/microbiology
RevDate: 2026-07-16
CmpDate: 2026-07-16
Elevation shapes the seed endophytic bacteria richness and composition of Taraxacum officinale.
AIMS microbiology, 12(2):377-392.
Taraxacum officinale, a widely invasive plant species in New Zealand, thrives across environments, yet little is known about the seed endophytic microbial communities contributing to its adaptability. In this study, we characterized the bacterial community within T. officinale seeds across an elevation gradient of 10 to 720 meters above sea level. Using PCR-DGGE fingerprinting and 16S rRNA gene sequencing, we characterized bacterial community structures and assessed variations across sites. Bacterial richness declined significantly with increasing elevation, accompanied by distinct shifts in community composition. Non-metric multidimensional scaling revealed clear clustering of communities according to elevation, with higher elevation sites exhibiting more similar and less diverse microbiomes compared to lower elevation locations. A total of six dominant bacterial genera were identified: Pseudomonas, Streptomyces, Clavibacter, Xanthomonas, Stenotrophomonas, and Erwinia. These included core genera detected across sites and location-specific genera associated with particular elevations. These results suggested that elevation acts as an environmental filter shaping seed microbiome assembly, with potential implications for microbial transmission and plant adaptation. The functional consequences of these shifts for plant performance, adaptation, and invasion success remain unknown and require further investigation.
Additional Links: PMID-42459389
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Citation:
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@article {pmid42459389,
year = {2026},
author = {Moukarzel, R and Costan, CA and Hulme, PE},
title = {Elevation shapes the seed endophytic bacteria richness and composition of Taraxacum officinale.},
journal = {AIMS microbiology},
volume = {12},
number = {2},
pages = {377-392},
pmid = {42459389},
issn = {2471-1888},
abstract = {Taraxacum officinale, a widely invasive plant species in New Zealand, thrives across environments, yet little is known about the seed endophytic microbial communities contributing to its adaptability. In this study, we characterized the bacterial community within T. officinale seeds across an elevation gradient of 10 to 720 meters above sea level. Using PCR-DGGE fingerprinting and 16S rRNA gene sequencing, we characterized bacterial community structures and assessed variations across sites. Bacterial richness declined significantly with increasing elevation, accompanied by distinct shifts in community composition. Non-metric multidimensional scaling revealed clear clustering of communities according to elevation, with higher elevation sites exhibiting more similar and less diverse microbiomes compared to lower elevation locations. A total of six dominant bacterial genera were identified: Pseudomonas, Streptomyces, Clavibacter, Xanthomonas, Stenotrophomonas, and Erwinia. These included core genera detected across sites and location-specific genera associated with particular elevations. These results suggested that elevation acts as an environmental filter shaping seed microbiome assembly, with potential implications for microbial transmission and plant adaptation. The functional consequences of these shifts for plant performance, adaptation, and invasion success remain unknown and require further investigation.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
Effects of cover cropping on orchard soil microbiomes: Mechanisms and perspectives.
AIMS microbiology, 12(2):224-251.
Orchards have long faced severe soil erosion, acidification of red soils, low nutrient-use efficiency, and frequent soil-borne diseases. Conventional clean tillage combined with intensive chemical inputs often fails to simultaneously improve fruit yield and quality while safeguarding orchard ecological security. Cover cropping (i.e., managed groundcover vegetation) introduces persistent surface plant cover and introduces continuous inputs of root exudates, litter, and residues, while simultaneously modifying soil moisture, temperature, aggregation, porosity, and nutrient availability. Consequently, it reorganizes the soil microbiome from the rhizosphere scale to community-network scales and drives key ecological processes such as carbon sequestration, nitrogen and phosphorus turnover, and disease suppression. Mechanistically, cover crops (i) enhance the supply of labile carbon through root exudation and residue return, stimulating microbial assimilation and enzyme-mediated decomposition and promoting SOC stabilization via microbial necromass formation-mineral association/aggregate protection; and (ii) optimize microbial habitats by improving aggregate architecture, pore structure, and water-holding capacity, and by regulating pH and nutrient availability, thereby increasing the abundance and functional potential of key guilds (e.g., diazotrophs, nitrifiers/denitrifiers, and microorganisms involved in organic-P mineralization) and their functional gene repertoires. In addition, cover cropping may strengthen system stability and suppressiveness through multi-trophic interactions and reconstruction of the soil micro-food web. However, under drought conditions or during the juvenile-tree stage, trade-offs can emerge due to context-dependent tree-groundcover competition for water and nutrients. Future progress requires long-term field experiments integrating multi-omics, isotope tracing, and process-based flux measurements to establish causal evidence chains and scenario-specific models linking management-microbial mechanisms-ecosystem services. Developing operational microbiome-based indicators will provide a scientific basis for groundcover species selection, cover pattern optimization, and fertilizer reduction with improved efficiency, as well as disease mitigation and fruit-quality enhancement.
Additional Links: PMID-42459390
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@article {pmid42459390,
year = {2026},
author = {Guan, G and He, P and Miao, Y and Zhou, G and Liu, G},
title = {Effects of cover cropping on orchard soil microbiomes: Mechanisms and perspectives.},
journal = {AIMS microbiology},
volume = {12},
number = {2},
pages = {224-251},
pmid = {42459390},
issn = {2471-1888},
abstract = {Orchards have long faced severe soil erosion, acidification of red soils, low nutrient-use efficiency, and frequent soil-borne diseases. Conventional clean tillage combined with intensive chemical inputs often fails to simultaneously improve fruit yield and quality while safeguarding orchard ecological security. Cover cropping (i.e., managed groundcover vegetation) introduces persistent surface plant cover and introduces continuous inputs of root exudates, litter, and residues, while simultaneously modifying soil moisture, temperature, aggregation, porosity, and nutrient availability. Consequently, it reorganizes the soil microbiome from the rhizosphere scale to community-network scales and drives key ecological processes such as carbon sequestration, nitrogen and phosphorus turnover, and disease suppression. Mechanistically, cover crops (i) enhance the supply of labile carbon through root exudation and residue return, stimulating microbial assimilation and enzyme-mediated decomposition and promoting SOC stabilization via microbial necromass formation-mineral association/aggregate protection; and (ii) optimize microbial habitats by improving aggregate architecture, pore structure, and water-holding capacity, and by regulating pH and nutrient availability, thereby increasing the abundance and functional potential of key guilds (e.g., diazotrophs, nitrifiers/denitrifiers, and microorganisms involved in organic-P mineralization) and their functional gene repertoires. In addition, cover cropping may strengthen system stability and suppressiveness through multi-trophic interactions and reconstruction of the soil micro-food web. However, under drought conditions or during the juvenile-tree stage, trade-offs can emerge due to context-dependent tree-groundcover competition for water and nutrients. Future progress requires long-term field experiments integrating multi-omics, isotope tracing, and process-based flux measurements to establish causal evidence chains and scenario-specific models linking management-microbial mechanisms-ecosystem services. Developing operational microbiome-based indicators will provide a scientific basis for groundcover species selection, cover pattern optimization, and fertilizer reduction with improved efficiency, as well as disease mitigation and fruit-quality enhancement.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
Yogurt as a modulator of gut and beyond gut: Mechanisms, health effects, and clinical translation.
AIMS microbiology, 12(2):393-421.
Yogurt, a fermented dairy food, has been increasingly recognized for its potential to modulate gut microbiota and promote host health. Accumulating evidence suggests that yogurt consumption influences gut microbial composition, diversity, and functional activity. In this narrative review, we synthesized the findings on yogurt-related effects on the gut microbiota, intestinal barrier, microbial metabolites, immune responses, and selected extra-intestinal outcomes. We distinguished traditional yogurt, probiotic yogurt, synbiotic yogurt, fortified yogurt, and non-dairy or regional yogurt-like fermented products, and then organized proposed mechanisms into a hierarchical framework that separated direct yogurt-derived inputs, including starter cultures, added probiotic strains, fermentation-derived compounds, and dairy matrix components, from resident microbiota-mediated secondary metabolites and host downstream responses. Importantly, limitations and controversies, such as variability in yogurt formulations, strain-specific effects, and inter-individual responses, were critically evaluated. Finally, we highlighted future research directions that emphasize standardized study designs, defined endpoints, long-term randomized controlled trials, and integrative multi-omics approaches to support the development of personalized dietary strategies. Together, this review provides a structured framework for understanding the complex interactions between yogurt, gut microbiota, and host physiology, while outlining key steps needed to translate evidence into actionable nutritional recommendations.
Additional Links: PMID-42459398
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Citation:
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@article {pmid42459398,
year = {2026},
author = {Yang, D and Zhao, H and He, K and Chen, W and Xu, H and Li, S and Xiao, Q and Yang, J and Wu, D},
title = {Yogurt as a modulator of gut and beyond gut: Mechanisms, health effects, and clinical translation.},
journal = {AIMS microbiology},
volume = {12},
number = {2},
pages = {393-421},
pmid = {42459398},
issn = {2471-1888},
abstract = {Yogurt, a fermented dairy food, has been increasingly recognized for its potential to modulate gut microbiota and promote host health. Accumulating evidence suggests that yogurt consumption influences gut microbial composition, diversity, and functional activity. In this narrative review, we synthesized the findings on yogurt-related effects on the gut microbiota, intestinal barrier, microbial metabolites, immune responses, and selected extra-intestinal outcomes. We distinguished traditional yogurt, probiotic yogurt, synbiotic yogurt, fortified yogurt, and non-dairy or regional yogurt-like fermented products, and then organized proposed mechanisms into a hierarchical framework that separated direct yogurt-derived inputs, including starter cultures, added probiotic strains, fermentation-derived compounds, and dairy matrix components, from resident microbiota-mediated secondary metabolites and host downstream responses. Importantly, limitations and controversies, such as variability in yogurt formulations, strain-specific effects, and inter-individual responses, were critically evaluated. Finally, we highlighted future research directions that emphasize standardized study designs, defined endpoints, long-term randomized controlled trials, and integrative multi-omics approaches to support the development of personalized dietary strategies. Together, this review provides a structured framework for understanding the complex interactions between yogurt, gut microbiota, and host physiology, while outlining key steps needed to translate evidence into actionable nutritional recommendations.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
Computational formulation of a broad-spectrum multi-epitope vaccine against bacterial pathogens implicated in periodontal and systemic diseases.
3 Biotech, 16(8):323.
UNLABELLED: Periodontitis is a chronic inflammatory disease driven by dysbiosis of the oral microbiome and is associated with both oral and systemic complications. Key pathogens from the red and orange complexes, along with Chlamydia pneumoniae, contribute significantly to disease progression and related systemic disorders. In this study, emerging biotechnological approaches, including immunoinformatics-driven vaccine design, were employed to develop a multi-epitope vaccine candidate (MEVC) targeting these polymicrobial infections. The MEVC was constructed using 13 B-cell epitopes, 15 cytotoxic T lymphocyte (CTL) epitopes, and 14 helper T lymphocyte (HTL) epitopes identified through experimental evidence and computational prediction. Immunostimulatory linkers and cholera toxin subunit B were incorporated as an adjuvant to enhance immunogenicity. Molecular docking demonstrated strong binding affinities between T-cell epitopes and HLA alleles. Physicochemical analysis indicated that the MEVC is stable, soluble, and exhibits a favourable half-life across biological systems. The construct ws predicted to be antigenic, non-allergenic, and host-compatible. Population coverage analysis of the selected HLA alleles indicated broad global applicability. The tertiary structure of the MEVC was modelled, refined, and docked with TLR2. HADDOCK 2.4 server yielded a binding score of - 196.2 ± 0.0, while PRODIGY predicted a binding affinity of - 13.2 kcal/mol for the MEVC-TLR2 complex. Codon optimization and in silico cloning into the pET-28(+) vector confirmed suitability for expression in Escherichia coli. Molecular dynamics simulations indicated stability of the MEVC-TLR2 complex, while immune simulations predicted strong humoral and cellular responses with sustained IgG, IFN-γ, and IL-2 production upon injection of MEVC into the host. Overall, the MEVC represents a promising therapeutic candidate warranting further experimental validation.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-026-04958-x.
Additional Links: PMID-42459414
PubMed:
Citation:
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@article {pmid42459414,
year = {2026},
author = {Khatrawi, EM},
title = {Computational formulation of a broad-spectrum multi-epitope vaccine against bacterial pathogens implicated in periodontal and systemic diseases.},
journal = {3 Biotech},
volume = {16},
number = {8},
pages = {323},
pmid = {42459414},
issn = {2190-572X},
abstract = {UNLABELLED: Periodontitis is a chronic inflammatory disease driven by dysbiosis of the oral microbiome and is associated with both oral and systemic complications. Key pathogens from the red and orange complexes, along with Chlamydia pneumoniae, contribute significantly to disease progression and related systemic disorders. In this study, emerging biotechnological approaches, including immunoinformatics-driven vaccine design, were employed to develop a multi-epitope vaccine candidate (MEVC) targeting these polymicrobial infections. The MEVC was constructed using 13 B-cell epitopes, 15 cytotoxic T lymphocyte (CTL) epitopes, and 14 helper T lymphocyte (HTL) epitopes identified through experimental evidence and computational prediction. Immunostimulatory linkers and cholera toxin subunit B were incorporated as an adjuvant to enhance immunogenicity. Molecular docking demonstrated strong binding affinities between T-cell epitopes and HLA alleles. Physicochemical analysis indicated that the MEVC is stable, soluble, and exhibits a favourable half-life across biological systems. The construct ws predicted to be antigenic, non-allergenic, and host-compatible. Population coverage analysis of the selected HLA alleles indicated broad global applicability. The tertiary structure of the MEVC was modelled, refined, and docked with TLR2. HADDOCK 2.4 server yielded a binding score of - 196.2 ± 0.0, while PRODIGY predicted a binding affinity of - 13.2 kcal/mol for the MEVC-TLR2 complex. Codon optimization and in silico cloning into the pET-28(+) vector confirmed suitability for expression in Escherichia coli. Molecular dynamics simulations indicated stability of the MEVC-TLR2 complex, while immune simulations predicted strong humoral and cellular responses with sustained IgG, IFN-γ, and IL-2 production upon injection of MEVC into the host. Overall, the MEVC represents a promising therapeutic candidate warranting further experimental validation.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-026-04958-x.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
Neighborhood-level socioeconomic disadvantage is associated with gut microbial composition and diversity across many chronic disease states.
Frontiers in public health, 14:1847540.
BACKGROUND: Socioeconomic disparities play a major role in health and disease. Growing evidence suggests that healthcare access accounts for only part of these outcomes, and additional biological mechanisms remain to be elucidated. The gut microbiome is a central component of health and disease and can be affected by environmental factors and socioeconomic disparities.
METHODS: Using a large cohort with diverse comorbidities identified in the Elixhauser comorbidity index, we tested for association between area deprivation index (ADI), a neighborhood-level measurement of socioeconomic disadvantage in the United States, and taxonomic profiles of gut microbiota (16S rRNA gene sequences) to examine the effect of (1) covariates (age, sex, and smoking), ADI, and microbiota on comorbidities and (2) covariates, ADI, and comorbidities on microbiota.
FINDINGS: Covariates explained several associations, and ADI was associated with multiple comorbidities as assessed using generalized linear models (GLMs) augmented with ADI regression splines. Most associations with ADI were nonlinear, and the associations were most frequent among individuals living in more disadvantaged neighborhoods. Multivariate analysis of variance (MANOVA) revealed a significant effect of ADI on the collective microbiota of the cohort. Individual microbial taxa were identified in association with ADI, ranging from potentially more beneficial to human health to more disease-promoting, whereas microbial diversity was negatively associated with over half of the disease associations.
INTERPRETATION: These findings indicate that ADI is associated with alterations to the gut microbiome and common disease states.
Additional Links: PMID-42459469
PubMed:
Citation:
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@article {pmid42459469,
year = {2026},
author = {Radder, JE and Li, K and Saul, M and Nouraie, M and Gentry, H and Patel, A and Kessinger, C and Fitch, A and Dunlap, DG and Kitsios, GD and Zhang, Y and Methé, BA and Morris, A},
title = {Neighborhood-level socioeconomic disadvantage is associated with gut microbial composition and diversity across many chronic disease states.},
journal = {Frontiers in public health},
volume = {14},
number = {},
pages = {1847540},
pmid = {42459469},
issn = {2296-2565},
mesh = {Humans ; Chronic Disease/epidemiology ; Socioeconomic Disparities in Health ; Female ; *Gastrointestinal Microbiome ; Male ; United States/epidemiology ; Middle Aged ; *Neighborhood Characteristics/statistics & numerical data ; Comorbidity ; Aged ; Low Socioeconomic Status ; RNA, Ribosomal, 16S ; Socioeconomic Factors ; Adult ; Cohort Studies ; },
abstract = {BACKGROUND: Socioeconomic disparities play a major role in health and disease. Growing evidence suggests that healthcare access accounts for only part of these outcomes, and additional biological mechanisms remain to be elucidated. The gut microbiome is a central component of health and disease and can be affected by environmental factors and socioeconomic disparities.
METHODS: Using a large cohort with diverse comorbidities identified in the Elixhauser comorbidity index, we tested for association between area deprivation index (ADI), a neighborhood-level measurement of socioeconomic disadvantage in the United States, and taxonomic profiles of gut microbiota (16S rRNA gene sequences) to examine the effect of (1) covariates (age, sex, and smoking), ADI, and microbiota on comorbidities and (2) covariates, ADI, and comorbidities on microbiota.
FINDINGS: Covariates explained several associations, and ADI was associated with multiple comorbidities as assessed using generalized linear models (GLMs) augmented with ADI regression splines. Most associations with ADI were nonlinear, and the associations were most frequent among individuals living in more disadvantaged neighborhoods. Multivariate analysis of variance (MANOVA) revealed a significant effect of ADI on the collective microbiota of the cohort. Individual microbial taxa were identified in association with ADI, ranging from potentially more beneficial to human health to more disease-promoting, whereas microbial diversity was negatively associated with over half of the disease associations.
INTERPRETATION: These findings indicate that ADI is associated with alterations to the gut microbiome and common disease states.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Chronic Disease/epidemiology
Socioeconomic Disparities in Health
Female
*Gastrointestinal Microbiome
Male
United States/epidemiology
Middle Aged
*Neighborhood Characteristics/statistics & numerical data
Comorbidity
Aged
Low Socioeconomic Status
RNA, Ribosomal, 16S
Socioeconomic Factors
Adult
Cohort Studies
RevDate: 2026-07-16
CmpDate: 2026-07-16
Effects of dietary Inonotus obliquus fermentation product supplementation on growth performance, immune function, blood glucose level, and gut microbiota in cats.
Frontiers in veterinary science, 13:1815007.
Inonotus obliquus is a medicinal fungus rich in bioactive compounds that has demonstrated significant efficacy in animals when supplemented in the diet. However, its effects on key health parameters in cats remain unclear. This study evaluated the effects of Inonotus obliquus fermentation product (IOFP) as a functional preparation for cats. A total of 20 weaned kittens were divided into two groups, and each group was fed a basal diet or a diet supplemented with 0.8% IOFP (w/w) for 45 days. Growth performance, fasting blood glucose levels, and relative immune indicators were determined every 15 days. Post-trial intestinal samples were subjected to gut morphology, microbiota, and metabolomic analysis. Results indicated that IOFP supplementation significantly enhanced average daily gain and feed conversion efficiency, moderately lowered blood glucose levels, improved immune indicators, and reduced inflammatory cytokines. In addition, IOFP significantly increased gut microbial diversity and altered its composition. Metabolomic changes were consistent with anti-inflammatory and antitumor effects, with increased production of short-chain fatty acids, whereas metabolites linked to toxicity and metabolic disruption decreased. Pearson correlation analysis indicated that most metabolites were regulated by various bacteria. In conclusion, dietary IOFP supplementation improved growth performance and immunity, reduced blood glucose levels, and likely alleviated inflammation, probably by modulating the gut microbiota and its metabolites in cats, supporting its potential as a novel functional preparation for cats.
Additional Links: PMID-42459542
PubMed:
Citation:
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@article {pmid42459542,
year = {2026},
author = {Zhang, L and Gao, X and Wang, J and Sun, W and Cheng, W and Lian, L and Li, Y},
title = {Effects of dietary Inonotus obliquus fermentation product supplementation on growth performance, immune function, blood glucose level, and gut microbiota in cats.},
journal = {Frontiers in veterinary science},
volume = {13},
number = {},
pages = {1815007},
pmid = {42459542},
issn = {2297-1769},
abstract = {Inonotus obliquus is a medicinal fungus rich in bioactive compounds that has demonstrated significant efficacy in animals when supplemented in the diet. However, its effects on key health parameters in cats remain unclear. This study evaluated the effects of Inonotus obliquus fermentation product (IOFP) as a functional preparation for cats. A total of 20 weaned kittens were divided into two groups, and each group was fed a basal diet or a diet supplemented with 0.8% IOFP (w/w) for 45 days. Growth performance, fasting blood glucose levels, and relative immune indicators were determined every 15 days. Post-trial intestinal samples were subjected to gut morphology, microbiota, and metabolomic analysis. Results indicated that IOFP supplementation significantly enhanced average daily gain and feed conversion efficiency, moderately lowered blood glucose levels, improved immune indicators, and reduced inflammatory cytokines. In addition, IOFP significantly increased gut microbial diversity and altered its composition. Metabolomic changes were consistent with anti-inflammatory and antitumor effects, with increased production of short-chain fatty acids, whereas metabolites linked to toxicity and metabolic disruption decreased. Pearson correlation analysis indicated that most metabolites were regulated by various bacteria. In conclusion, dietary IOFP supplementation improved growth performance and immunity, reduced blood glucose levels, and likely alleviated inflammation, probably by modulating the gut microbiota and its metabolites in cats, supporting its potential as a novel functional preparation for cats.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
Gut microbiota and gut-derived metabolites in defining multiple sclerosis phenotypic continuum.
Frontiers in immunology, 17:1858047.
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system in which environmental factors play an important role in shaping disease risk, activity, and progression. Over the past decade, human and experimental studies have consistently shown alterations in the gut microbiome across the phenotypic spectrum of MS and have linked these changes to immune dysregulation, barrier dysfunction, neuroinflammation, and demyelination. Additionally, emerging evidence indicates that microbial function, particularly metabolite production plays a more direct role in shaping immune responses and associated neuropathology. Evidence from both human studies and experimental autoimmune encephalomyelitis models supports a functional role for microbial metabolites in shaping neuroimmune responses. Bacterially derived metabolites such as short-chain fatty acids, bile acids, polyamines, phytoestrogen metabolites, and tryptophan-derived compounds can influence T-cell differentiation, glial activation, epithelial integrity, and neuroimmune communication. Recent longitudinal studies also show associations between metabolite profiles and disability worsening. Because disease-modifying therapies, diet, and microbiome-directed interventions can reshape microbial metabolism, microbial metabolites may represent promising therapeutic targets in the gut-immune-brain axis. In this Review, we integrate current evidence to propose a mechanistic framework in which microbial metabolites act as central regulators of mucosal and systemic immunity that influence different aspects of MS biology. We discuss how this perspective shifts gut microbiome research from descriptive associations to biological mechanisms that more directly link the gut to immune responses and downstream neuropathology. We then evaluate therapeutic strategies that target microbial metabolism and outline key priorities for longitudinal, multi-omics, and interventional studies that are needed to enable microbiome-informed precision therapies in MS.
Additional Links: PMID-42459649
PubMed:
Citation:
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@article {pmid42459649,
year = {2026},
author = {Montini, F and Mangalam, A and Zeydan, B and Murray, J and Kantarci, OH},
title = {Gut microbiota and gut-derived metabolites in defining multiple sclerosis phenotypic continuum.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1858047},
pmid = {42459649},
issn = {1664-3224},
mesh = {Humans ; *Multiple Sclerosis/metabolism/immunology/microbiology/etiology ; Animals ; *Gastrointestinal Microbiome/immunology ; Phenotype ; },
abstract = {Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system in which environmental factors play an important role in shaping disease risk, activity, and progression. Over the past decade, human and experimental studies have consistently shown alterations in the gut microbiome across the phenotypic spectrum of MS and have linked these changes to immune dysregulation, barrier dysfunction, neuroinflammation, and demyelination. Additionally, emerging evidence indicates that microbial function, particularly metabolite production plays a more direct role in shaping immune responses and associated neuropathology. Evidence from both human studies and experimental autoimmune encephalomyelitis models supports a functional role for microbial metabolites in shaping neuroimmune responses. Bacterially derived metabolites such as short-chain fatty acids, bile acids, polyamines, phytoestrogen metabolites, and tryptophan-derived compounds can influence T-cell differentiation, glial activation, epithelial integrity, and neuroimmune communication. Recent longitudinal studies also show associations between metabolite profiles and disability worsening. Because disease-modifying therapies, diet, and microbiome-directed interventions can reshape microbial metabolism, microbial metabolites may represent promising therapeutic targets in the gut-immune-brain axis. In this Review, we integrate current evidence to propose a mechanistic framework in which microbial metabolites act as central regulators of mucosal and systemic immunity that influence different aspects of MS biology. We discuss how this perspective shifts gut microbiome research from descriptive associations to biological mechanisms that more directly link the gut to immune responses and downstream neuropathology. We then evaluate therapeutic strategies that target microbial metabolism and outline key priorities for longitudinal, multi-omics, and interventional studies that are needed to enable microbiome-informed precision therapies in MS.},
}
MeSH Terms:
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Humans
*Multiple Sclerosis/metabolism/immunology/microbiology/etiology
Animals
*Gastrointestinal Microbiome/immunology
Phenotype
RevDate: 2026-07-16
CmpDate: 2026-07-16
Duodenal dysbiosis is linked to altered ferroportin related transcriptomics programs in iron deficiency anemia.
Frontiers in nutrition, 13:1836940.
BACKGROUND & AIMS: Iron deficiency anemia (IDA) affects over two billion people, yet up to half of patients show inadequate response to oral iron therapy. We hypothesized that IDA is a primary duodenal mucosal disorder where dysbiosis and immune polarization converge to impair enterocyte iron export. This study integrates mucosal-associated microbiome and transcriptomic profiling to elucidate mechanisms underlying impaired iron handling.
METHODS: Duodenal biopsies from women with IDA (n = 11) and matched controls (n = 9) underwent paired 16S rRNA and RNA-Seq. A Microbial Redox Index (MRI) quantified oxygen-tolerant taxa. Multilayer network modeling linked microbial hubs to epithelial transcriptional remodeling in iron-handling, inflammatory, and barrier-integrity pathways.
RESULTS: IDA subjects demonstrated expected hematological deficits (hemoglobin 10.02 ± 0.82 vs. 12.69 ± 0.67 g/dL; ferritin 10.7 [8.2-35.3] vs. 49.7 [28.4-58.7] ng/mL; P < 0.05). Although the overall ratio of oxygen-tolerant to anaerobic taxa was comparable between groups (P = 0.44), IDA was marked by a collapse of homeostatic ecological control. In controls, Group V a/V b anaerobes showed a strong inverse correlation with Shannon diversity (P = 0.009), indicating a stable, niche-restricting anaerobic core. This relationship was lost in IDA, where both oxygen-tolerant and anaerobic taxa displayed positive correlations with Th17 skewed inflammation (IL17A log2FC = +3.59), hypoxic stress (EGLN3 log2FC = +1.31), and sensitized BMP signaling (BMPR2 log2FC = +0.50). These transcriptomic signatures could reflect a functional ferroportin blockade, as reflected by SLC40A1 mRNA upregulation (log2FC = +1.02) concurrent with a proposed model of post translational ferroportin suppression, despite profound cellular iron starvation (TFRC log2FC = +1.58; SLC11A2 log2FC = +2.2). Together, these features are consistent with a possible enterocyte iron retention phenotype. The lncRNA LOC124902620 emerged as a central regulatory hub linking dysbiosis to iron-handling genes.
CONCLUSIONS: IDA is a duodenal mucosal disorder where dysbiosis-driven redox shifts and immune activation could support a model of hepcidin associated ferroportin downregulation. This is consistent with a proposed enterocyte iron retention phenotype. Microbial hubs and the LOC124902620 axis are promising targets for precision interventions to restore mucosal iron export.
Additional Links: PMID-42459794
PubMed:
Citation:
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@article {pmid42459794,
year = {2026},
author = {Agrawal, S and Dash, R and Jumin, P and Samal, SC and Mishra, S and Raghav, SK and Ramakrishna, BS and Ramadass, B},
title = {Duodenal dysbiosis is linked to altered ferroportin related transcriptomics programs in iron deficiency anemia.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1836940},
pmid = {42459794},
issn = {2296-861X},
abstract = {BACKGROUND & AIMS: Iron deficiency anemia (IDA) affects over two billion people, yet up to half of patients show inadequate response to oral iron therapy. We hypothesized that IDA is a primary duodenal mucosal disorder where dysbiosis and immune polarization converge to impair enterocyte iron export. This study integrates mucosal-associated microbiome and transcriptomic profiling to elucidate mechanisms underlying impaired iron handling.
METHODS: Duodenal biopsies from women with IDA (n = 11) and matched controls (n = 9) underwent paired 16S rRNA and RNA-Seq. A Microbial Redox Index (MRI) quantified oxygen-tolerant taxa. Multilayer network modeling linked microbial hubs to epithelial transcriptional remodeling in iron-handling, inflammatory, and barrier-integrity pathways.
RESULTS: IDA subjects demonstrated expected hematological deficits (hemoglobin 10.02 ± 0.82 vs. 12.69 ± 0.67 g/dL; ferritin 10.7 [8.2-35.3] vs. 49.7 [28.4-58.7] ng/mL; P < 0.05). Although the overall ratio of oxygen-tolerant to anaerobic taxa was comparable between groups (P = 0.44), IDA was marked by a collapse of homeostatic ecological control. In controls, Group V a/V b anaerobes showed a strong inverse correlation with Shannon diversity (P = 0.009), indicating a stable, niche-restricting anaerobic core. This relationship was lost in IDA, where both oxygen-tolerant and anaerobic taxa displayed positive correlations with Th17 skewed inflammation (IL17A log2FC = +3.59), hypoxic stress (EGLN3 log2FC = +1.31), and sensitized BMP signaling (BMPR2 log2FC = +0.50). These transcriptomic signatures could reflect a functional ferroportin blockade, as reflected by SLC40A1 mRNA upregulation (log2FC = +1.02) concurrent with a proposed model of post translational ferroportin suppression, despite profound cellular iron starvation (TFRC log2FC = +1.58; SLC11A2 log2FC = +2.2). Together, these features are consistent with a possible enterocyte iron retention phenotype. The lncRNA LOC124902620 emerged as a central regulatory hub linking dysbiosis to iron-handling genes.
CONCLUSIONS: IDA is a duodenal mucosal disorder where dysbiosis-driven redox shifts and immune activation could support a model of hepcidin associated ferroportin downregulation. This is consistent with a proposed enterocyte iron retention phenotype. Microbial hubs and the LOC124902620 axis are promising targets for precision interventions to restore mucosal iron export.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
Lentinan alleviates metabolic dysfunction implicating Parabacteroides goldsteinii-enriched gut microbiota and hepatic lipid metabolism reprogramming through gut-liver axis-associated mechanisms.
Frontiers in nutrition, 13:1841358.
Metabolic disorders represent a global health challenge requiring novel therapeutic strategies targeting the gut-liver axis. This study investigates the protective effects and mechanisms of lentinan, a bioactive polysaccharide from Lentinus edodes, against high-fat diet (HFD)-induced metabolic dysfunction. HFD-fed mice were treated with lentinan. Comprehensive phenotypic assessments, metagenome sequencing, hepatic transcriptomics, and correlation analyses were performed to elucidate mechanisms. Lentinan intervention significantly ameliorated dyslipidemia, hepatic steatosis, systemic inflammation, and intestinal barrier dysfunction in HFD-fed mice. Mechanistically, lentinan induced taxonomically selective gut microbiota remodeling, characterized by substantial enrichment of Parabacteroides goldsteinii (positively correlated with hepatic Plppr3 expression) and reduction of Romboutsia ilealis (negatively correlated with Dgkh and Nfat5), while paradoxically decreasing Akkermansia muciniphila despite metabolic improvements. Hepatic transcriptomics revealed significant downregulation of glycerolipid metabolism and oxidative phosphorylation pathways, directly correlating with reduced lipid accumulation and improved serum biochemistry. Unlike conventional prebiotics, lentinan functions as a precision modulator of specific microbial metabolic functions, particularly L-arginine and uridine 5'-monophosphate (UMP) biosynthesis pathways, which interface with host inflammatory and lipid metabolism. These findings establish lentinan as a promising therapeutic candidate for metabolic syndrome management through coordinated gut microbiota-liver axis modulation, providing a conceptual framework for developing precision microbiome-targeted interventions.
Additional Links: PMID-42459798
PubMed:
Citation:
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@article {pmid42459798,
year = {2026},
author = {Cao, D and Huang, L and Zhang, X and Zhang, X and Zhao, Z and Long, X and Zhu, X and Li, Y},
title = {Lentinan alleviates metabolic dysfunction implicating Parabacteroides goldsteinii-enriched gut microbiota and hepatic lipid metabolism reprogramming through gut-liver axis-associated mechanisms.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1841358},
pmid = {42459798},
issn = {2296-861X},
abstract = {Metabolic disorders represent a global health challenge requiring novel therapeutic strategies targeting the gut-liver axis. This study investigates the protective effects and mechanisms of lentinan, a bioactive polysaccharide from Lentinus edodes, against high-fat diet (HFD)-induced metabolic dysfunction. HFD-fed mice were treated with lentinan. Comprehensive phenotypic assessments, metagenome sequencing, hepatic transcriptomics, and correlation analyses were performed to elucidate mechanisms. Lentinan intervention significantly ameliorated dyslipidemia, hepatic steatosis, systemic inflammation, and intestinal barrier dysfunction in HFD-fed mice. Mechanistically, lentinan induced taxonomically selective gut microbiota remodeling, characterized by substantial enrichment of Parabacteroides goldsteinii (positively correlated with hepatic Plppr3 expression) and reduction of Romboutsia ilealis (negatively correlated with Dgkh and Nfat5), while paradoxically decreasing Akkermansia muciniphila despite metabolic improvements. Hepatic transcriptomics revealed significant downregulation of glycerolipid metabolism and oxidative phosphorylation pathways, directly correlating with reduced lipid accumulation and improved serum biochemistry. Unlike conventional prebiotics, lentinan functions as a precision modulator of specific microbial metabolic functions, particularly L-arginine and uridine 5'-monophosphate (UMP) biosynthesis pathways, which interface with host inflammatory and lipid metabolism. These findings establish lentinan as a promising therapeutic candidate for metabolic syndrome management through coordinated gut microbiota-liver axis modulation, providing a conceptual framework for developing precision microbiome-targeted interventions.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
The effects of 12-weeks resveratrol supplementation on cognition, gastrointestinal microbiota, and systemic inflammation, in an overweight and obese human population: a randomized, double-blind, placebo controlled, parallel groups trial.
Frontiers in nutrition, 13:1839709.
BACKGROUND: Resveratrol appears to offer greater cognitive benefit to compromised models, such as in type II diabetes mellitus, menopause, and high body mass index (BMI), relative to healthy cohorts. With regards high BMI, hypertension, insulin resistance, oxidative stress, and inflammation have been posited as mechanisms underpinning cognitive decrements, and recent advancements in gut-brain-axis research have linked high BMI with inflammation via gut dysbiosis. Polyphenols have been evidenced to act prebiotically in the gut, to mediate anti-inflammatory effects in animal models, and this presents a mechanism by which resveratrol could bolster cognition in high BMI individuals.
AIMS: The current study investigates whether resveratrol can confer cognitive benefit to individuals with a high BMI, and whether these effects coincide with changes in the gut microbiome, urinary metabolome and biological markers of adiposity (anthropomorphic and blood biomarkers) and inflammation/oxidation.
METHODS: N = 99 male and females (35-60 years, mean age 47.51 years), with a BMI between 25 and 42 kg/m[2], received either 500 mg Veri-te™ resveratrol, or placebo, daily for 12 weeks. This supplementation period was bookended by visits to the laboratory for urine, blood, and stool sampling, and cognitive testing, which was assessed pre-and post-dose during both the acute and chronic testing visit.
RESULTS: Participants in the placebo control group presented with existing differences on cognitive outcomes at baseline, which makes interpretation of apparent improvements in this group relative to resveratrol, problematic. No significant differences were observed within or between groups on any microbiome, urinary metabolome, biological markers of adiposity or inflammation/oxidation markers.
CONCLUSION: The absence of effects on the underlying biological mechanisms rationalized to underpin cognitive improvements in high BMI individuals likely explains the null results in the resveratrol intervention group. Effects attributed to the placebo control condition are explained as the persistence of pre-existing effects in this group of participants, and this may underlie the need to factor pre-enrolment aptitude into randomization in nutritional intervention trials. The lack of change in the gut microbiome of a healthy human cohort, following 12 weeks of resveratrol supplementation, is a positive indication, showing no deleterious disruption within this environment. Future studies may wish to investigate these effects in those with a disrupted gut microbiome.
CLINICAL TRIAL REGISTRATION: The study was pre-registered on clinicaltrials.gov (identifier: NCT03448094).
Additional Links: PMID-42459802
PubMed:
Citation:
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@article {pmid42459802,
year = {2026},
author = {Wightman, E and Lodge, J and Kennedy, D and Bowerbank, S and Cheung, W and Cuthbertson, L and Nelson, A and Smith, D},
title = {The effects of 12-weeks resveratrol supplementation on cognition, gastrointestinal microbiota, and systemic inflammation, in an overweight and obese human population: a randomized, double-blind, placebo controlled, parallel groups trial.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1839709},
pmid = {42459802},
issn = {2296-861X},
abstract = {BACKGROUND: Resveratrol appears to offer greater cognitive benefit to compromised models, such as in type II diabetes mellitus, menopause, and high body mass index (BMI), relative to healthy cohorts. With regards high BMI, hypertension, insulin resistance, oxidative stress, and inflammation have been posited as mechanisms underpinning cognitive decrements, and recent advancements in gut-brain-axis research have linked high BMI with inflammation via gut dysbiosis. Polyphenols have been evidenced to act prebiotically in the gut, to mediate anti-inflammatory effects in animal models, and this presents a mechanism by which resveratrol could bolster cognition in high BMI individuals.
AIMS: The current study investigates whether resveratrol can confer cognitive benefit to individuals with a high BMI, and whether these effects coincide with changes in the gut microbiome, urinary metabolome and biological markers of adiposity (anthropomorphic and blood biomarkers) and inflammation/oxidation.
METHODS: N = 99 male and females (35-60 years, mean age 47.51 years), with a BMI between 25 and 42 kg/m[2], received either 500 mg Veri-te™ resveratrol, or placebo, daily for 12 weeks. This supplementation period was bookended by visits to the laboratory for urine, blood, and stool sampling, and cognitive testing, which was assessed pre-and post-dose during both the acute and chronic testing visit.
RESULTS: Participants in the placebo control group presented with existing differences on cognitive outcomes at baseline, which makes interpretation of apparent improvements in this group relative to resveratrol, problematic. No significant differences were observed within or between groups on any microbiome, urinary metabolome, biological markers of adiposity or inflammation/oxidation markers.
CONCLUSION: The absence of effects on the underlying biological mechanisms rationalized to underpin cognitive improvements in high BMI individuals likely explains the null results in the resveratrol intervention group. Effects attributed to the placebo control condition are explained as the persistence of pre-existing effects in this group of participants, and this may underlie the need to factor pre-enrolment aptitude into randomization in nutritional intervention trials. The lack of change in the gut microbiome of a healthy human cohort, following 12 weeks of resveratrol supplementation, is a positive indication, showing no deleterious disruption within this environment. Future studies may wish to investigate these effects in those with a disrupted gut microbiome.
CLINICAL TRIAL REGISTRATION: The study was pre-registered on clinicaltrials.gov (identifier: NCT03448094).},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
Partial enteral nutrition combined with an exclusion diet promotes a healthy gut microbiome in patients with mild to moderately active ulcerative colitis: a quasi-experimental study.
Crohn's & colitis 360, 8(3):otag068.
BACKGROUND AND AIMS: The therapeutic role of enteral nutrition and diet in patients with ulcerative colitis (UC) has not been adequately explored. We aimed to evaluate the effectiveness of partial enteral nutrition (PEN) in combination with an exclusion diet (ED) in patients with UC.
METHODS: In this prospective, open-label, non-randomized, quasi-experimental study, patients with mild-to-moderate UC (simple clinical colitis activity index [SCCAI]3-9) were non-randomly allocated to either PEN+ED along with standard of care (SOC) or SOC alone for 4 weeks. The primary outcome was clinical remission (SCCAI ≤2) at week 4. In addition, fecal microbiota analysis was performed at baseline and at week 4 for 14 participants in the PEN+ED group.
RESULTS: Sixty patients were included (PEN+ED = 30; SOC = 30). Baseline disease activity parameters were similar between the two groups. At week 4, 66.7% (20/30) of patients in the PEN+ED arm achieved clinical remission compared to 83.3% (25/30) receiving SOC. The proportion of patients with rectal bleeding score "0" was significantly lower in PEN+ED (56.7% vs 86.7%, P = .01) arm at week 4. A numerically higher number of patients required steroids in SOC arm compared to the PEN+ED arm, but it was not significant (23.3% vs 16.7%, P = .748). Microbiome analysis showed significant improvements in alpha diversity, increased relative abundance of beneficial gut microbes, depletion of pathobionts, and shift toward a healthier microbial profile, which was in turn shown to be negatively associated with disease severity.
CONCLUSIONS: Although PEN+ED does not appear to have additional clinical benefit to SOC at week 4, it was associated with significant improvement in gut microbiota. Long-term benefits of dietary interventions should be explored in future studies.
ISRCTN15559229.
Additional Links: PMID-42459866
PubMed:
Citation:
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@article {pmid42459866,
year = {2026},
author = {Vuyyuru, SK and Madan, D and Goswami, S and Kante, B and Shete, O and Kumar, P and Ranjan, MK and Mundhra, S and Golla, R and Narang, H and Monga, N and Singh, N and Makharia, G and Ghosh, TS and Kedia, S and Ahuja, V},
title = {Partial enteral nutrition combined with an exclusion diet promotes a healthy gut microbiome in patients with mild to moderately active ulcerative colitis: a quasi-experimental study.},
journal = {Crohn's & colitis 360},
volume = {8},
number = {3},
pages = {otag068},
pmid = {42459866},
issn = {2631-827X},
abstract = {BACKGROUND AND AIMS: The therapeutic role of enteral nutrition and diet in patients with ulcerative colitis (UC) has not been adequately explored. We aimed to evaluate the effectiveness of partial enteral nutrition (PEN) in combination with an exclusion diet (ED) in patients with UC.
METHODS: In this prospective, open-label, non-randomized, quasi-experimental study, patients with mild-to-moderate UC (simple clinical colitis activity index [SCCAI]3-9) were non-randomly allocated to either PEN+ED along with standard of care (SOC) or SOC alone for 4 weeks. The primary outcome was clinical remission (SCCAI ≤2) at week 4. In addition, fecal microbiota analysis was performed at baseline and at week 4 for 14 participants in the PEN+ED group.
RESULTS: Sixty patients were included (PEN+ED = 30; SOC = 30). Baseline disease activity parameters were similar between the two groups. At week 4, 66.7% (20/30) of patients in the PEN+ED arm achieved clinical remission compared to 83.3% (25/30) receiving SOC. The proportion of patients with rectal bleeding score "0" was significantly lower in PEN+ED (56.7% vs 86.7%, P = .01) arm at week 4. A numerically higher number of patients required steroids in SOC arm compared to the PEN+ED arm, but it was not significant (23.3% vs 16.7%, P = .748). Microbiome analysis showed significant improvements in alpha diversity, increased relative abundance of beneficial gut microbes, depletion of pathobionts, and shift toward a healthier microbial profile, which was in turn shown to be negatively associated with disease severity.
CONCLUSIONS: Although PEN+ED does not appear to have additional clinical benefit to SOC at week 4, it was associated with significant improvement in gut microbiota. Long-term benefits of dietary interventions should be explored in future studies.
ISRCTN15559229.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
Next-generation soil monitoring: linking metagenomics, biosensors, and ecological modeling for sustainable agriculture.
Frontiers in microbiology, 17:1861333.
Soils represent one of the most complex and dynamic biological systems on Earth, where microbial communities play a central role in regulating ecosystem functions, including nutrient cycling, carbon sequestration, and plant productivity. However, increasing pressures from land-use intensification and climate change threaten soil health and biodiversity, highlighting the need for innovative monitoring and management approaches. In this review, we synthesize current advances in soil microbial ecology, sustainable soil management, environmental sensing technologies, and metagenomics to propose an integrative framework for soil monitoring and prediction. This review integrates environmental sensing, microbiome characterization, ecological modeling, and AI-based analytics into a unified framework for next-generation predictive soil monitoring systems. We discuss how high-resolution environmental sensors enable real-time characterization of soil physicochemical dynamics, while metagenomic approaches provide unprecedented insights into the taxonomic and functional diversity of soil microbiomes. Furthermore, we explore the role of microbial network analysis and ecological modeling in uncovering interaction patterns and predicting ecosystem responses to environmental change. The integration of these tools through machine learning and data-driven approaches is transforming soil science from a descriptive to a predictive discipline. We also address key challenges, including data standardization, scalability, and the interpretation of complex biological datasets. Finally, we highlight emerging directions such as microbiome-informed precision agriculture, microbiome engineering, and the development of soil digital twins. Together, these advances pave the way toward sustainable soil management strategies that enhance ecosystem resilience and agricultural productivity in the face of global change.
Additional Links: PMID-42459877
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42459877,
year = {2026},
author = {Romero-Arguelles, R and Ruiz-Ayma, G and Rodriguez-Castro, VA and Gonzalez-Rojas, JI and Gomez-Govea, MA},
title = {Next-generation soil monitoring: linking metagenomics, biosensors, and ecological modeling for sustainable agriculture.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1861333},
pmid = {42459877},
issn = {1664-302X},
abstract = {Soils represent one of the most complex and dynamic biological systems on Earth, where microbial communities play a central role in regulating ecosystem functions, including nutrient cycling, carbon sequestration, and plant productivity. However, increasing pressures from land-use intensification and climate change threaten soil health and biodiversity, highlighting the need for innovative monitoring and management approaches. In this review, we synthesize current advances in soil microbial ecology, sustainable soil management, environmental sensing technologies, and metagenomics to propose an integrative framework for soil monitoring and prediction. This review integrates environmental sensing, microbiome characterization, ecological modeling, and AI-based analytics into a unified framework for next-generation predictive soil monitoring systems. We discuss how high-resolution environmental sensors enable real-time characterization of soil physicochemical dynamics, while metagenomic approaches provide unprecedented insights into the taxonomic and functional diversity of soil microbiomes. Furthermore, we explore the role of microbial network analysis and ecological modeling in uncovering interaction patterns and predicting ecosystem responses to environmental change. The integration of these tools through machine learning and data-driven approaches is transforming soil science from a descriptive to a predictive discipline. We also address key challenges, including data standardization, scalability, and the interpretation of complex biological datasets. Finally, we highlight emerging directions such as microbiome-informed precision agriculture, microbiome engineering, and the development of soil digital twins. Together, these advances pave the way toward sustainable soil management strategies that enhance ecosystem resilience and agricultural productivity in the face of global change.},
}
RevDate: 2026-07-16
CmpDate: 2026-07-16
Transcutaneous auricular vagus nerve stimulation improves depressive-like behaviors in CUMS rats through regulation of gut microbiome, serum metabolites, and immune factors.
Frontiers in microbiology, 17:1820578.
BACKGROUND: Depression is associated with microbiota-gut-brain (MGB) axis dysregulation. Transcutaneous auricular vagus nerve stimulation (taVNS) has shown antidepressant effects and modulated gut microbiota, but its potential to alleviate depression specifically via modulation of the MGB axis remains largely unexplored.
METHODS: Rats subjected to chronic unpredictable mild stress (CUMS) received taVNS for 3 weeks. We assessed depressive-like behaviors, gut microbiota, plasma metabolism, and inflammatory marker levels. Pearson correlation analyses examined relationships among these factors.
RESULTS: taVNS significantly improved depressive behaviors in CUMS rats. It shifted gut microbiota composition, enriching beneficial Lactobacillus murinus, Bifidobacterium animalis, and Prevotellaceae while reducing harmful Bacteroidales and Romboutsia. Metabolomics revealed taVNS modulated plasma metabolism, especially metabolism of cofactor/vitamin, sphingolipid metabolism, amino and organic acid metabolism, increasing the levels of indole-3-lactic acid (ILA), riboflavin, sphingosine-1-phosphate (S1P), sphinganine-1-phosphate (Sa1P) and sphingosine (SP), and creatine. taVNS also reduced blood, hippocampus and prefrontal cortex inflammation. Pearson correlation analysis showed that alleviation of depressive behaviors positively correlated with Lactobacillus murinus, Bifidobacterium animalis, and plasma ILA, riboflavin, S1P, Sa1P, SP, and creatine and all these parameters inversely associated with pro-inflammatory factors.
CONCLUSION: These findings indicate that taVNS may alleviate depression by enriching Lactobacillus murinus and Bifidobacterium animalis to enhance biosynthesis of microbiota-derived metabolites (ILA, riboflavin) and modulate host plasma metabolites (S1P, Sa1P, SP, creatine), thereby attenuating systemic and neuroinflammatory processes.
Additional Links: PMID-42459878
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42459878,
year = {2026},
author = {Tan, C and Qiao, M and Ma, Y and Wang, X and Xing, M and Sun, S and Shi, Y and Wang, Y and Fang, J and Yang, Y},
title = {Transcutaneous auricular vagus nerve stimulation improves depressive-like behaviors in CUMS rats through regulation of gut microbiome, serum metabolites, and immune factors.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1820578},
pmid = {42459878},
issn = {1664-302X},
abstract = {BACKGROUND: Depression is associated with microbiota-gut-brain (MGB) axis dysregulation. Transcutaneous auricular vagus nerve stimulation (taVNS) has shown antidepressant effects and modulated gut microbiota, but its potential to alleviate depression specifically via modulation of the MGB axis remains largely unexplored.
METHODS: Rats subjected to chronic unpredictable mild stress (CUMS) received taVNS for 3 weeks. We assessed depressive-like behaviors, gut microbiota, plasma metabolism, and inflammatory marker levels. Pearson correlation analyses examined relationships among these factors.
RESULTS: taVNS significantly improved depressive behaviors in CUMS rats. It shifted gut microbiota composition, enriching beneficial Lactobacillus murinus, Bifidobacterium animalis, and Prevotellaceae while reducing harmful Bacteroidales and Romboutsia. Metabolomics revealed taVNS modulated plasma metabolism, especially metabolism of cofactor/vitamin, sphingolipid metabolism, amino and organic acid metabolism, increasing the levels of indole-3-lactic acid (ILA), riboflavin, sphingosine-1-phosphate (S1P), sphinganine-1-phosphate (Sa1P) and sphingosine (SP), and creatine. taVNS also reduced blood, hippocampus and prefrontal cortex inflammation. Pearson correlation analysis showed that alleviation of depressive behaviors positively correlated with Lactobacillus murinus, Bifidobacterium animalis, and plasma ILA, riboflavin, S1P, Sa1P, SP, and creatine and all these parameters inversely associated with pro-inflammatory factors.
CONCLUSION: These findings indicate that taVNS may alleviate depression by enriching Lactobacillus murinus and Bifidobacterium animalis to enhance biosynthesis of microbiota-derived metabolites (ILA, riboflavin) and modulate host plasma metabolites (S1P, Sa1P, SP, creatine), thereby attenuating systemic and neuroinflammatory processes.},
}
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ESP Quick Facts
ESP Origins
In the early 1990's, Robert Robbins was a faculty member at Johns Hopkins, where he directed the informatics core of GDB — the human gene-mapping database of the international human genome project. To share papers with colleagues around the world, he set up a small paper-sharing section on his personal web page. This small project evolved into The Electronic Scholarly Publishing Project.
ESP Support
In 1995, Robbins became the VP/IT of the Fred Hutchinson Cancer Research Center in Seattle, WA. Soon after arriving in Seattle, Robbins secured funding, through the ELSI component of the US Human Genome Project, to create the original ESP.ORG web site, with the formal goal of providing free, world-wide access to the literature of classical genetics.
ESP Rationale
Although the methods of molecular biology can seem almost magical to the uninitiated, the original techniques of classical genetics are readily appreciated by one and all: cross individuals that differ in some inherited trait, collect all of the progeny, score their attributes, and propose mechanisms to explain the patterns of inheritance observed.
ESP Goal
In reading the early works of classical genetics, one is drawn, almost inexorably, into ever more complex models, until molecular explanations begin to seem both necessary and natural. At that point, the tools for understanding genome research are at hand. Assisting readers reach this point was the original goal of The Electronic Scholarly Publishing Project.
ESP Usage
Usage of the site grew rapidly and has remained high. Faculty began to use the site for their assigned readings. Other on-line publishers, ranging from The New York Times to Nature referenced ESP materials in their own publications. Nobel laureates (e.g., Joshua Lederberg) regularly used the site and even wrote to suggest changes and improvements.
ESP Content
When the site began, no journals were making their early content available in digital format. As a result, ESP was obliged to digitize classic literature before it could be made available. For many important papers — such as Mendel's original paper or the first genetic map — ESP had to produce entirely new typeset versions of the works, if they were to be available in a high-quality format.
ESP Help
Early support from the DOE component of the Human Genome Project was critically important for getting the ESP project on a firm foundation. Since that funding ended (nearly 20 years ago), the project has been operated as a purely volunteer effort. Anyone wishing to assist in these efforts should send an email to Robbins.
ESP Plans
With the development of methods for adding typeset side notes to PDF files, the ESP project now plans to add annotated versions of some classical papers to its holdings. We also plan to add new reference and pedagogical material. We have already started providing regularly updated, comprehensive bibliographies to the ESP.ORG site.
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Dinosaur tail, complete with feathers, found preserved in amber.
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Mysterious fast radio burst (FRB) detected in the distant universe.
Big Data & Informatics
Big Data: Buzzword or Big Deal?
Hacking the genome: Identifying anonymized human subjects using publicly available data.