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ESP: PubMed Auto Bibliography 01 Aug 2026 at 01:56 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: 2026-07-31
Correspondence to editorial on "Bacteroides eggerthii ameliorates metabolic dysfunction-associated steatotic liver disease through host-microbe signaling and highlights 2-hydroxyisocaproate as a potential effector".
Clinical and molecular hepatology, 32(3):e361-e364.
Additional Links: PMID-41430052
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@article {pmid41430052,
year = {2026},
author = {Kim, SS and Cheong, JY and Eun, JW},
title = {Correspondence to editorial on "Bacteroides eggerthii ameliorates metabolic dysfunction-associated steatotic liver disease through host-microbe signaling and highlights 2-hydroxyisocaproate as a potential effector".},
journal = {Clinical and molecular hepatology},
volume = {32},
number = {3},
pages = {e361-e364},
doi = {10.3350/cmh.2025.1416},
pmid = {41430052},
issn = {2287-285X},
support = {//Korea Health Industry Development Institute/ ; HR21C1003//Ministry of Health and Welfare/ ; RS-2022-NR070489//Ministry of Science and ICT/ ; RS-2024-00422549//Ministry of Science and ICT/ ; RS-2025-00521818//Ministry of Science and ICT/ ; RS-2025-00562556//Ministry of Science and ICT/ ; },
}
RevDate: 2026-07-30
Gut microbiome associations in male reproductive endocrine-skeletal physiology: a taxonomic-resolution Mendelian randomization study.
Molecular and cellular endocrinology pii:S0303-7207(26)00155-3 [Epub ahead of print].
The gut microbiome is increasingly linked to endocrine physiology, but human evidence that individual microbial traits contribute to male reproductive and skeletal phenotypes remains largely observational. We integrated MiBioGen genus-level and Dutch Microbiome Project species-level microbiome genome-wide association studies with sex-stratified steroid traits, sex hormone-binding globulin (SHBG), and heel estimated bone mineral density (eBMD) in a two-sample Mendelian randomization (MR) screen of 1,204 microbe-outcome tests. The leading male endocrine association linked genetically proxied abundance of the MiBioGen-defined Eubacterium rectale group to greater odds of detectable male estradiol (odds ratio = 1.36; 95% CI, 1.12-1.65; P = 0.00246; eight instruments). This binary endpoint denotes assay detectability above 175 pmol/L, not circulating estradiol concentration. Independent GTEx V10/SuSiE fine-mapping of CYP19A1 expression in subcutaneous adipose provided aromatase-relevant tissue context but did not localize or mediate the microbial association. Complementary associations linked Roseburia hominis with SHBG and Alistipes finegoldii with heel eBMD; the latter was the only study-wide Bonferroni-significant result (P = 6.55 × 10[-8]). A Bifidobacterium longum-female testosterone association attenuated after exclusion of the LCT/MCM6 region, indicating substantial host-diet genetic influence. Across 172 matched genus-species pairs, effect estimates showed little correlation, directional agreement was no better than chance, and no pair shared clumped instruments. These findings nominate the E. rectale group for targeted male endocrine follow-up and show that taxonomic resolution is part of the exposure definition in microbiome MR.
Additional Links: PMID-42532253
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@article {pmid42532253,
year = {2026},
author = {Ha, GD and Li, Y and Liu, Q and Shi, H and Zhang, Z and Tian, Z and Wang, Y and Bian, X and Wan, G and Meng, Y and Huang, M and Sankoh, MA and Qiu, T and Li, J and Li, H and Ge, H and Wei, J and Ma, J and Tang, Q and Wu, W},
title = {Gut microbiome associations in male reproductive endocrine-skeletal physiology: a taxonomic-resolution Mendelian randomization study.},
journal = {Molecular and cellular endocrinology},
volume = {},
number = {},
pages = {112878},
doi = {10.1016/j.mce.2026.112878},
pmid = {42532253},
issn = {1872-8057},
abstract = {The gut microbiome is increasingly linked to endocrine physiology, but human evidence that individual microbial traits contribute to male reproductive and skeletal phenotypes remains largely observational. We integrated MiBioGen genus-level and Dutch Microbiome Project species-level microbiome genome-wide association studies with sex-stratified steroid traits, sex hormone-binding globulin (SHBG), and heel estimated bone mineral density (eBMD) in a two-sample Mendelian randomization (MR) screen of 1,204 microbe-outcome tests. The leading male endocrine association linked genetically proxied abundance of the MiBioGen-defined Eubacterium rectale group to greater odds of detectable male estradiol (odds ratio = 1.36; 95% CI, 1.12-1.65; P = 0.00246; eight instruments). This binary endpoint denotes assay detectability above 175 pmol/L, not circulating estradiol concentration. Independent GTEx V10/SuSiE fine-mapping of CYP19A1 expression in subcutaneous adipose provided aromatase-relevant tissue context but did not localize or mediate the microbial association. Complementary associations linked Roseburia hominis with SHBG and Alistipes finegoldii with heel eBMD; the latter was the only study-wide Bonferroni-significant result (P = 6.55 × 10[-8]). A Bifidobacterium longum-female testosterone association attenuated after exclusion of the LCT/MCM6 region, indicating substantial host-diet genetic influence. Across 172 matched genus-species pairs, effect estimates showed little correlation, directional agreement was no better than chance, and no pair shared clumped instruments. These findings nominate the E. rectale group for targeted male endocrine follow-up and show that taxonomic resolution is part of the exposure definition in microbiome MR.},
}
RevDate: 2026-07-30
The Microbiota-Gut-Brain Axis in Neuropsychiatric Disorders: Mechanisms, Advances, and Clinical Applications.
Brain research bulletin pii:S0361-9230(26)00349-7 [Epub ahead of print].
Neuropsychiatric disorders are increasingly recognized as systemic conditions arising from dynamic interactions within the gut-brain-immune network. The Microbiota-Gut-Brain Axis (MGBA) serves as a central regulatory system orchestrating neurodevelopment, neural homeostasis, and immune-metabolic balance. This review summarizes evidence across seven major neuropsychiatric disorders, Depression, Autism Spectrum Disorder, Attention-Deficit/Hyperactivity Disorder, Alzheimer's disease, Schizophrenia, Anxiety and Obsessive Compulsive Disorder, demonstrating that dysregulation of the MGBA constitutes a shared pathological mechanism. On this common basis, we delineate disorder specific neurochemical and immunological features and highlight the clinical potential of microbiota-targeted interventions. Moreover, psychotropic medications profoundly alter microbial physiology, influencing bacterial growth and metabolism, thereby complicating interpretation of MGBA-disease relationships. Future research should define strain-specific therapeutic actions and integrate multi-omics approaches to unravel causal pathways, ultimately enabling precision microbiome modulation in neuropsychiatric medicine.
Additional Links: PMID-42532353
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@article {pmid42532353,
year = {2026},
author = {Li, T and Chang, Y and Tang, S and Chen, Y and Li, X and Wang, Y},
title = {The Microbiota-Gut-Brain Axis in Neuropsychiatric Disorders: Mechanisms, Advances, and Clinical Applications.},
journal = {Brain research bulletin},
volume = {},
number = {},
pages = {112062},
doi = {10.1016/j.brainresbull.2026.112062},
pmid = {42532353},
issn = {1873-2747},
abstract = {Neuropsychiatric disorders are increasingly recognized as systemic conditions arising from dynamic interactions within the gut-brain-immune network. The Microbiota-Gut-Brain Axis (MGBA) serves as a central regulatory system orchestrating neurodevelopment, neural homeostasis, and immune-metabolic balance. This review summarizes evidence across seven major neuropsychiatric disorders, Depression, Autism Spectrum Disorder, Attention-Deficit/Hyperactivity Disorder, Alzheimer's disease, Schizophrenia, Anxiety and Obsessive Compulsive Disorder, demonstrating that dysregulation of the MGBA constitutes a shared pathological mechanism. On this common basis, we delineate disorder specific neurochemical and immunological features and highlight the clinical potential of microbiota-targeted interventions. Moreover, psychotropic medications profoundly alter microbial physiology, influencing bacterial growth and metabolism, thereby complicating interpretation of MGBA-disease relationships. Future research should define strain-specific therapeutic actions and integrate multi-omics approaches to unravel causal pathways, ultimately enabling precision microbiome modulation in neuropsychiatric medicine.},
}
RevDate: 2026-07-30
[Research progress on the bidirectional relationship between oral infectious diseases and mental health issues].
Zhonghua kou qiang yi xue za zhi = Zhonghua kouqiang yixue zazhi = Chinese journal of stomatology, 61(8):1243-1250 [Epub ahead of print].
Infectious oral diseases represent the most prevalent categories of oral conditions, including dental caries, periodontitis, periapical lesions, and pericoronitis. Their bidirectional relationship with mental health has emerged as a critical interdisciplinary research frontier. This paper integrates epidemiological findings and molecular mechanism evidence to analyze the significant comorbidity and correlation characteristics between infectious oral diseases such as caries and periodontitis, and psychological disorders including depression and anxiety. Oral diseases not only directly impair mental well-being through pain, functional impairment, and social anxiety, but also induce systemic inflammatory responses that disrupt the blood-brain barrier, activate microglia, and alter neurotransmitter metabolism, thereby contributing to functional dysregulation within emotional regulatory centers. The dysbiosis of the oral microbiota caused by infectious oral diseases plays a central role in the vicious cycle of "oral infection-mental health disorders" through the"oral-gut-brain axis", inflammation-mediated neuroimmune cascades, and hypothalamic-pituitary-adrenal axis dysregulation. Meanwhile, mental disorders exacerbate oral microbial imbalance and tissue destruction through poor oral hygiene behaviors, xerostomia induced by psychotropic medications, and stress-related neuroendocrine alterations. This paper advocates for synergistically integrate oral clinical interventions with mental health improvement strategies, and for the development of microbiome-targeted precision modulation approaches. It further proposes an integrated health management paradigm that bridges dentistry and psychiatry, providing both theoretical foundations and practical pathways to transcend traditional disciplinary boundaries and achieve holistic oral-mental co-management.
Additional Links: PMID-42532542
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@article {pmid42532542,
year = {2026},
author = {Yang, JM and Yuan, ML and Zhang, YY and Chen, Y and Qu, X},
title = {[Research progress on the bidirectional relationship between oral infectious diseases and mental health issues].},
journal = {Zhonghua kou qiang yi xue za zhi = Zhonghua kouqiang yixue zazhi = Chinese journal of stomatology},
volume = {61},
number = {8},
pages = {1243-1250},
doi = {10.3760/cma.j.cn112144-20251031-00437},
pmid = {42532542},
issn = {1002-0098},
support = {72374146//National Natural Science Foundation of China/ ; },
abstract = {Infectious oral diseases represent the most prevalent categories of oral conditions, including dental caries, periodontitis, periapical lesions, and pericoronitis. Their bidirectional relationship with mental health has emerged as a critical interdisciplinary research frontier. This paper integrates epidemiological findings and molecular mechanism evidence to analyze the significant comorbidity and correlation characteristics between infectious oral diseases such as caries and periodontitis, and psychological disorders including depression and anxiety. Oral diseases not only directly impair mental well-being through pain, functional impairment, and social anxiety, but also induce systemic inflammatory responses that disrupt the blood-brain barrier, activate microglia, and alter neurotransmitter metabolism, thereby contributing to functional dysregulation within emotional regulatory centers. The dysbiosis of the oral microbiota caused by infectious oral diseases plays a central role in the vicious cycle of "oral infection-mental health disorders" through the"oral-gut-brain axis", inflammation-mediated neuroimmune cascades, and hypothalamic-pituitary-adrenal axis dysregulation. Meanwhile, mental disorders exacerbate oral microbial imbalance and tissue destruction through poor oral hygiene behaviors, xerostomia induced by psychotropic medications, and stress-related neuroendocrine alterations. This paper advocates for synergistically integrate oral clinical interventions with mental health improvement strategies, and for the development of microbiome-targeted precision modulation approaches. It further proposes an integrated health management paradigm that bridges dentistry and psychiatry, providing both theoretical foundations and practical pathways to transcend traditional disciplinary boundaries and achieve holistic oral-mental co-management.},
}
RevDate: 2026-07-30
Arbuscular mycorrhizal fungi orchestrate belowground microbiomes in plant holobionts.
Trends in plant science pii:S1360-1385(26)00218-9 [Epub ahead of print].
The traditional model of plant-arbuscular mycorrhizal (AM) fungal coevolution, based solely on interactions between plants and AM fungi, became obsolete with the discovery of the critical roles that belowground microbiomes play in the function of mycorrhizal symbiosis. Based on insights into hyphosphere microbiota, we expand the plant-AM fungus-bacterium continuum into a multipartite AM fungal-orchestrated holobiont (H-AMF) framework, where AM fungi integrate plant roots with soil microbiota into a cross-kingdom ecological unit. A division of labor exists among plants, AM fungi, and hyphosphere microbes in the mycocentric H-AMF perspective. We summarize mechanisms by which AM fungi sustain cooperative relationships with plants and hyphosphere microbiota and propose holobiont-scale methodologies to advance understanding of plant-fungal-microbial interactions and their ecological functions.
Additional Links: PMID-42532766
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@article {pmid42532766,
year = {2026},
author = {Wang, L and Zhang, L and Rillig, MC and van der Heijden, MGA and Johnson, NC and Feng, G},
title = {Arbuscular mycorrhizal fungi orchestrate belowground microbiomes in plant holobionts.},
journal = {Trends in plant science},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tplants.2026.07.003},
pmid = {42532766},
issn = {1878-4372},
abstract = {The traditional model of plant-arbuscular mycorrhizal (AM) fungal coevolution, based solely on interactions between plants and AM fungi, became obsolete with the discovery of the critical roles that belowground microbiomes play in the function of mycorrhizal symbiosis. Based on insights into hyphosphere microbiota, we expand the plant-AM fungus-bacterium continuum into a multipartite AM fungal-orchestrated holobiont (H-AMF) framework, where AM fungi integrate plant roots with soil microbiota into a cross-kingdom ecological unit. A division of labor exists among plants, AM fungi, and hyphosphere microbes in the mycocentric H-AMF perspective. We summarize mechanisms by which AM fungi sustain cooperative relationships with plants and hyphosphere microbiota and propose holobiont-scale methodologies to advance understanding of plant-fungal-microbial interactions and their ecological functions.},
}
RevDate: 2026-07-30
Next-Generation Sequencing in Companion Animal Practice for Infectious Disease Diagnostics and Characterizing Normal Microbiomes.
The Veterinary clinics of North America. Small animal practice pii:S0195-5616(26)00086-0 [Epub ahead of print].
The purpose of this article is to review and compare the most common and emergent next-generation sequencing methodologies used in small animal veterinary practice, with a focus on their applications to bacterial diagnostics and assessment of the healthy gut microbiome. These methodologies include whole genome sequencing, amplicon sequencing, shotgun metagenomic sequencing, and transcriptomics. Understanding the benefits and limitations of each methodology will help small animal practitioners to make informed decisions for their patients and maximize the utility of each test as part of a complete patient health assessment.
Additional Links: PMID-42532775
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PubMed:
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@article {pmid42532775,
year = {2026},
author = {Nealon, NJ},
title = {Next-Generation Sequencing in Companion Animal Practice for Infectious Disease Diagnostics and Characterizing Normal Microbiomes.},
journal = {The Veterinary clinics of North America. Small animal practice},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cvsm.2026.06.005},
pmid = {42532775},
issn = {1878-1306},
abstract = {The purpose of this article is to review and compare the most common and emergent next-generation sequencing methodologies used in small animal veterinary practice, with a focus on their applications to bacterial diagnostics and assessment of the healthy gut microbiome. These methodologies include whole genome sequencing, amplicon sequencing, shotgun metagenomic sequencing, and transcriptomics. Understanding the benefits and limitations of each methodology will help small animal practitioners to make informed decisions for their patients and maximize the utility of each test as part of a complete patient health assessment.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Site-specific oral microbiome profiles in healthy young Korean women.
Scientific reports, 16(1):.
We characterized site-specific organization of the oral microbiome in 59 healthy, non-smoking women in their twenties using 16S rRNA (V3-V4) sequencing of dental plaque (DQ), mouthwash (MW), and tongue coating (TC) samples (177 libraries; rarefied to 29,853 reads). The order of alpha diversity was DQ > MW > TC (p < 0.001), with mean Observed Features of 227.6, 208.7, and 142.4, respectively, consistent with differences in local niche structure within the oral cavity. Beta diversity (Bray-Curtis; weighted/unweighted UniFrac) showed clear separation by site (PERMANOVA overall p < 0.001), with DQ most distinct from MW and TC. At the phylum level, DQ was enriched for Actinobacteriota and Proteobacteria, whereas Firmicutes predominated in MW and TC, indicating compositional shifts across oral microenvironments. Dominant genera included Streptococcus (20.6%), Neisseria (11.7%), Haemophilus (10.1%), Prevotella (7.1%), Veillonella (6.0%), Rothia (5.1%), and Lactobacillus (4.4%). Site-associated taxa included Cardiobacterium, Corynebacterium, and Campylobacter in DQ; Actinobacillus in MW; and Absconditabacteriales (SR1) and Lactobacillus in TC. TC exhibited the lowest alpha diversity but the highest genus richness (n = 340), indicating an uneven community with many low-abundance taxa. LEfSe identified discriminant taxa, including Rothia, Actinomyces, Fusobacterium (DQ), Streptococcus, and Gemella (MW); and Lactobacillus, Prevotella, Veillonella, and Haemophilus (TC). These results demonstrate pronounced site specificity within the oral cavity of a well-defined healthy cohort and indicate that multi-site resolution is essential for advancing mechanistic and translational oral microbiome research.
Additional Links: PMID-42533020
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@article {pmid42533020,
year = {2026},
author = {Cho, MY and Eom, JH and Kim, JW and Kim, YW and Hwang, J and Lee, D and Kim, YY and Kim, HS and Hwang, I},
title = {Site-specific oral microbiome profiles in healthy young Korean women.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {42533020},
issn = {2045-2322},
support = {2024ER050700//Korea National Institute of Health/ ; },
mesh = {Humans ; Female ; *Microbiota/genetics ; *Mouth/microbiology ; RNA, Ribosomal, 16S/genetics ; Republic of Korea ; *Bacteria/genetics/classification ; Dental Plaque/microbiology ; Tongue/microbiology ; Adult ; Young Adult ; },
abstract = {We characterized site-specific organization of the oral microbiome in 59 healthy, non-smoking women in their twenties using 16S rRNA (V3-V4) sequencing of dental plaque (DQ), mouthwash (MW), and tongue coating (TC) samples (177 libraries; rarefied to 29,853 reads). The order of alpha diversity was DQ > MW > TC (p < 0.001), with mean Observed Features of 227.6, 208.7, and 142.4, respectively, consistent with differences in local niche structure within the oral cavity. Beta diversity (Bray-Curtis; weighted/unweighted UniFrac) showed clear separation by site (PERMANOVA overall p < 0.001), with DQ most distinct from MW and TC. At the phylum level, DQ was enriched for Actinobacteriota and Proteobacteria, whereas Firmicutes predominated in MW and TC, indicating compositional shifts across oral microenvironments. Dominant genera included Streptococcus (20.6%), Neisseria (11.7%), Haemophilus (10.1%), Prevotella (7.1%), Veillonella (6.0%), Rothia (5.1%), and Lactobacillus (4.4%). Site-associated taxa included Cardiobacterium, Corynebacterium, and Campylobacter in DQ; Actinobacillus in MW; and Absconditabacteriales (SR1) and Lactobacillus in TC. TC exhibited the lowest alpha diversity but the highest genus richness (n = 340), indicating an uneven community with many low-abundance taxa. LEfSe identified discriminant taxa, including Rothia, Actinomyces, Fusobacterium (DQ), Streptococcus, and Gemella (MW); and Lactobacillus, Prevotella, Veillonella, and Haemophilus (TC). These results demonstrate pronounced site specificity within the oral cavity of a well-defined healthy cohort and indicate that multi-site resolution is essential for advancing mechanistic and translational oral microbiome research.},
}
MeSH Terms:
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Humans
Female
*Microbiota/genetics
*Mouth/microbiology
RNA, Ribosomal, 16S/genetics
Republic of Korea
*Bacteria/genetics/classification
Dental Plaque/microbiology
Tongue/microbiology
Adult
Young Adult
RevDate: 2026-07-31
CmpDate: 2026-07-30
Microbiota-derived 10-hydroxystearic acid activates PPARα to restore gut epithelial barrier integrity and enhance anti-retroviral therapy.
Nature microbiology, 11(8):2365-2383.
HIV infection disrupts gut epithelial barrier integrity and mucosal immunity, driving chronic inflammation and disease progression which are not fully resolved despite anti-retroviral therapy. Here we identify the microbiota-derived octadecanoid-hydroxy-fatty-acid metabolite 10-hydroxystearic acid (10-HSA), produced by Lactiplantibacillus plantarum, as a key mediator of gut epithelial barrier repair in human intestinal epithelial cells in vitro, ex vivo and in the non-human primate model of HIV/AIDS. X-ray crystallography and transcriptomics combined with functional analyses revealed that 10-HSA directly binds PPARα, inducing lipid metabolism, mitochondrial regeneration and subsequent epigenetic histone crotonylation, thereby promoting gut epithelial renewal. Co-administration of 10-HSA with anti-retroviral therapy in SIV-infected macaques accelerated viral suppression, resolved systemic inflammation, repaired gut epithelial integrity and recovered the gut microbiota. These findings identify a microbiota-derived lipid metabolite-PPARα-histone crotonylation axis that activates gut epithelial regeneration. This study defines a host-microbiome metabolic pathway that restores epithelial-immune homeostasis and enhances the efficacy of anti-retroviral therapy.
Additional Links: PMID-42533069
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@article {pmid42533069,
year = {2026},
author = {Kramer, D and Santos Rocha, C and Gaulke, CA and Nearing, M and Sankaran-Walters, S and Loque, I and Kidigannappa, A and Pham, E and Hu, S and Wanakumjorn, P and Abbattista, R and Dandekar, A and Faller, R and Dandekar, S},
title = {Microbiota-derived 10-hydroxystearic acid activates PPARα to restore gut epithelial barrier integrity and enhance anti-retroviral therapy.},
journal = {Nature microbiology},
volume = {11},
number = {8},
pages = {2365-2383},
pmid = {42533069},
issn = {2058-5276},
support = {R37 AI 153025//U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; AI123105//U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; T32 AI060555/AI/NIAID NIH HHS/United States ; R37 AI 153025//U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; R37 AI 153025//U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; R37 AI 153025//U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; R37 AI 153025//U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; R37 AI 153025//U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; R37 AI 153025//U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; R37 AI 153025//U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; R37 AI 153025//U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; R37 AI 153025//U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; R37 AI 153025//U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; R37 AI 153025//U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; R37 AI 153025//U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; P51 OD011107/CD/ODCDC CDC HHS/United States ; },
mesh = {Animals ; *PPAR alpha/metabolism/genetics ; Humans ; Intestinal Barrier Function ; *Intestinal Mucosa/drug effects/metabolism ; Epithelial Cells/drug effects/metabolism ; HIV Infections/drug therapy ; *Gastrointestinal Microbiome ; Lipid Metabolism/drug effects ; *Anti-Retroviral Agents/therapeutic use/pharmacology ; Macaca mulatta ; Simian Immunodeficiency Virus/drug effects ; Disease Models, Animal ; },
abstract = {HIV infection disrupts gut epithelial barrier integrity and mucosal immunity, driving chronic inflammation and disease progression which are not fully resolved despite anti-retroviral therapy. Here we identify the microbiota-derived octadecanoid-hydroxy-fatty-acid metabolite 10-hydroxystearic acid (10-HSA), produced by Lactiplantibacillus plantarum, as a key mediator of gut epithelial barrier repair in human intestinal epithelial cells in vitro, ex vivo and in the non-human primate model of HIV/AIDS. X-ray crystallography and transcriptomics combined with functional analyses revealed that 10-HSA directly binds PPARα, inducing lipid metabolism, mitochondrial regeneration and subsequent epigenetic histone crotonylation, thereby promoting gut epithelial renewal. Co-administration of 10-HSA with anti-retroviral therapy in SIV-infected macaques accelerated viral suppression, resolved systemic inflammation, repaired gut epithelial integrity and recovered the gut microbiota. These findings identify a microbiota-derived lipid metabolite-PPARα-histone crotonylation axis that activates gut epithelial regeneration. This study defines a host-microbiome metabolic pathway that restores epithelial-immune homeostasis and enhances the efficacy of anti-retroviral therapy.},
}
MeSH Terms:
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hide MeSH Terms
Animals
*PPAR alpha/metabolism/genetics
Humans
Intestinal Barrier Function
*Intestinal Mucosa/drug effects/metabolism
Epithelial Cells/drug effects/metabolism
HIV Infections/drug therapy
*Gastrointestinal Microbiome
Lipid Metabolism/drug effects
*Anti-Retroviral Agents/therapeutic use/pharmacology
Macaca mulatta
Simian Immunodeficiency Virus/drug effects
Disease Models, Animal
RevDate: 2026-07-30
CmpDate: 2026-07-30
Comparative microbiome profiling of plant- and animal-derived traditional fermented foods from Mizoram, India using full-length 16S rRNA sequencing.
Antonie van Leeuwenhoek, 119(8):.
Traditional fermented foods represent complex microbial ecosystems shaped by substrate composition, indigenous processing practices, and local environmental conditions. However, the microbiomes of many traditional fermented foods from Northeast India remain poorly characterized. In this study, the bacterial communities associated with thirteen traditional fermented foods from Mizoram, India, representing both plant- and animal-derived fermentations, were characterized using full-length 16S rRNA gene sequencing on the Oxford Nanopore platform. Sequencing generated approximately 1.94 million high-quality reads, enabling high-resolution taxonomic profiling of the fermented food microbiomes. The microbial communities were predominantly composed of Bacillota, Pseudomonadota, and Cyanobacteriota, although their relative abundances varied considerably among fermented food types. Plant-derived fermented foods were enriched with fermentative bacterial genera, including Bacillus, Lactobacillus, Lacticaseibacillus, Pediococcus, and Weissella, whereas animal-derived fermented foods showed a greater abundance of anaerobic taxa, particularly Clostridium. Alpha diversity analyses demonstrated higher microbial richness in plant-derived fermented foods, while beta diversity revealed clear substrate-dependent clustering of microbial communities. Functional prediction indicated that metabolism-related pathways, particularly carbohydrate and amino acid metabolism, predominated across the fermented food microbiomes, and LEfSe analysis identified distinct microbial biomarkers associated with plant- and animal-derived fermentations. Collectively, these findings provide the first comprehensive microbiome characterization of traditional fermented foods from Mizoram and demonstrate that fermentation substrate is a major determinant of microbial community composition and predicted functional potential. Although full-length 16S rRNA gene sequencing improved taxonomic resolution, taxonomic interpretations were made cautiously at the genus level where appropriate because of the inherent limitations of 16S rRNA gene-based classification.
Additional Links: PMID-42533119
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@article {pmid42533119,
year = {2026},
author = {Lalhmunsangi, J and Sudharsan, R and Laldinmawii, G and Lalngaihzuali, R and Das, M and Das, S and Mukherjee, S and Bhattacharyya, S and Ramamurthy, T and Roychoudhury, P and Akter, F and Mukhopadhyay, A and Roy, A and Kesavan, M and Senthil Kumar, N and Roy, S and Dutta, T},
title = {Comparative microbiome profiling of plant- and animal-derived traditional fermented foods from Mizoram, India using full-length 16S rRNA sequencing.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {8},
pages = {},
pmid = {42533119},
issn = {1572-9699},
support = {Order No. ER/FBS/Phase-II/2023/DR/MD(Part-C) [e-177060]//Indian Council of Medical Research/ ; },
mesh = {*RNA, Ribosomal, 16S/genetics ; India ; Animals ; *Fermented Foods/microbiology ; *Microbiota/genetics ; *Bacteria/classification/genetics/isolation & purification ; Fermentation ; Phylogeny ; Food Microbiology ; DNA, Bacterial/genetics ; Sequence Analysis, DNA ; Plants/microbiology ; },
abstract = {Traditional fermented foods represent complex microbial ecosystems shaped by substrate composition, indigenous processing practices, and local environmental conditions. However, the microbiomes of many traditional fermented foods from Northeast India remain poorly characterized. In this study, the bacterial communities associated with thirteen traditional fermented foods from Mizoram, India, representing both plant- and animal-derived fermentations, were characterized using full-length 16S rRNA gene sequencing on the Oxford Nanopore platform. Sequencing generated approximately 1.94 million high-quality reads, enabling high-resolution taxonomic profiling of the fermented food microbiomes. The microbial communities were predominantly composed of Bacillota, Pseudomonadota, and Cyanobacteriota, although their relative abundances varied considerably among fermented food types. Plant-derived fermented foods were enriched with fermentative bacterial genera, including Bacillus, Lactobacillus, Lacticaseibacillus, Pediococcus, and Weissella, whereas animal-derived fermented foods showed a greater abundance of anaerobic taxa, particularly Clostridium. Alpha diversity analyses demonstrated higher microbial richness in plant-derived fermented foods, while beta diversity revealed clear substrate-dependent clustering of microbial communities. Functional prediction indicated that metabolism-related pathways, particularly carbohydrate and amino acid metabolism, predominated across the fermented food microbiomes, and LEfSe analysis identified distinct microbial biomarkers associated with plant- and animal-derived fermentations. Collectively, these findings provide the first comprehensive microbiome characterization of traditional fermented foods from Mizoram and demonstrate that fermentation substrate is a major determinant of microbial community composition and predicted functional potential. Although full-length 16S rRNA gene sequencing improved taxonomic resolution, taxonomic interpretations were made cautiously at the genus level where appropriate because of the inherent limitations of 16S rRNA gene-based classification.},
}
MeSH Terms:
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*RNA, Ribosomal, 16S/genetics
India
Animals
*Fermented Foods/microbiology
*Microbiota/genetics
*Bacteria/classification/genetics/isolation & purification
Fermentation
Phylogeny
Food Microbiology
DNA, Bacterial/genetics
Sequence Analysis, DNA
Plants/microbiology
RevDate: 2026-07-31
CmpDate: 2026-07-31
Nanopore sequencing reveals coordinated host and microbiome responses across barley genotypes.
BMC biology, 24(1):.
BACKGROUND: Barley (Hordeum vulgare L.) provides a suitable model for studying domestication-driven plant-microbiome interactions. Although wild, landrace, and modern genotypes host distinct rhizosphere communities, the extent to which roots and microbes reciprocally influence each other remains unclear. Here, we applied an integrated multi-omics approach combining long-read metagenomics, root transcriptomics, and plant genomics to understand genotype-specific host-microbiome coordination.
RESULTS: Oxford Nanopore whole metagenome sequencing (WMS) revealed genotype-associated shifts in rhizosphere communities across seasons. Functional profiling showed a conserved metabolic backbone including amino acid metabolism, energy production, and secondary metabolite biosynthesis, alongside genotype-dependent variation in carbohydrate metabolism and transport-associated pathways. Genome-resolved analysis through metagenome-assembled genomes (MAGs) further detailed the taxonomic and functional architecture of key rhizosphere lineages. Root transcriptome profiling identified extensive differential expression associated with microbial perception, signaling, defense, and metabolic processes. Integration of host and microbiome data revealed coordinated molecular patterns, indicating that barley genotypes are associated with distinct microbial assemblages and corresponding transcriptional responses.
CONCLUSIONS: These findings indicate that domestication has shaped coordinated associations between barley genotypes and their rhizosphere microbiomes, reflected in both microbial community composition and host transcriptional regulation. This work provides new insights into the evolutionary tuning of plant-microbiome relationships and highlights opportunities for microbiome-informed strategies in barley improvement.
Additional Links: PMID-42533345
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Citation:
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@article {pmid42533345,
year = {2026},
author = {Devasahayam, BRF and McNeil, T and Wubet, T and Schmutzer, T},
title = {Nanopore sequencing reveals coordinated host and microbiome responses across barley genotypes.},
journal = {BMC biology},
volume = {24},
number = {1},
pages = {},
pmid = {42533345},
issn = {1741-7007},
mesh = {*Hordeum/genetics/microbiology ; *Microbiota/genetics ; *Genotype ; Nanopore Sequencing ; Rhizosphere ; Plant Roots/microbiology/genetics ; Metagenome ; Metagenomics ; Transcriptome ; },
abstract = {BACKGROUND: Barley (Hordeum vulgare L.) provides a suitable model for studying domestication-driven plant-microbiome interactions. Although wild, landrace, and modern genotypes host distinct rhizosphere communities, the extent to which roots and microbes reciprocally influence each other remains unclear. Here, we applied an integrated multi-omics approach combining long-read metagenomics, root transcriptomics, and plant genomics to understand genotype-specific host-microbiome coordination.
RESULTS: Oxford Nanopore whole metagenome sequencing (WMS) revealed genotype-associated shifts in rhizosphere communities across seasons. Functional profiling showed a conserved metabolic backbone including amino acid metabolism, energy production, and secondary metabolite biosynthesis, alongside genotype-dependent variation in carbohydrate metabolism and transport-associated pathways. Genome-resolved analysis through metagenome-assembled genomes (MAGs) further detailed the taxonomic and functional architecture of key rhizosphere lineages. Root transcriptome profiling identified extensive differential expression associated with microbial perception, signaling, defense, and metabolic processes. Integration of host and microbiome data revealed coordinated molecular patterns, indicating that barley genotypes are associated with distinct microbial assemblages and corresponding transcriptional responses.
CONCLUSIONS: These findings indicate that domestication has shaped coordinated associations between barley genotypes and their rhizosphere microbiomes, reflected in both microbial community composition and host transcriptional regulation. This work provides new insights into the evolutionary tuning of plant-microbiome relationships and highlights opportunities for microbiome-informed strategies in barley improvement.},
}
MeSH Terms:
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*Hordeum/genetics/microbiology
*Microbiota/genetics
*Genotype
Nanopore Sequencing
Rhizosphere
Plant Roots/microbiology/genetics
Metagenome
Metagenomics
Transcriptome
RevDate: 2026-07-31
CmpDate: 2026-07-31
Gut microbial composition modulates endogenous food-specific CD4+ T cells in food allergy.
Journal of immunology (Baltimore, Md. : 1950), 215(7):.
The growing food allergy epidemic is thought to be related to changing environmental factors, particularly changes in the gut microbiome. While prior work has demonstrated that food allergy can be modulated by gut microbes, little is known about how food allergen-specific CD4+ T cells are affected by gut microbial composition. Here, we report that food allergy severity differs between mice obtained from 2 different specific pathogen-free mouse vendors (Jackson Labs [Jax] and Taconic Biosciences [Tac]). Mice from Tac develop diarrhea and anaphylaxis after fewer allergen exposures than mice from Jax. Using food allergen peptide: MHCII tetramers, we also find that Tac mice have fewer allergen-specific regulatory T cells in the small intestine compared to mice from Jax with concomitant increase in allergen-specific Th2 cells. In addition, Tac mice have increased intestinal permeability. Increased food allergy severity, phenotype of allergen-specific T cells, and increased gut permeability were transferable to Jax animals via co-housing, which corresponded to a shift in Jax microbial communities towards those found in Tac mice. Our findings demonstrate that food allergen-specific Treg cells can be modulated by gut microbial community composition, which in turn is correlated to food allergy severity.
Additional Links: PMID-42533363
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PubMed:
Citation:
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@article {pmid42533363,
year = {2026},
author = {Weingarden, AR and Dahlberg, FS and Broude, CN and Meng, X and Jain, S and Weakley, AM and Cabrera, AV and Dileepan, T and Fischbach, MA and Jenkins, MK},
title = {Gut microbial composition modulates endogenous food-specific CD4+ T cells in food allergy.},
journal = {Journal of immunology (Baltimore, Md. : 1950)},
volume = {215},
number = {7},
pages = {},
doi = {10.1093/jimmun/vkag172},
pmid = {42533363},
issn = {1550-6606},
support = {R01AI187164//National Institute of Allergy and Infectious Diseases (NIAID)/ ; //Life Science Research Foundation postdoctoral fellowship and Open Philanthropy/ ; },
mesh = {Animals ; *Food Hypersensitivity/immunology/microbiology ; Mice ; *Gastrointestinal Microbiome/immunology ; Allergens/immunology ; *T-Lymphocytes, Regulatory/immunology ; *CD4-Positive T-Lymphocytes/immunology ; Female ; Th2 Cells/immunology ; Disease Models, Animal ; },
abstract = {The growing food allergy epidemic is thought to be related to changing environmental factors, particularly changes in the gut microbiome. While prior work has demonstrated that food allergy can be modulated by gut microbes, little is known about how food allergen-specific CD4+ T cells are affected by gut microbial composition. Here, we report that food allergy severity differs between mice obtained from 2 different specific pathogen-free mouse vendors (Jackson Labs [Jax] and Taconic Biosciences [Tac]). Mice from Tac develop diarrhea and anaphylaxis after fewer allergen exposures than mice from Jax. Using food allergen peptide: MHCII tetramers, we also find that Tac mice have fewer allergen-specific regulatory T cells in the small intestine compared to mice from Jax with concomitant increase in allergen-specific Th2 cells. In addition, Tac mice have increased intestinal permeability. Increased food allergy severity, phenotype of allergen-specific T cells, and increased gut permeability were transferable to Jax animals via co-housing, which corresponded to a shift in Jax microbial communities towards those found in Tac mice. Our findings demonstrate that food allergen-specific Treg cells can be modulated by gut microbial community composition, which in turn is correlated to food allergy severity.},
}
MeSH Terms:
show MeSH Terms
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Animals
*Food Hypersensitivity/immunology/microbiology
Mice
*Gastrointestinal Microbiome/immunology
Allergens/immunology
*T-Lymphocytes, Regulatory/immunology
*CD4-Positive T-Lymphocytes/immunology
Female
Th2 Cells/immunology
Disease Models, Animal
RevDate: 2026-07-31
Letter: The Microbiome-Mediated Impact of Proton Pump Inhibitors on Spontaneous Bacterial Peritonitis.
Additional Links: PMID-42533399
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PubMed:
Citation:
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@article {pmid42533399,
year = {2026},
author = {Simeoni, S and Ponziani, FR and Gasbarrini, G and Gasbarrini, A and Ianiro, G},
title = {Letter: The Microbiome-Mediated Impact of Proton Pump Inhibitors on Spontaneous Bacterial Peritonitis.},
journal = {Alimentary pharmacology & therapeutics},
volume = {},
number = {},
pages = {},
doi = {10.1111/apt.70883},
pmid = {42533399},
issn = {1365-2036},
}
RevDate: 2026-07-31
CmpDate: 2026-07-31
Host phylogeny and diet shape gut microbiome and virome in wild small mammals of Gongga Mountain, China.
Zoological research, 47(4):1332-1352.
Gut microbiotas play pivotal roles in host adaptation, yet their composition and function in high-altitude small mammals remain poorly characterized. This study investigated how host phylogeny (order-level) and dietary habits shape the gut microbiome and virome of three mammalian orders (Eulipotyphla, Rodentia, Lagomorpha) in Gongga Mountain, a biodiversity hotspot on the Qinghai-Xizang Plateau. Metagenomic sequencing of 219 samples from 22 species revealed order-specific microbial signatures: Eulipotyphla (carnivorous) harbored higher abundances of potential pathogens (e.g., Helicobacter, Hafnia) and Retroviridae; Lagomorpha (herbivorous) was enriched in cellulolytic bacteria (e.g., Lachnospiraceae, Prevotella) and carbohydrate-active enzymes (CAZymes); Rodentia (omnivorous) showed intermediate traits. We reconstructed 1 385 high-quality metagenome-assembled genomes (MAGs), 1 328 representing novel species, and identified 749 viral operational taxonomic units (vOTUs), >80% being Caudoviricetes. Crucially, Retroviridae abundance in Eulipotyphla suggests zoonotic risk. Phage-host network analysis indicated Caudoviricetes regulates cellulolytic bacteria in Lagomorpha. Host phylogeny and diet jointly drive gut microbiome divergence in small mammals. We establish the first gut microbiome and virome resource of small mammals in the high-altitude area of Gongga Mountain, highlighting Eulipotyphla as a potential vector for zoonotic pathogens.
Additional Links: PMID-42533584
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PubMed:
Citation:
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@article {pmid42533584,
year = {2026},
author = {He, LW and Tang, RX and Liu, SY and Zhang, ZJ and Li, Y and Wang, XM and Yue, BS and Fan, ZX},
title = {Host phylogeny and diet shape gut microbiome and virome in wild small mammals of Gongga Mountain, China.},
journal = {Zoological research},
volume = {47},
number = {4},
pages = {1332-1352},
doi = {10.24272/j.issn.2095-8137.2025.448},
pmid = {42533584},
issn = {2095-8137},
mesh = {Animals ; *Gastrointestinal Microbiome ; *Phylogeny ; *Virome ; *Diet/veterinary ; China ; *Rodentia ; *Mammals/virology ; },
abstract = {Gut microbiotas play pivotal roles in host adaptation, yet their composition and function in high-altitude small mammals remain poorly characterized. This study investigated how host phylogeny (order-level) and dietary habits shape the gut microbiome and virome of three mammalian orders (Eulipotyphla, Rodentia, Lagomorpha) in Gongga Mountain, a biodiversity hotspot on the Qinghai-Xizang Plateau. Metagenomic sequencing of 219 samples from 22 species revealed order-specific microbial signatures: Eulipotyphla (carnivorous) harbored higher abundances of potential pathogens (e.g., Helicobacter, Hafnia) and Retroviridae; Lagomorpha (herbivorous) was enriched in cellulolytic bacteria (e.g., Lachnospiraceae, Prevotella) and carbohydrate-active enzymes (CAZymes); Rodentia (omnivorous) showed intermediate traits. We reconstructed 1 385 high-quality metagenome-assembled genomes (MAGs), 1 328 representing novel species, and identified 749 viral operational taxonomic units (vOTUs), >80% being Caudoviricetes. Crucially, Retroviridae abundance in Eulipotyphla suggests zoonotic risk. Phage-host network analysis indicated Caudoviricetes regulates cellulolytic bacteria in Lagomorpha. Host phylogeny and diet jointly drive gut microbiome divergence in small mammals. We establish the first gut microbiome and virome resource of small mammals in the high-altitude area of Gongga Mountain, highlighting Eulipotyphla as a potential vector for zoonotic pathogens.},
}
MeSH Terms:
show MeSH Terms
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Animals
*Gastrointestinal Microbiome
*Phylogeny
*Virome
*Diet/veterinary
China
*Rodentia
*Mammals/virology
RevDate: 2026-07-31
Zinc-stabilized stannous fluoride modulates the periodontal microbiome, reducing Fusobacteria, key Gram-negative species, and overall inflammation within an experimental gingivitis clinical trial.
Journal of periodontology [Epub ahead of print].
BACKGROUND: This study aimed to evaluate the effects of a dentifrice containing stannous fluoride stabilized with zinc phosphate on subgingival microbiome composition and clinical inflammation during experimental gingivitis, compared with a sodium fluoride control.
METHODS: This investigation was conducted as a secondary analysis of a randomized, parallel-arm, double-blind, controlled clinical trial. Clinical resolution of experimental gingivitis was assessed using bleeding on probing, gingival index, and plaque index. Deeply sequenced subgingival plaque metagenomic data were analyzed to compare microbial composition and functional potential between a stannous fluoride stabilized with zinc phosphate dentifrice (test) and a sodium fluoride dentifrice (control) over a 21-day experimental gingivitis period.
RESULTS: Use of the stannous fluoride stabilized with zinc phosphate dentifrice was associated with depletion of periodontal disease-associated Gram-negative bacteria, including Fusobacterium nucleatum and multiple Porphyromonas and Prevotella species. This reduction in Gram-negative taxa corresponded with shifts in microbial community metabolic functions and was associated with significantly reduced clinical inflammation compared with the control over the 21-day period.
CONCLUSIONS: Short-term use of stannous fluoride stabilized with zinc phosphate may provide additional protection against gingival inflammation by limiting the outgrowth of key periodontal pathogens, including the bridging organism Fusobacterium nucleatum, and by altering plaque functional capacity. These effects were associated with improved periodontal health outcomes compared with a standard sodium fluoride dentifrice.
PLAIN LANGUAGE SUMMARY: In this study, we analyzed bacteria within the periodontal pocket using deep metagenomic sequencing to better resolve bacterial species and their functions. Results from this study show that using a toothpaste containing stannous fluoride stabilized with zinc phosphate was associated with the reduction of several important Gram-negative bacteria associated with periodontal disease, including Fusobacterium nucleatum and species of Porphyromonas and Prevotella compared with a control toothpaste. These bacteria are well‑known contributors to gingival inflammation and biofilm maturation. When levels of these specific bacteria decreased within the stannous fluoride treatment group, the overall subgingival microbiome shifted which notably persisted during the subsequent 21-day oral hygiene abstention period in this experimental gingivitis model - resulting in significantly lower clinical inflammation. Our findings suggest that even short‑term use of stannous fluoride stabilized with zinc phosphate may provide added protection against early gingival inflammation. Notably, stannous fluoride stabilized with zinc phosphate appears to limit the growth of key periodontal pathogens-particularly Fusobacterium nucleatum, an important bridging organism in subgingival biofilms-and may alter the functional activity of dental plaque in ways that support improved periodontal health when compared with a standard sodium fluoride toothpaste.
Additional Links: PMID-42533623
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PubMed:
Citation:
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@article {pmid42533623,
year = {2026},
author = {Kerns, KA and Naumann, AA and Soon, LY and Hendrickson, EL and Barbour, A and Chen, D and Trivedi, HM and Glogauer, M and McLean, JS},
title = {Zinc-stabilized stannous fluoride modulates the periodontal microbiome, reducing Fusobacteria, key Gram-negative species, and overall inflammation within an experimental gingivitis clinical trial.},
journal = {Journal of periodontology},
volume = {},
number = {},
pages = {},
doi = {10.1002/jper.70168},
pmid = {42533623},
issn = {1943-3670},
abstract = {BACKGROUND: This study aimed to evaluate the effects of a dentifrice containing stannous fluoride stabilized with zinc phosphate on subgingival microbiome composition and clinical inflammation during experimental gingivitis, compared with a sodium fluoride control.
METHODS: This investigation was conducted as a secondary analysis of a randomized, parallel-arm, double-blind, controlled clinical trial. Clinical resolution of experimental gingivitis was assessed using bleeding on probing, gingival index, and plaque index. Deeply sequenced subgingival plaque metagenomic data were analyzed to compare microbial composition and functional potential between a stannous fluoride stabilized with zinc phosphate dentifrice (test) and a sodium fluoride dentifrice (control) over a 21-day experimental gingivitis period.
RESULTS: Use of the stannous fluoride stabilized with zinc phosphate dentifrice was associated with depletion of periodontal disease-associated Gram-negative bacteria, including Fusobacterium nucleatum and multiple Porphyromonas and Prevotella species. This reduction in Gram-negative taxa corresponded with shifts in microbial community metabolic functions and was associated with significantly reduced clinical inflammation compared with the control over the 21-day period.
CONCLUSIONS: Short-term use of stannous fluoride stabilized with zinc phosphate may provide additional protection against gingival inflammation by limiting the outgrowth of key periodontal pathogens, including the bridging organism Fusobacterium nucleatum, and by altering plaque functional capacity. These effects were associated with improved periodontal health outcomes compared with a standard sodium fluoride dentifrice.
PLAIN LANGUAGE SUMMARY: In this study, we analyzed bacteria within the periodontal pocket using deep metagenomic sequencing to better resolve bacterial species and their functions. Results from this study show that using a toothpaste containing stannous fluoride stabilized with zinc phosphate was associated with the reduction of several important Gram-negative bacteria associated with periodontal disease, including Fusobacterium nucleatum and species of Porphyromonas and Prevotella compared with a control toothpaste. These bacteria are well‑known contributors to gingival inflammation and biofilm maturation. When levels of these specific bacteria decreased within the stannous fluoride treatment group, the overall subgingival microbiome shifted which notably persisted during the subsequent 21-day oral hygiene abstention period in this experimental gingivitis model - resulting in significantly lower clinical inflammation. Our findings suggest that even short‑term use of stannous fluoride stabilized with zinc phosphate may provide added protection against early gingival inflammation. Notably, stannous fluoride stabilized with zinc phosphate appears to limit the growth of key periodontal pathogens-particularly Fusobacterium nucleatum, an important bridging organism in subgingival biofilms-and may alter the functional activity of dental plaque in ways that support improved periodontal health when compared with a standard sodium fluoride toothpaste.},
}
RevDate: 2026-07-31
CmpDate: 2026-07-31
Bacillus thuringiensis and nucleopolyhedrovirus combination against Spodoptera litura alters the cigar tobacco leaves microbiome during air curing.
Frontiers in microbiology, 17:1855531.
INTRODUCTION: Spodoptera litura continues feeding on cigar tobacco leaves during air curing, causing substantial economic losses. This study evaluated the synergistic efficacy of a Bacillus thuringiensis (Bt) and nucleopolyhedrovirus (NPV) combination for controlling Spodoptera litura and investigated its effects on the bacterial and fungal microbiomes of cigar tobacco leaves during air curing.
METHODS: Laboratory bioassays were conducted to determine the optimal Bt:NPV ratio and evaluate the synergistic toxicity. The selected formulation was subsequently validated under field conditions. Cigar tobacco leaves treated with the optimal Bt-NPV mixture were air-cured for 23 days, after which bacterial (16s rRNA) and fungal (ITS) communities were characterized using Illumina NovaSeq high-throughput sequencing.
RESULTS: The Bt:NPV mixture at a 4:1 ratio exhibited the strongest synergistic activity against second-instar Spodoptera litura, with an LC50 of 0.64 ml L[-1] and a co-toxicity coefficient of 153.8. Bt-NPV treatment significantly altered the leaf microbiomes by reducing microbial richness while increasing microbial diversity and evenness. Compared with the control, treated leaves showed increased relative abundances of Pantoea, Pseudomonas, and Eurotiales, together with reduced abundances of Staphylococcus and Cladosporiales. These findings demonstrate that Bt-NPV treatment effectively controlled Spodoptera litura while reshaping bacterial and fungal community composition during air curing.
DISCUSSION: The synergistic Bt-NPV formulation represents an effective and environmentally friendly strategy for controlling Spodoptera litura during air curing while promoting an ecological framework that may support leaf preservation. However, the direct effects of Bt-NPV-induced microbiome changes on cigar tobacco quality, aroma development, and chemical maturation were not evaluated and should be investigated through integrated chemical, metabolomic, and sensory analyses in future studies.
Additional Links: PMID-42534264
PubMed:
Citation:
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@article {pmid42534264,
year = {2026},
author = {Adam, A and Khan, R and Lu, B and Lin, T and Liao, H and Peng, L},
title = {Bacillus thuringiensis and nucleopolyhedrovirus combination against Spodoptera litura alters the cigar tobacco leaves microbiome during air curing.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1855531},
pmid = {42534264},
issn = {1664-302X},
abstract = {INTRODUCTION: Spodoptera litura continues feeding on cigar tobacco leaves during air curing, causing substantial economic losses. This study evaluated the synergistic efficacy of a Bacillus thuringiensis (Bt) and nucleopolyhedrovirus (NPV) combination for controlling Spodoptera litura and investigated its effects on the bacterial and fungal microbiomes of cigar tobacco leaves during air curing.
METHODS: Laboratory bioassays were conducted to determine the optimal Bt:NPV ratio and evaluate the synergistic toxicity. The selected formulation was subsequently validated under field conditions. Cigar tobacco leaves treated with the optimal Bt-NPV mixture were air-cured for 23 days, after which bacterial (16s rRNA) and fungal (ITS) communities were characterized using Illumina NovaSeq high-throughput sequencing.
RESULTS: The Bt:NPV mixture at a 4:1 ratio exhibited the strongest synergistic activity against second-instar Spodoptera litura, with an LC50 of 0.64 ml L[-1] and a co-toxicity coefficient of 153.8. Bt-NPV treatment significantly altered the leaf microbiomes by reducing microbial richness while increasing microbial diversity and evenness. Compared with the control, treated leaves showed increased relative abundances of Pantoea, Pseudomonas, and Eurotiales, together with reduced abundances of Staphylococcus and Cladosporiales. These findings demonstrate that Bt-NPV treatment effectively controlled Spodoptera litura while reshaping bacterial and fungal community composition during air curing.
DISCUSSION: The synergistic Bt-NPV formulation represents an effective and environmentally friendly strategy for controlling Spodoptera litura during air curing while promoting an ecological framework that may support leaf preservation. However, the direct effects of Bt-NPV-induced microbiome changes on cigar tobacco quality, aroma development, and chemical maturation were not evaluated and should be investigated through integrated chemical, metabolomic, and sensory analyses in future studies.},
}
RevDate: 2026-07-31
CmpDate: 2026-07-31
Comparative 16S rRNA Gene Amplicon Sequencing of the Fecal Microbiome in Pet Dogs and Cats of Different Breeds in Dhaka City, Bangladesh: With Preliminary Insights Into Zoonotic Relevance.
International journal of microbiology, 2026:8738439.
Dogs and cats are the most commonly kept pets, and the popularity of different breeds of them continues to increase in Dhaka City, Bangladesh. Pets naturally harbor a diverse gut microbiome that plays a significant role in digestion, immunity, and overall health. Although pets provide valuable companionship, their feces may occasionally harbor bacteria with zoonotic potential. However, little is known about the fecal microbial diversity and its zoonotic relevance in Bangladesh. This study investigated the diversity of pets' fecal microbiome using 16S rRNA metagenomics and explored the zoonotic bacterial taxa. Fecal samples were collected from 24 apparently healthy pets, including 12 dogs and 12 cats, from randomly selected households in Dhaka City. High-throughput sequencing revealed a diverse microbial community comprising 1,148 amplicon sequence variants (ASVs) distributed across 20 phyla and 258 genera. Although cats showed slightly higher microbial richness and diversity, both species shared common bacterial phyla such as Firmicutes, Proteobacteria, Actinobacteria, and Bacteroidetes. Relative abundance of bacterial taxa varied between pet species and among breeds rather than the presence of distinct microbial groups. Furthermore, Enterococcus cecorum, Schaalia canis, Campylobacter helveticus, and Sutterella wadsworthensis were the explored bacterial taxa with zoonotic relevance rather than a direct assessment of zoonotic risk; however, they were very low in number than the dominating bacteria. This study provides the first 16S rRNA-based metagenomic snapshot of the fecal microbiome of 24 urban pets in Bangladesh and highlights the need for routine microbial surveillance and public awareness about zoonoses.
Additional Links: PMID-42534357
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Citation:
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@article {pmid42534357,
year = {2026},
author = {Tania, MNT and Sabrin, MS and Mannan, MA and Islam, MM and Hossain, MT and Rahman, MH and Islam, MR and Sultana, S and Hossain, MS and Islam, M},
title = {Comparative 16S rRNA Gene Amplicon Sequencing of the Fecal Microbiome in Pet Dogs and Cats of Different Breeds in Dhaka City, Bangladesh: With Preliminary Insights Into Zoonotic Relevance.},
journal = {International journal of microbiology},
volume = {2026},
number = {},
pages = {8738439},
pmid = {42534357},
issn = {1687-918X},
abstract = {Dogs and cats are the most commonly kept pets, and the popularity of different breeds of them continues to increase in Dhaka City, Bangladesh. Pets naturally harbor a diverse gut microbiome that plays a significant role in digestion, immunity, and overall health. Although pets provide valuable companionship, their feces may occasionally harbor bacteria with zoonotic potential. However, little is known about the fecal microbial diversity and its zoonotic relevance in Bangladesh. This study investigated the diversity of pets' fecal microbiome using 16S rRNA metagenomics and explored the zoonotic bacterial taxa. Fecal samples were collected from 24 apparently healthy pets, including 12 dogs and 12 cats, from randomly selected households in Dhaka City. High-throughput sequencing revealed a diverse microbial community comprising 1,148 amplicon sequence variants (ASVs) distributed across 20 phyla and 258 genera. Although cats showed slightly higher microbial richness and diversity, both species shared common bacterial phyla such as Firmicutes, Proteobacteria, Actinobacteria, and Bacteroidetes. Relative abundance of bacterial taxa varied between pet species and among breeds rather than the presence of distinct microbial groups. Furthermore, Enterococcus cecorum, Schaalia canis, Campylobacter helveticus, and Sutterella wadsworthensis were the explored bacterial taxa with zoonotic relevance rather than a direct assessment of zoonotic risk; however, they were very low in number than the dominating bacteria. This study provides the first 16S rRNA-based metagenomic snapshot of the fecal microbiome of 24 urban pets in Bangladesh and highlights the need for routine microbial surveillance and public awareness about zoonoses.},
}
RevDate: 2026-07-31
CmpDate: 2026-07-31
Wohlfahrtiimonas chitiniclastica Bacteremia Associated With Maggot-Infested Ulcers and Tumor Lysis Syndrome in Ohio, USA: A Case Report.
Case reports in infectious diseases, 2026:6760136.
BACKGROUND: Wohlfahrtiimonas chitiniclastica is an emerging Gram-negative bacillus historically linked to larvae of the parasitic fly Wohlfahrtia magnifica. Although most human infections have been reported in Europe and Asia, cases are increasingly recognized in North America.
CASE SUMMARY: A 74-year-old man from Ohio presented with sepsis and maggot-infested decubitus ulcers. Blood cultures grew Gram-negative, oxidase-positive rods that could not be identified at the home institution. The isolate was referred to an outside hospital, where it was initially misidentified as Edwardsiella species before definitive identification as W. chitiniclastica by MALDI-TOF MS (Bruker MALDI Biotyper), confirmed by supplementary biochemical testing, 6 days after the initial culture draw. Additional testing identified the rare anaerobe Tissierella praeacuta. Blood cultures at the home institution also identified Proteus mirabilis and Staphylococcus aureus. The clinical course was complicated by metastatic cancer and spontaneous tumor lysis syndrome (uric acid 14.6 mg/dL, LDH 2157 U/L) that improved following rasburicase therapy. The patient received empiric intravenous piperacillin-tazobactam for approximately 24 days, followed by de-escalation to ceftriaxone. Follow-up blood cultures were sterile. Goals of care were transitioned to palliation, and the patient died on hospital day 30.
CONCLUSION: This case illustrates W. chitiniclastica bacteremia in Ohio, USA, and highlights diagnostic challenges including initial misidentification by conventional methods, the importance of MALDI-TOF MS for definitive identification, and possible vector adaptation to regional muscid fly species. The coisolation of T. praeacuta underscores the complex wound microbiome associated with chronic neglected ulcers.
Additional Links: PMID-42534410
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Citation:
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@article {pmid42534410,
year = {2026},
author = {Menon, A and Morelli, MK and Hulec, H},
title = {Wohlfahrtiimonas chitiniclastica Bacteremia Associated With Maggot-Infested Ulcers and Tumor Lysis Syndrome in Ohio, USA: A Case Report.},
journal = {Case reports in infectious diseases},
volume = {2026},
number = {},
pages = {6760136},
pmid = {42534410},
issn = {2090-6625},
abstract = {BACKGROUND: Wohlfahrtiimonas chitiniclastica is an emerging Gram-negative bacillus historically linked to larvae of the parasitic fly Wohlfahrtia magnifica. Although most human infections have been reported in Europe and Asia, cases are increasingly recognized in North America.
CASE SUMMARY: A 74-year-old man from Ohio presented with sepsis and maggot-infested decubitus ulcers. Blood cultures grew Gram-negative, oxidase-positive rods that could not be identified at the home institution. The isolate was referred to an outside hospital, where it was initially misidentified as Edwardsiella species before definitive identification as W. chitiniclastica by MALDI-TOF MS (Bruker MALDI Biotyper), confirmed by supplementary biochemical testing, 6 days after the initial culture draw. Additional testing identified the rare anaerobe Tissierella praeacuta. Blood cultures at the home institution also identified Proteus mirabilis and Staphylococcus aureus. The clinical course was complicated by metastatic cancer and spontaneous tumor lysis syndrome (uric acid 14.6 mg/dL, LDH 2157 U/L) that improved following rasburicase therapy. The patient received empiric intravenous piperacillin-tazobactam for approximately 24 days, followed by de-escalation to ceftriaxone. Follow-up blood cultures were sterile. Goals of care were transitioned to palliation, and the patient died on hospital day 30.
CONCLUSION: This case illustrates W. chitiniclastica bacteremia in Ohio, USA, and highlights diagnostic challenges including initial misidentification by conventional methods, the importance of MALDI-TOF MS for definitive identification, and possible vector adaptation to regional muscid fly species. The coisolation of T. praeacuta underscores the complex wound microbiome associated with chronic neglected ulcers.},
}
RevDate: 2026-07-31
Beyond omics: From descriptive profiling to causal and scalable design of fermentation microbiomes.
Fermentation microbiomes play essential roles in food production, feed preservation, waste valorization, and diverse sustainable industrial processes. Although multi-omics and systems biology have substantially advanced our understanding of their assembly, interactions, and functional dynamics, industrial translation remains constrained by fragmented datasets, limited causal validation, and transport constraints during scale-up. Large language models act as upper-level knowledge and workflow orchestrators, accelerating data integration, hybrid AI-mechanistic modeling, hypothesis generation, and perturbation-guided learning. Collectively, these advances enable fermentation microbiome research to move beyond descriptive omics toward mechanism-guided synthetic microbial community design, causal validation, and scalable biomanufacturing.
Additional Links: PMID-42534443
PubMed:
Citation:
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@article {pmid42534443,
year = {2026},
author = {Niu, D and Pang, H and Wang, X and Song, L and Zhang, J and Terry, A and Li, J and Cao, J and Liu, Q and Han, D and Wang, J and Kim, JG and Ataku, K and Bureenok, S and Tan, Z and Bai, F and Shao, T and Huhe, T and Wang, L and Han, P and Xu, C and Yang, F and Cai, Y},
title = {Beyond omics: From descriptive profiling to causal and scalable design of fermentation microbiomes.},
journal = {iMeta},
volume = {},
number = {},
pages = {e70161},
pmid = {42534443},
issn = {2770-596X},
abstract = {Fermentation microbiomes play essential roles in food production, feed preservation, waste valorization, and diverse sustainable industrial processes. Although multi-omics and systems biology have substantially advanced our understanding of their assembly, interactions, and functional dynamics, industrial translation remains constrained by fragmented datasets, limited causal validation, and transport constraints during scale-up. Large language models act as upper-level knowledge and workflow orchestrators, accelerating data integration, hybrid AI-mechanistic modeling, hypothesis generation, and perturbation-guided learning. Collectively, these advances enable fermentation microbiome research to move beyond descriptive omics toward mechanism-guided synthetic microbial community design, causal validation, and scalable biomanufacturing.},
}
RevDate: 2026-07-31
CmpDate: 2026-07-31
Knowledge mapping and bibliometric analysis of metabolic phenotypes in childhood and adolescent obesity: research hotspots and emerging trends from 2000 to 2026.
Frontiers in public health, 14:1907434.
BACKGROUND: Childhood and adolescent obesity is increasingly understood as a heterogeneous condition in which excess adiposity may be accompanied by distinct cardiometabolic phenotypes. Metabolically healthy obesity and metabolically unhealthy obesity have become important concepts for risk stratification, but the overall knowledge structure and emerging research directions in this field remain insufficiently mapped.
METHODS: Records on metabolic phenotypes in childhood and adolescent obesity published between 1 January 2000 and 20 February 2026 were retrieved from the Web of Science Core Collection and PubMed on 20 February 2026. English-language articles and reviews were independently screened by two researchers. After database merging, deduplication and data cleaning, 4,963 records were retained for bibliometric analysis, including 4,384 WoSCC-retained records and 579 PubMed-only records. CiteSpace 6.4. R1, VOSviewer 1.6.20, R 4.5.2 and bibliometrix 5.4.1 were used to analyze annual publication trends, country and institutional collaboration, author and reference co-citation, keyword co-occurrence, clustering and burst terms. Citation-dependent analyses were based on WoSCC-retained records with complete cited-reference metadata.
RESULTS: Publication output increased overall and showed three broad phases: an initial phase centered on BMI criteria, obesity prevalence and metabolic syndrome recognition; a rapid growth phase associated with insulin resistance, glucose-lipid abnormalities and metabolic heterogeneity; and a recent consolidation phase emphasizing phenotype transition, gut microbiota, non-alcoholic fatty liver disease, physical activity, cardiometabolic health and precision intervention. The United States, Spain, China and England were leading contributors, although cross-regional collaboration remained uneven. Co-cited references, author networks and keyword clusters indicated that the field has moved from weight-based classification toward integrated cardiometabolic risk identification, with emerging attention to central adiposity, visceral fat, microbiome-related mechanisms and phenotype-guided management.
CONCLUSION: Research on metabolic phenotypes in childhood and adolescent obesity is shifting from BMI-centered description toward risk-stratified interpretation of metabolic heterogeneity. Future studies should harmonize pediatric phenotype definitions, strengthen multicenter longitudinal cohorts and integrate body composition, fat distribution, insulin sensitivity, liver fat, inflammatory markers, lifestyle exposure and gut microbiota to support early identification and precision prevention of cardiometabolic risk.
Additional Links: PMID-42534462
PubMed:
Citation:
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@article {pmid42534462,
year = {2026},
author = {Ren, G and Feng, Z and Wang, X and He, J and Yu, Z and Cao, L},
title = {Knowledge mapping and bibliometric analysis of metabolic phenotypes in childhood and adolescent obesity: research hotspots and emerging trends from 2000 to 2026.},
journal = {Frontiers in public health},
volume = {14},
number = {},
pages = {1907434},
pmid = {42534462},
issn = {2296-2565},
mesh = {Humans ; *Bibliometrics ; Phenotype ; Adolescent ; *Pediatric Obesity/epidemiology/metabolism ; Child ; },
abstract = {BACKGROUND: Childhood and adolescent obesity is increasingly understood as a heterogeneous condition in which excess adiposity may be accompanied by distinct cardiometabolic phenotypes. Metabolically healthy obesity and metabolically unhealthy obesity have become important concepts for risk stratification, but the overall knowledge structure and emerging research directions in this field remain insufficiently mapped.
METHODS: Records on metabolic phenotypes in childhood and adolescent obesity published between 1 January 2000 and 20 February 2026 were retrieved from the Web of Science Core Collection and PubMed on 20 February 2026. English-language articles and reviews were independently screened by two researchers. After database merging, deduplication and data cleaning, 4,963 records were retained for bibliometric analysis, including 4,384 WoSCC-retained records and 579 PubMed-only records. CiteSpace 6.4. R1, VOSviewer 1.6.20, R 4.5.2 and bibliometrix 5.4.1 were used to analyze annual publication trends, country and institutional collaboration, author and reference co-citation, keyword co-occurrence, clustering and burst terms. Citation-dependent analyses were based on WoSCC-retained records with complete cited-reference metadata.
RESULTS: Publication output increased overall and showed three broad phases: an initial phase centered on BMI criteria, obesity prevalence and metabolic syndrome recognition; a rapid growth phase associated with insulin resistance, glucose-lipid abnormalities and metabolic heterogeneity; and a recent consolidation phase emphasizing phenotype transition, gut microbiota, non-alcoholic fatty liver disease, physical activity, cardiometabolic health and precision intervention. The United States, Spain, China and England were leading contributors, although cross-regional collaboration remained uneven. Co-cited references, author networks and keyword clusters indicated that the field has moved from weight-based classification toward integrated cardiometabolic risk identification, with emerging attention to central adiposity, visceral fat, microbiome-related mechanisms and phenotype-guided management.
CONCLUSION: Research on metabolic phenotypes in childhood and adolescent obesity is shifting from BMI-centered description toward risk-stratified interpretation of metabolic heterogeneity. Future studies should harmonize pediatric phenotype definitions, strengthen multicenter longitudinal cohorts and integrate body composition, fat distribution, insulin sensitivity, liver fat, inflammatory markers, lifestyle exposure and gut microbiota to support early identification and precision prevention of cardiometabolic risk.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Bibliometrics
Phenotype
Adolescent
*Pediatric Obesity/epidemiology/metabolism
Child
RevDate: 2026-07-31
CmpDate: 2026-07-31
Mechanistic and clinical investigation of Jiajiang Xuming decoction in multi-modal programmed cell death in stroke-associated pneumonia.
Frontiers in cell and developmental biology, 14:1889833.
BACKGROUND: Stroke-Associated Pneumonia (SAP) is one of the leading causes of sepsis and ICU mortality among stroke patients, attributed to dysregulated immune responses as well as multiple MODES of cell death. Jiajiang Xuming Decoction (JXD) is a traditional Chinese medicine (TCM) formula to treat the symptoms of Wind-Phlegm-Stasis Obstruction Syndrome, blamed for all SAP-related sepsis.
METHODS: A single-centre retrospective cohort study was conducted in 100 ICU patients with microbiologically confirmed sepsis (Sepsis-3 criteria): 58 Stroke-Associated Pneumonia (SAP) and 42 non-SAP sepsis, compared to thirty healthy controls. On admission, Day 3 and Day 7, serial inflammatory markers (IL-6, IL-1β, TNF-α PCT CRP) and organ-function indicators were measured (hepatic: ALT AST; renal: creatinine (BUN); cardiac: cTnI† NT-proBNP). Therapeutic efficacy of JXD was evaluated in a propensity-score-matched (JXD n = 29; conventional treatment n = 29) sub-cohort. Mechanistic evidence were derived from scRNA-seq and an in vitro LPS + OGD cell model as well as ferroptosis characterisation (GEO: GSM5319987).
RESULTS: Compared to non-SAP sepsis, SAP patients had significantly higher levels of inflammatory cytokines, markers of hepatic injury (ALT, AST), renal impairment (creatinine, BUN), and cardiac injury (cTnI, NT-proBNP) all P < 0.001; FDR q < 0.001). An AUC = 0.872 for SAP diagnosis with a combination of four markers (PCT + IL-6 + ALT + creatinine) was established. Supplemental JXD therapy provided a significant advantage over conventional treatment in Day-7 clinical improvement rate (72.4% vs. 48.3%, P = 0.048) and shortened ICU stay (12.1 vs. 16.3 days, P = 0.002), along with markers of mode microbiome-related inflammation and injury reduction in this population of patients with acute disturbances post-septic organs (Galluzzi et al., Cell Death Differ, 2018, 25(3), 486-541). JXD basically inhibited apoptosis (CASP3), pyroptosis (NLRP3), necroptosis (RIPK3) in vitro, and reversed ferroptotic death by restoring GPX4, downregulating MDA, as well as inhibiting ACSL4.
CONCLUSION: Multi-organ dysfunction biomarkers independently predicts sepsis sequelae post-SAP (AUC = 0.872)) and track treatments response Conclusions: JXD modulates a number of cellular death pathways in vitro, and markedly improves clinical outcomes in SAP-associated sepsis.
Additional Links: PMID-42534689
PubMed:
Citation:
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@article {pmid42534689,
year = {2026},
author = {Li, Z and Wang, J and Hong, Z and Li, M and Liu, T and Wang, Y and Men, L},
title = {Mechanistic and clinical investigation of Jiajiang Xuming decoction in multi-modal programmed cell death in stroke-associated pneumonia.},
journal = {Frontiers in cell and developmental biology},
volume = {14},
number = {},
pages = {1889833},
pmid = {42534689},
issn = {2296-634X},
abstract = {BACKGROUND: Stroke-Associated Pneumonia (SAP) is one of the leading causes of sepsis and ICU mortality among stroke patients, attributed to dysregulated immune responses as well as multiple MODES of cell death. Jiajiang Xuming Decoction (JXD) is a traditional Chinese medicine (TCM) formula to treat the symptoms of Wind-Phlegm-Stasis Obstruction Syndrome, blamed for all SAP-related sepsis.
METHODS: A single-centre retrospective cohort study was conducted in 100 ICU patients with microbiologically confirmed sepsis (Sepsis-3 criteria): 58 Stroke-Associated Pneumonia (SAP) and 42 non-SAP sepsis, compared to thirty healthy controls. On admission, Day 3 and Day 7, serial inflammatory markers (IL-6, IL-1β, TNF-α PCT CRP) and organ-function indicators were measured (hepatic: ALT AST; renal: creatinine (BUN); cardiac: cTnI† NT-proBNP). Therapeutic efficacy of JXD was evaluated in a propensity-score-matched (JXD n = 29; conventional treatment n = 29) sub-cohort. Mechanistic evidence were derived from scRNA-seq and an in vitro LPS + OGD cell model as well as ferroptosis characterisation (GEO: GSM5319987).
RESULTS: Compared to non-SAP sepsis, SAP patients had significantly higher levels of inflammatory cytokines, markers of hepatic injury (ALT, AST), renal impairment (creatinine, BUN), and cardiac injury (cTnI, NT-proBNP) all P < 0.001; FDR q < 0.001). An AUC = 0.872 for SAP diagnosis with a combination of four markers (PCT + IL-6 + ALT + creatinine) was established. Supplemental JXD therapy provided a significant advantage over conventional treatment in Day-7 clinical improvement rate (72.4% vs. 48.3%, P = 0.048) and shortened ICU stay (12.1 vs. 16.3 days, P = 0.002), along with markers of mode microbiome-related inflammation and injury reduction in this population of patients with acute disturbances post-septic organs (Galluzzi et al., Cell Death Differ, 2018, 25(3), 486-541). JXD basically inhibited apoptosis (CASP3), pyroptosis (NLRP3), necroptosis (RIPK3) in vitro, and reversed ferroptotic death by restoring GPX4, downregulating MDA, as well as inhibiting ACSL4.
CONCLUSION: Multi-organ dysfunction biomarkers independently predicts sepsis sequelae post-SAP (AUC = 0.872)) and track treatments response Conclusions: JXD modulates a number of cellular death pathways in vitro, and markedly improves clinical outcomes in SAP-associated sepsis.},
}
RevDate: 2026-07-31
CmpDate: 2026-07-31
Metagenomic insights into potential PET hydrolases from Antarctic soils and rhizospheres.
Frontiers in microbiology, 17:1749101.
Polyethylene terephthalate (PET) is a persistent synthetic polymer that is increasingly detected in terrestrial environments, where it influences soil microbial activity and carbon cycling. Microorganisms capable of hydrolyzing PET and related polyesters constitute a valuable enzymatic resource for developing low-temperature biocatalysts and for advancing the understanding of soil functional adaptation to plastic pollution. Here, we conducted a metagenomic analysis of soil and rhizosphere samples from the Antarctic vascular plants Deschampsia antarctica and Colobanthus quitensis, as sources of microbial enzymes with potential PET-hydrolytic activity. Hidden Markov Models constructed from experimentally validated PET hydrolases identified 152 putative PET hydrolases (pPETHs) spanning multiple protein families. Four candidates exhibited amino acid motifs characteristic of Ideonella sakaiensis PETase, including the conserved alpha/beta hydrolase fold and the Ser-His-Asp catalytic triad. One candidate from a Duganella genome also contained a tryptophan residue associated with efficient product release during PET hydrolysis. Molecular docking and molecular dynamics analyses revealed that candidates retain the core catalytic architecture of established PET hydrolases, while simultaneously displaying structural signatures of cold adaptation. These findings demonstrate the diversity of PET-hydrolase-like genes within Antarctic rhizosphere and soil microbiomes, broadening the current understanding of microbial enzymatic potential under cold, oligotrophic conditions. The identified sequences highlight the rhizosphere as a reservoir of functional diversity relevant to soil biotechnology, cold-adapted catalysis, and microbial strategies for transforming recalcitrant carbon substrates.
Additional Links: PMID-42534735
PubMed:
Citation:
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@article {pmid42534735,
year = {2026},
author = {Berríos-Farías, V and Guajardo-Leiva, S and Gallardo-Cerda, J and Galbán-Malagón, C and Egas, C and Molina-Montenegro, MA and Castro-Nallar, E},
title = {Metagenomic insights into potential PET hydrolases from Antarctic soils and rhizospheres.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1749101},
pmid = {42534735},
issn = {1664-302X},
abstract = {Polyethylene terephthalate (PET) is a persistent synthetic polymer that is increasingly detected in terrestrial environments, where it influences soil microbial activity and carbon cycling. Microorganisms capable of hydrolyzing PET and related polyesters constitute a valuable enzymatic resource for developing low-temperature biocatalysts and for advancing the understanding of soil functional adaptation to plastic pollution. Here, we conducted a metagenomic analysis of soil and rhizosphere samples from the Antarctic vascular plants Deschampsia antarctica and Colobanthus quitensis, as sources of microbial enzymes with potential PET-hydrolytic activity. Hidden Markov Models constructed from experimentally validated PET hydrolases identified 152 putative PET hydrolases (pPETHs) spanning multiple protein families. Four candidates exhibited amino acid motifs characteristic of Ideonella sakaiensis PETase, including the conserved alpha/beta hydrolase fold and the Ser-His-Asp catalytic triad. One candidate from a Duganella genome also contained a tryptophan residue associated with efficient product release during PET hydrolysis. Molecular docking and molecular dynamics analyses revealed that candidates retain the core catalytic architecture of established PET hydrolases, while simultaneously displaying structural signatures of cold adaptation. These findings demonstrate the diversity of PET-hydrolase-like genes within Antarctic rhizosphere and soil microbiomes, broadening the current understanding of microbial enzymatic potential under cold, oligotrophic conditions. The identified sequences highlight the rhizosphere as a reservoir of functional diversity relevant to soil biotechnology, cold-adapted catalysis, and microbial strategies for transforming recalcitrant carbon substrates.},
}
RevDate: 2026-07-31
CmpDate: 2026-07-31
Gut microbiota derived indoles are altered and associate with immune activation in moderate and severe carotid stenosis.
Frontiers in immunology, 17:1796312.
BACKGROUND: An imbalance of gut microbiota, their metabolites as well as inflammatory mediators have been increasingly linked to both atherosclerosis and stroke. However, data on microbiota derived tryptophan and histidine metabolites in carotid atherosclerosis are scarce.
PURPOSE: We investigated serum microbiota derived indoles, imidazole propionate (ImP) and trimethylamine N-oxide (TMAO), representing three distinct gut bacterial-related metabolites, in patients with carotid atherosclerosis compared with healthy controls with normal findings on carotid ultrasound. We aimed to examine their relation to plaque characteristics, immune activation markers and traditional cardiovascular risk factors.
METHODS: Thirty patients scheduled for carotid endarterectomy and 18 control subjects were included in this cross-sectional study. Carotid arteries were investigated with ultrasound. Indoles, ImP and TMAO were analyzed by liquid chromatography-tandem mass spectrometry, and Lipopolysaccharide (LPS) by a Limulus Amebocyte Lysate chromogenic assay.
RESULTS: Compared to controls, patients exhibited lower levels of indole-3-propionic acid (IPA) (p=0.004) and indole-3-acetic acid (IAA) (p = 0.030). In patients, higher levels of indole metabolites were associated with lower C-reactive protein. ImP and TMAO did not differ between patients and controls.
CONCLUSION: Patients with carotid atherosclerosis exhibited reduced serum concentrations of IPA and IAA, thought to have anti-inflammatory effects, and increased inflammatory markers, possibly suggesting disruptions in the gut-vascular-immune axis.
Additional Links: PMID-42534803
PubMed:
Citation:
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@article {pmid42534803,
year = {2026},
author = {Stø, K and Skagen, K and Bjerkeli, V and Ueland, PM and Hov, JR and Trøseid, M and Aukrust, P and Ueland, T and Halvorsen, B and Skjelland, M},
title = {Gut microbiota derived indoles are altered and associate with immune activation in moderate and severe carotid stenosis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1796312},
pmid = {42534803},
issn = {1664-3224},
mesh = {Humans ; Male ; *Indoles/blood/metabolism ; *Carotid Stenosis/immunology/microbiology/metabolism/surgery ; Female ; *Gastrointestinal Microbiome/immunology ; Aged ; Biomarkers/blood ; Cross-Sectional Studies ; Middle Aged ; Methylamines/blood ; Severity of Illness Index ; },
abstract = {BACKGROUND: An imbalance of gut microbiota, their metabolites as well as inflammatory mediators have been increasingly linked to both atherosclerosis and stroke. However, data on microbiota derived tryptophan and histidine metabolites in carotid atherosclerosis are scarce.
PURPOSE: We investigated serum microbiota derived indoles, imidazole propionate (ImP) and trimethylamine N-oxide (TMAO), representing three distinct gut bacterial-related metabolites, in patients with carotid atherosclerosis compared with healthy controls with normal findings on carotid ultrasound. We aimed to examine their relation to plaque characteristics, immune activation markers and traditional cardiovascular risk factors.
METHODS: Thirty patients scheduled for carotid endarterectomy and 18 control subjects were included in this cross-sectional study. Carotid arteries were investigated with ultrasound. Indoles, ImP and TMAO were analyzed by liquid chromatography-tandem mass spectrometry, and Lipopolysaccharide (LPS) by a Limulus Amebocyte Lysate chromogenic assay.
RESULTS: Compared to controls, patients exhibited lower levels of indole-3-propionic acid (IPA) (p=0.004) and indole-3-acetic acid (IAA) (p = 0.030). In patients, higher levels of indole metabolites were associated with lower C-reactive protein. ImP and TMAO did not differ between patients and controls.
CONCLUSION: Patients with carotid atherosclerosis exhibited reduced serum concentrations of IPA and IAA, thought to have anti-inflammatory effects, and increased inflammatory markers, possibly suggesting disruptions in the gut-vascular-immune axis.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Male
*Indoles/blood/metabolism
*Carotid Stenosis/immunology/microbiology/metabolism/surgery
Female
*Gastrointestinal Microbiome/immunology
Aged
Biomarkers/blood
Cross-Sectional Studies
Middle Aged
Methylamines/blood
Severity of Illness Index
RevDate: 2026-07-31
CmpDate: 2026-07-31
Dynamics of archaeal diversity and functionality in the piglet gut microbiome under common antimicrobial treatments.
Frontiers in cellular and infection microbiology, 16:1833734.
INTRODUCTION: The gut microbiota comprises a diverse and dynamic community of microorganisms that collectively enhance host metabolism, physiology, and overall functionality. In this context, the swine archaeome remains largely underexplored despite growing evidence that archaea may greatly influence host health. Advances in high-throughput approaches provide new opportunities to reveal the dynamics and composition of archaea. Herein, we uncover the taxonomic and functional landscape of the piglet archaeome during the weaning transition under multiple experimental conditions, integrating shotgun metagenomic and metatranscriptomic analyses to elucidate its contribution to gut microbial ecology.
METHODS: The seven experimental conditions included four antibiotic treatments for post-weaning diarrhoea (trimethoprim/sulfamethoxazole, colistin, gentamicin, amoxicillin), an oral vaccine, acidifiers in drinking water, and a no-intervention group. A total of 280 faecal samples were collected longitudinally one day before weaning (ST1), three days (ST2), two weeks (ST3), and four weeks (ST4) after the start of the treatment. Treatment was initiated eleven days after arrival at the experimental farm following the onset of clinical signs. Shotgun metagenomics was used to assess archaeal taxonomic diversity and recover archaeal metagenome-assembled genomes (aMAGs), while metatranscriptomics was integrated to assess differentially expressed genes at ST1, ST2, and ST4.
RESULTS: The results revealed archaea as the second most abundant microorganism, exhibiting a longitudinal increase in diversity over the experimental time. The most predominant genus was Methanobrevibacter, including Methanobrevibacter smithii. Eleven high-quality aMAGs were recovered, belonging to the Methanobacteriota and Thermoplasmatota phyla. Genome-inferred functional analyses revealed that the predominant metabolic processes included the biosynthesis of nucleic acids, amino acids, organic anions, and vitamins. Additional functional traits suggested potential roles in the degradation of sugars, amino acids, and antibiotics were also observed. Moreover, significant differences were detected on the archaeal metatranscriptome between the experimental groups treated with antibiotics and the rest of the groups, underscoring their response to changes in microbial interactions, substrate availability and, in some cases, direct effect of the antimicrobials on metabolic pathways.
DISCUSSION: Altogether, this study highlights the biological significance of archaeal dynamics during initial life stages and demonstrates how combining metagenomics and metatranscriptomics uncovers their functional potential and the pathways actively expressed in the piglets' gut.
Additional Links: PMID-42534899
PubMed:
Citation:
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@article {pmid42534899,
year = {2026},
author = {Guitart-Matas, J and Bravo, M and Tort-Miró, C and Giler-Baquerizo, N and Fraile, L and Caldas-Ramayo, Y and Ballester, M and Migura-Garcia, L},
title = {Dynamics of archaeal diversity and functionality in the piglet gut microbiome under common antimicrobial treatments.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1833734},
pmid = {42534899},
issn = {2235-2988},
mesh = {Animals ; *Archaea/classification/genetics/drug effects ; Swine ; Metagenomics ; *Gastrointestinal Microbiome/drug effects ; Feces/microbiology ; Metagenome ; Weaning ; *Biodiversity ; *Anti-Infective Agents/administration & dosage/pharmacology ; Gene Expression Profiling ; Phylogeny ; Diarrhea/drug therapy/veterinary ; Anti-Bacterial Agents ; },
abstract = {INTRODUCTION: The gut microbiota comprises a diverse and dynamic community of microorganisms that collectively enhance host metabolism, physiology, and overall functionality. In this context, the swine archaeome remains largely underexplored despite growing evidence that archaea may greatly influence host health. Advances in high-throughput approaches provide new opportunities to reveal the dynamics and composition of archaea. Herein, we uncover the taxonomic and functional landscape of the piglet archaeome during the weaning transition under multiple experimental conditions, integrating shotgun metagenomic and metatranscriptomic analyses to elucidate its contribution to gut microbial ecology.
METHODS: The seven experimental conditions included four antibiotic treatments for post-weaning diarrhoea (trimethoprim/sulfamethoxazole, colistin, gentamicin, amoxicillin), an oral vaccine, acidifiers in drinking water, and a no-intervention group. A total of 280 faecal samples were collected longitudinally one day before weaning (ST1), three days (ST2), two weeks (ST3), and four weeks (ST4) after the start of the treatment. Treatment was initiated eleven days after arrival at the experimental farm following the onset of clinical signs. Shotgun metagenomics was used to assess archaeal taxonomic diversity and recover archaeal metagenome-assembled genomes (aMAGs), while metatranscriptomics was integrated to assess differentially expressed genes at ST1, ST2, and ST4.
RESULTS: The results revealed archaea as the second most abundant microorganism, exhibiting a longitudinal increase in diversity over the experimental time. The most predominant genus was Methanobrevibacter, including Methanobrevibacter smithii. Eleven high-quality aMAGs were recovered, belonging to the Methanobacteriota and Thermoplasmatota phyla. Genome-inferred functional analyses revealed that the predominant metabolic processes included the biosynthesis of nucleic acids, amino acids, organic anions, and vitamins. Additional functional traits suggested potential roles in the degradation of sugars, amino acids, and antibiotics were also observed. Moreover, significant differences were detected on the archaeal metatranscriptome between the experimental groups treated with antibiotics and the rest of the groups, underscoring their response to changes in microbial interactions, substrate availability and, in some cases, direct effect of the antimicrobials on metabolic pathways.
DISCUSSION: Altogether, this study highlights the biological significance of archaeal dynamics during initial life stages and demonstrates how combining metagenomics and metatranscriptomics uncovers their functional potential and the pathways actively expressed in the piglets' gut.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Archaea/classification/genetics/drug effects
Swine
Metagenomics
*Gastrointestinal Microbiome/drug effects
Feces/microbiology
Metagenome
Weaning
*Biodiversity
*Anti-Infective Agents/administration & dosage/pharmacology
Gene Expression Profiling
Phylogeny
Diarrhea/drug therapy/veterinary
Anti-Bacterial Agents
RevDate: 2026-07-31
CmpDate: 2026-07-31
Reappraising traumatic brain injury and ventilator-associated pneumonia through the brain-lung-immune-microbiome axis.
Frontiers in neurology, 17:1844556.
Ventilator-associated pneumonia (VAP) remains the most prevalent and lethal infectious complication among patients with severe traumatic brain injury (TBI) requiring invasive mechanical ventilation. Historically, the pathogenesis of VAP within neurocritical care settings has been attributed to mechanical and physical factors. This traditional paradigm posits that the endotracheal tube bypasses natural upper airway defenses, impairs glottic reflexes, and allows for the continuous micro-aspiration of pathogen-laden oropharyngeal secretions into the lower respiratory tract. However, this biomechanical model fails to adequately explain the disproportionately high incidence of VAP in TBI patients compared to other critically ill populations. A profound conceptual paradigm shift is transitioning the focus from isolated airway mechanics toward multidimensional biological construct: the Brain-Lung-Immune-Microbiome Axis. The fundamental catalyst for respiratory vulnerability following neurotrauma is central nervous system injury-induced immunodepression syndrome (CIDS), a profound systemic immune remodeling driven by acute neuroendocrine and autonomic dysregulation, as well as the translocation of pathogenic gut microbiota to the lungs. By synthesizing evidence from neuroimmunology, microbiology, and critical care medicine, this narrative review details the tripartite interplay of neurological trauma, immune exhaustion, and microbiome evolution. Ultimately, this review evaluates emerging host-directed immunomodulatory therapies and microbiome-targeted interventions, advocating for a critical transition from simple mechanical airway hygiene to precision immuno-microbiome therapeutics in the neuro-intensive care unit.
Additional Links: PMID-42534910
PubMed:
Citation:
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@article {pmid42534910,
year = {2026},
author = {Mao, L and Yang, Z and Jiang, F},
title = {Reappraising traumatic brain injury and ventilator-associated pneumonia through the brain-lung-immune-microbiome axis.},
journal = {Frontiers in neurology},
volume = {17},
number = {},
pages = {1844556},
pmid = {42534910},
issn = {1664-2295},
abstract = {Ventilator-associated pneumonia (VAP) remains the most prevalent and lethal infectious complication among patients with severe traumatic brain injury (TBI) requiring invasive mechanical ventilation. Historically, the pathogenesis of VAP within neurocritical care settings has been attributed to mechanical and physical factors. This traditional paradigm posits that the endotracheal tube bypasses natural upper airway defenses, impairs glottic reflexes, and allows for the continuous micro-aspiration of pathogen-laden oropharyngeal secretions into the lower respiratory tract. However, this biomechanical model fails to adequately explain the disproportionately high incidence of VAP in TBI patients compared to other critically ill populations. A profound conceptual paradigm shift is transitioning the focus from isolated airway mechanics toward multidimensional biological construct: the Brain-Lung-Immune-Microbiome Axis. The fundamental catalyst for respiratory vulnerability following neurotrauma is central nervous system injury-induced immunodepression syndrome (CIDS), a profound systemic immune remodeling driven by acute neuroendocrine and autonomic dysregulation, as well as the translocation of pathogenic gut microbiota to the lungs. By synthesizing evidence from neuroimmunology, microbiology, and critical care medicine, this narrative review details the tripartite interplay of neurological trauma, immune exhaustion, and microbiome evolution. Ultimately, this review evaluates emerging host-directed immunomodulatory therapies and microbiome-targeted interventions, advocating for a critical transition from simple mechanical airway hygiene to precision immuno-microbiome therapeutics in the neuro-intensive care unit.},
}
RevDate: 2026-07-31
CmpDate: 2026-07-31
Stage-associated enrichment of Dietzia in the conjunctival microbiome of calves with infectious bovine keratoconjunctivitis: a cross-sectional microbiome and genomic characterization study.
Frontiers in veterinary science, 13:1890304.
BACKGROUND: Infectious bovine keratoconjunctivitis (IBK) is a major ocular disease of cattle. Although the bovine conjunctival microbiome has been studied in IBK-affected and healthy animals, microbiome patterns across clinically defined lesion stages remain poorly understood, and the occurrence of Dietzia on the diseased bovine ocular surface has not been systematically investigated.
METHODS: This cross-sectional study enrolled 57 calves from two commercial farms in Kazakhstan, stratified across six clinical stages of IBK severity (0-5). Conjunctival swabs were analyzed by culture-based Dietzia recovery and 16S rRNA gene amplicon sequencing. Alpha and beta diversity were assessed using standard ecological metrics, and stage-associated Dietzia abundance was evaluated using Kruskal-Wallis testing and quadratic regression. Two representative Dietzia isolates were subjected to whole-genome sequencing, phylogenomic placement and homology-based screening against resistance and virulence-factor databases.
RESULTS: IBK stage was not associated with significant global restructuring of the conjunctival microbiome. Alpha-diversity indices did not differ significantly across stages, and PERMANOVA showed no stage-specific beta-diversity separation (R [2] = 0.098, p = 0.323). In contrast, Dietzia showed a non-linear stage-associated abundance pattern in a quadratic model, with the highest reads-per-million (RPM) abundance in samples classified at stages 2-3, which are clinically characterized by active corneal ulceration. Culture-based recovery of Dietzia was frequent overall (42/57 samples; 73.7%) but showed no monotonic relationship with lesion severity. Whole-genome analysis of two isolates revealed phylogenomic heterogeneity: one isolate clustered within phylogenomic Group A, whereas the second was positioned outside the four major Dietzia groups, adjacent to the divergent animal isolate Dietzia sp. B32. Both genomes contained conserved stress-response, regulatory and metabolic homologues, without clear evidence of specialized virulence systems.
CONCLUSION: IBK lesion stage was not associated with major alpha- or beta-diversity restructuring, but Dietzia displayed stage-associated enrichment during the active ulcerative phase. These findings support interpretation of bovine ocular Dietzia as a surface-accessible opportunistic colonizer rather than a confirmed primary aetiological agent of IBK.
Additional Links: PMID-42534989
PubMed:
Citation:
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@article {pmid42534989,
year = {2026},
author = {Abdigulov, B and Ordabayeva, A and Kuibagarov, M and Suminov, A and Ilderbayev, O and Dauletov, A and Kadyrova, M and Abdrakhmanov, S and Vergnaud, G and Shevtsov, A},
title = {Stage-associated enrichment of Dietzia in the conjunctival microbiome of calves with infectious bovine keratoconjunctivitis: a cross-sectional microbiome and genomic characterization study.},
journal = {Frontiers in veterinary science},
volume = {13},
number = {},
pages = {1890304},
pmid = {42534989},
issn = {2297-1769},
abstract = {BACKGROUND: Infectious bovine keratoconjunctivitis (IBK) is a major ocular disease of cattle. Although the bovine conjunctival microbiome has been studied in IBK-affected and healthy animals, microbiome patterns across clinically defined lesion stages remain poorly understood, and the occurrence of Dietzia on the diseased bovine ocular surface has not been systematically investigated.
METHODS: This cross-sectional study enrolled 57 calves from two commercial farms in Kazakhstan, stratified across six clinical stages of IBK severity (0-5). Conjunctival swabs were analyzed by culture-based Dietzia recovery and 16S rRNA gene amplicon sequencing. Alpha and beta diversity were assessed using standard ecological metrics, and stage-associated Dietzia abundance was evaluated using Kruskal-Wallis testing and quadratic regression. Two representative Dietzia isolates were subjected to whole-genome sequencing, phylogenomic placement and homology-based screening against resistance and virulence-factor databases.
RESULTS: IBK stage was not associated with significant global restructuring of the conjunctival microbiome. Alpha-diversity indices did not differ significantly across stages, and PERMANOVA showed no stage-specific beta-diversity separation (R [2] = 0.098, p = 0.323). In contrast, Dietzia showed a non-linear stage-associated abundance pattern in a quadratic model, with the highest reads-per-million (RPM) abundance in samples classified at stages 2-3, which are clinically characterized by active corneal ulceration. Culture-based recovery of Dietzia was frequent overall (42/57 samples; 73.7%) but showed no monotonic relationship with lesion severity. Whole-genome analysis of two isolates revealed phylogenomic heterogeneity: one isolate clustered within phylogenomic Group A, whereas the second was positioned outside the four major Dietzia groups, adjacent to the divergent animal isolate Dietzia sp. B32. Both genomes contained conserved stress-response, regulatory and metabolic homologues, without clear evidence of specialized virulence systems.
CONCLUSION: IBK lesion stage was not associated with major alpha- or beta-diversity restructuring, but Dietzia displayed stage-associated enrichment during the active ulcerative phase. These findings support interpretation of bovine ocular Dietzia as a surface-accessible opportunistic colonizer rather than a confirmed primary aetiological agent of IBK.},
}
RevDate: 2026-07-31
CmpDate: 2026-07-31
Multi-habitat microbiome profiling identifies habitat-dependent alterations and complementary discriminatory information in urolithiasis.
Frontiers in cellular and infection microbiology, 16:1853826.
BACKGROUND: Urolithiasis has been associated with microbial alterations in individual anatomical niches; however, whether microbial signatures across urinary, intestinal, and oral habitats represent shared, site-specific, or complementary disease-associated information remains unclear. This study aimed to characterize multi-habitat microbiome alterations associated with urolithiasis and to evaluate whether integrated multi-site profiling captures internally cross-validated disease-associated microbial information.
METHODS: Salivary, clean-catch midstream urinary, and fecal samples were collected from 80 stone formers (SF) and 40 healthy controls (HC) and profiled using 16S rRNA gene sequencing. After quality control, the final analytical dataset comprised 101 urinary, 117 fecal, and 120 salivary samples, with 98 participants contributing complete three-habitat profiles. Habitat-specific alpha- and beta-diversity, taxonomic alterations, and exploratory inferred-network and predicted-functional profiles were evaluated. Random forest models were assessed using repeated nested stratified cross-validation to examine internal discriminatory information from single- and multi-habitat microbial features.
RESULTS: Urolithiasis was associated with statistically detectable but modest differences in microbial community structure across all three habitats, with small PERMANOVA effect sizes and significant dispersion differences. Fecal samples from SF showed significantly reduced richness, including lower Sobs, Chao1, and ACE indices than HC after false discovery rate correction (all q = 0.022), whereas urinary and salivary alpha-diversity did not show broad loss. Taxonomic alterations were habitat dependent: saliva yielded the broadest covariate-robust genus-level candidate set, feces showed fewer stable HC-enriched genera alongside reduced richness, and urinary candidate associations were identified but require prospective contamination-controlled validation because of the low-biomass nature of urine and the absence of negative controls. In matched participants, the combined multi-habitat microbiome model achieved an area under the receiver operating characteristic curve of 0.865 (95% CI, 0.839-0.886), exceeding the limited clinical-only model based on age, sex, and body mass index (AUC, 0.738; delta-AUC, 0.128; 95% CI, 0.026-0.229). Improvement over the best single-habitat microbiome model was not statistically conclusive. External contextual analyses provided partial urinary community-level support in KiSMi and an inverse but FDR-non-significant NHANES oral-richness association after extensive covariate adjustment, supporting harmonized prospective validation.
CONCLUSIONS: These findings identify habitat-dependent microbiome alterations in urolithiasis and show that integrated multi-habitat profiling captures disease-associated microbial information beyond a limited clinical baseline. The combination of reduced fecal richness, broad salivary covariate-robust candidates, biologically proximal urinary candidates, and external contextual signals supports simultaneous multi-site profiling as a valuable framework for future mechanistic and translational studies. Prospective studies with rigorous low-biomass controls, comprehensive exposure metadata, direct functional measurements, and prespecified independent validation are warranted.
Additional Links: PMID-42535026
PubMed:
Citation:
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@article {pmid42535026,
year = {2026},
author = {Jia, Z and Peng, Y and Jiang, S and Tang, Y and Yin, H and Huang, L and Li, P and Mo, C and Wu, R},
title = {Multi-habitat microbiome profiling identifies habitat-dependent alterations and complementary discriminatory information in urolithiasis.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1853826},
pmid = {42535026},
issn = {2235-2988},
mesh = {Humans ; RNA, Ribosomal, 16S/genetics ; *Urolithiasis/microbiology ; *Microbiota/genetics ; Female ; Feces/microbiology ; Saliva/microbiology ; Male ; *Ecosystem ; Middle Aged ; Adult ; *Bacteria/classification/genetics/isolation & purification ; Urine/microbiology ; DNA, Bacterial/genetics ; },
abstract = {BACKGROUND: Urolithiasis has been associated with microbial alterations in individual anatomical niches; however, whether microbial signatures across urinary, intestinal, and oral habitats represent shared, site-specific, or complementary disease-associated information remains unclear. This study aimed to characterize multi-habitat microbiome alterations associated with urolithiasis and to evaluate whether integrated multi-site profiling captures internally cross-validated disease-associated microbial information.
METHODS: Salivary, clean-catch midstream urinary, and fecal samples were collected from 80 stone formers (SF) and 40 healthy controls (HC) and profiled using 16S rRNA gene sequencing. After quality control, the final analytical dataset comprised 101 urinary, 117 fecal, and 120 salivary samples, with 98 participants contributing complete three-habitat profiles. Habitat-specific alpha- and beta-diversity, taxonomic alterations, and exploratory inferred-network and predicted-functional profiles were evaluated. Random forest models were assessed using repeated nested stratified cross-validation to examine internal discriminatory information from single- and multi-habitat microbial features.
RESULTS: Urolithiasis was associated with statistically detectable but modest differences in microbial community structure across all three habitats, with small PERMANOVA effect sizes and significant dispersion differences. Fecal samples from SF showed significantly reduced richness, including lower Sobs, Chao1, and ACE indices than HC after false discovery rate correction (all q = 0.022), whereas urinary and salivary alpha-diversity did not show broad loss. Taxonomic alterations were habitat dependent: saliva yielded the broadest covariate-robust genus-level candidate set, feces showed fewer stable HC-enriched genera alongside reduced richness, and urinary candidate associations were identified but require prospective contamination-controlled validation because of the low-biomass nature of urine and the absence of negative controls. In matched participants, the combined multi-habitat microbiome model achieved an area under the receiver operating characteristic curve of 0.865 (95% CI, 0.839-0.886), exceeding the limited clinical-only model based on age, sex, and body mass index (AUC, 0.738; delta-AUC, 0.128; 95% CI, 0.026-0.229). Improvement over the best single-habitat microbiome model was not statistically conclusive. External contextual analyses provided partial urinary community-level support in KiSMi and an inverse but FDR-non-significant NHANES oral-richness association after extensive covariate adjustment, supporting harmonized prospective validation.
CONCLUSIONS: These findings identify habitat-dependent microbiome alterations in urolithiasis and show that integrated multi-habitat profiling captures disease-associated microbial information beyond a limited clinical baseline. The combination of reduced fecal richness, broad salivary covariate-robust candidates, biologically proximal urinary candidates, and external contextual signals supports simultaneous multi-site profiling as a valuable framework for future mechanistic and translational studies. Prospective studies with rigorous low-biomass controls, comprehensive exposure metadata, direct functional measurements, and prespecified independent validation are warranted.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
RNA, Ribosomal, 16S/genetics
*Urolithiasis/microbiology
*Microbiota/genetics
Female
Feces/microbiology
Saliva/microbiology
Male
*Ecosystem
Middle Aged
Adult
*Bacteria/classification/genetics/isolation & purification
Urine/microbiology
DNA, Bacterial/genetics
RevDate: 2026-07-31
CmpDate: 2026-07-31
Integrating gut‑brain axis insights into bundled nutrition care for critically ill patients: From mechanisms to implementation (Review).
Molecular medicine reports, 34(4):.
Critical illness induces a marked disruption of the gut‑brain axis, which is characterized by systemic inflammation and the rapid collapse of intestinal barrier integrity. These pathological shifts facilitate the translocation of pathogen‑associated molecular patterns, thereby driving neuroinflammation and exacerbating intensive care unit‑acquired syndromes such as delirium and muscular wasting. Although conventional nutritional strategies emphasize caloric and protein goals, emerging evidence has highlighted the necessity of modulating the host‑microbiome interface to preserve neurological and systemic homeostasis. The integration of fermentable fibers, probiotics and specialized lipid mediators into a standardized framework may effectively interrupt the self‑perpetuating cycle of dysbiosis and organ failure. The present review uniquely contributes to the field by integrating an implementation science framework for clinical bundle application and discussing artificial intelligence driven precision nutrition advances, which are topics that have not been comprehensively covered in the majority of previous reviews. Therefore, the present review bridges mechanistic insights with practical, scalable strategies to optimize nutritional care and improve recovery trajectories in patients with critical illness.
Additional Links: PMID-42535369
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PubMed:
Citation:
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@article {pmid42535369,
year = {2026},
author = {Zhang, L and Yang, S and Wu, H and Zhou, H},
title = {Integrating gut‑brain axis insights into bundled nutrition care for critically ill patients: From mechanisms to implementation (Review).},
journal = {Molecular medicine reports},
volume = {34},
number = {4},
pages = {},
doi = {10.3892/mmr.2026.13978},
pmid = {42535369},
issn = {1791-3004},
mesh = {Humans ; *Critical Illness/therapy ; Gastrointestinal Microbiome ; *Brain/metabolism ; Intestinal Barrier Function ; Dysbiosis ; *Brain-Gut Axis ; Enteral Nutrition/methods ; Critical Care/methods ; *Nutrition Therapy/methods ; },
abstract = {Critical illness induces a marked disruption of the gut‑brain axis, which is characterized by systemic inflammation and the rapid collapse of intestinal barrier integrity. These pathological shifts facilitate the translocation of pathogen‑associated molecular patterns, thereby driving neuroinflammation and exacerbating intensive care unit‑acquired syndromes such as delirium and muscular wasting. Although conventional nutritional strategies emphasize caloric and protein goals, emerging evidence has highlighted the necessity of modulating the host‑microbiome interface to preserve neurological and systemic homeostasis. The integration of fermentable fibers, probiotics and specialized lipid mediators into a standardized framework may effectively interrupt the self‑perpetuating cycle of dysbiosis and organ failure. The present review uniquely contributes to the field by integrating an implementation science framework for clinical bundle application and discussing artificial intelligence driven precision nutrition advances, which are topics that have not been comprehensively covered in the majority of previous reviews. Therefore, the present review bridges mechanistic insights with practical, scalable strategies to optimize nutritional care and improve recovery trajectories in patients with critical illness.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Critical Illness/therapy
Gastrointestinal Microbiome
*Brain/metabolism
Intestinal Barrier Function
Dysbiosis
*Brain-Gut Axis
Enteral Nutrition/methods
Critical Care/methods
*Nutrition Therapy/methods
RevDate: 2026-07-31
CmpDate: 2026-07-31
Association between periodontitis and heart failure: Mechanisms and clinical implications (Review).
Molecular medicine reports, 34(4):.
Periodontitis, a common oral disease, is increasingly recognized for its potential impact on systemic health, particularly its association with heart failure (HF). HF is a complex clinical syndrome with a multifactorial pathogenesis. Emerging evidence suggests that periodontitis may influence the cardiovascular system and contribute to the onset and progression of HF through mechanisms such as systemic inflammation, microbial shifts, and immune dysregulation. However, current research still faces limitations in establishing causality and elucidating the precise underlying mechanisms. Furthermore, clinical intervention strategies require further investigation. Relevant literature was identified from PubMed, Web of Science, and Scopus using keywords related to periodontitis and heart failure, and screened for relevance to epidemiological evidence, mechanistic insights, and clinical implications. The present review aimed to summarize the mechanisms linking periodontitis and HF, analyze their shared pathophysiological basis, and discuss the potential role of periodontal treatment in improving outcomes for patients with HF. Clinically, periodontal assessment may be considered in patients with heart failure as part of multidisciplinary care, but current evidence remains insufficient to support definitive recommendations that such evaluation or treatment improves HF outcomes.
Additional Links: PMID-42535384
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PubMed:
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@article {pmid42535384,
year = {2026},
author = {Zhang, X and An, X},
title = {Association between periodontitis and heart failure: Mechanisms and clinical implications (Review).},
journal = {Molecular medicine reports},
volume = {34},
number = {4},
pages = {},
doi = {10.3892/mmr.2026.13974},
pmid = {42535384},
issn = {1791-3004},
mesh = {Humans ; *Heart Failure/etiology/epidemiology/complications ; *Periodontitis/complications/microbiology/epidemiology/therapy ; Microbiota ; Inflammation ; Animals ; },
abstract = {Periodontitis, a common oral disease, is increasingly recognized for its potential impact on systemic health, particularly its association with heart failure (HF). HF is a complex clinical syndrome with a multifactorial pathogenesis. Emerging evidence suggests that periodontitis may influence the cardiovascular system and contribute to the onset and progression of HF through mechanisms such as systemic inflammation, microbial shifts, and immune dysregulation. However, current research still faces limitations in establishing causality and elucidating the precise underlying mechanisms. Furthermore, clinical intervention strategies require further investigation. Relevant literature was identified from PubMed, Web of Science, and Scopus using keywords related to periodontitis and heart failure, and screened for relevance to epidemiological evidence, mechanistic insights, and clinical implications. The present review aimed to summarize the mechanisms linking periodontitis and HF, analyze their shared pathophysiological basis, and discuss the potential role of periodontal treatment in improving outcomes for patients with HF. Clinically, periodontal assessment may be considered in patients with heart failure as part of multidisciplinary care, but current evidence remains insufficient to support definitive recommendations that such evaluation or treatment improves HF outcomes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Heart Failure/etiology/epidemiology/complications
*Periodontitis/complications/microbiology/epidemiology/therapy
Microbiota
Inflammation
Animals
RevDate: 2026-07-31
CAMEO: a CAZyme mapping engine optimized for HUMAnN.
Microbiology resource announcements [Epub ahead of print].
There are technical barriers to creating functional mapping databases and a dearth of validated databases that can be easily implemented by users. We present CAMEO, a precomputed and validated mapping file for carbohydrate-active enzymes, as well as an approach to building new CAZyme mapping files, for use with HUMAnN.
Additional Links: PMID-42535839
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PubMed:
Citation:
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@article {pmid42535839,
year = {2026},
author = {Bolino, MJ and Frese, SA},
title = {CAMEO: a CAZyme mapping engine optimized for HUMAnN.},
journal = {Microbiology resource announcements},
volume = {},
number = {},
pages = {e0070726},
doi = {10.1128/mra.00707-26},
pmid = {42535839},
issn = {2576-098X},
abstract = {There are technical barriers to creating functional mapping databases and a dearth of validated databases that can be easily implemented by users. We present CAMEO, a precomputed and validated mapping file for carbohydrate-active enzymes, as well as an approach to building new CAZyme mapping files, for use with HUMAnN.},
}
RevDate: 2026-07-31
Differential pro-tumorigenic effects of Helicobacter pylori and Streptococcus anginosus on AGS cells: contact-dependent versus metabolite-driven mechanisms.
mBio [Epub ahead of print].
Gastric cancer remains a major global health burden, ranking fifth worldwide in both incidence and mortality. While Helicobacter pylori is a well-established Group I carcinogen, increasing evidence suggests that non-H. pylori bacteria, including Streptococcus anginosus, may also contribute to gastric carcinogenesis. However, their comparative pathogenic roles and interactions remain poorly defined. In this study, public databases showed stage-dependent abundance changes of H. pylori and S. anginosus but no significant correlation during gastric cancer progression. We further quantified both bacteria in gastric fluid samples collected from 500 individuals using a non-invasive gastric string test and in fecal samples from an independent cohort of 500 individuals by qPCR. In the two cohorts, no significant correlations were observed between the two bacterial pathogens, suggesting distinct colonization and pathogenic patterns. To evaluate functional differences, AGS cell co-culture models were established to explore their pro-tumorigenic effects. H. pylori predominantly exerted tumor-promoting effects through bacterial cell-associated mechanisms, whereas S. anginosus exerted stronger pro-tumorigenic effects via its metabolites. In particular, transcriptomic analysis revealed that proliferation-associated genes, including DEK and RTF1, were significantly upregulated by 21.9-fold and 19.2-fold, respectively, in cells treated with Streptococcus anginosus metabolite (SAM). Metabolomic profiling of SAM identified increased levels of spermidine and polyamine-related metabolites. Among these, N-acetylcadaverine, N-acetyltyrosine, N-acetyltryptophan, and urocanic acid were experimentally validated to significantly promote AGS cell proliferation. Collectively, these findings demonstrate that H. pylori and S. anginosus drive gastric tumorigenesis through contact-dependent and metabolite-mediated mechanisms, respectively, highlighting bacterial metabolites as emerging contributors to gastric cancer progression.IMPORTANCEThe gastric microbiota plays a critical role in gastrointestinal health and disease. However, the ecological interactions between Helicobacter pylori and non-H. pylori bacteria remain poorly understood. Among established bacterial pathogens linked to gastric carcinogenesis, H. pylori and Streptococcus anginosus are recognized as major contributors. In this study, we systematically evaluated infection patterns and potential associations between these two pathogens using public metagenomic data sets and qPCR analysis of clinical samples (feces and gastric fluid) from multicenter cohorts. We found no significant association between their infection statuses (P > 0.05), indicating independent colonization patterns and likely differences in their pathogenic mechanisms within the human host. Complementary in vitro and cellular analyses further showed that H. pylori primarily acts through direct mucosal colonization and virulence factors, whereas S. anginosus influences host responses mainly via its metabolic products. These findings demonstrate that H. pylori and S. anginosus operate through distinct colonization strategies and pathogenic pathways. They underscore the importance of accounting for mechanistic heterogeneity in gastric microbiome research and provide a conceptual framework for future investigations into microbe-driven pathogenesis of gastric disease.
Additional Links: PMID-42535843
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PubMed:
Citation:
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@article {pmid42535843,
year = {2026},
author = {Luan, L and Song, X and Zeng, Y and Xie, Y and Hong, Y and Tang, J and Ma, C and Gu, B and Wang, L},
title = {Differential pro-tumorigenic effects of Helicobacter pylori and Streptococcus anginosus on AGS cells: contact-dependent versus metabolite-driven mechanisms.},
journal = {mBio},
volume = {},
number = {},
pages = {e0158926},
doi = {10.1128/mbio.01589-26},
pmid = {42535843},
issn = {2150-7511},
abstract = {Gastric cancer remains a major global health burden, ranking fifth worldwide in both incidence and mortality. While Helicobacter pylori is a well-established Group I carcinogen, increasing evidence suggests that non-H. pylori bacteria, including Streptococcus anginosus, may also contribute to gastric carcinogenesis. However, their comparative pathogenic roles and interactions remain poorly defined. In this study, public databases showed stage-dependent abundance changes of H. pylori and S. anginosus but no significant correlation during gastric cancer progression. We further quantified both bacteria in gastric fluid samples collected from 500 individuals using a non-invasive gastric string test and in fecal samples from an independent cohort of 500 individuals by qPCR. In the two cohorts, no significant correlations were observed between the two bacterial pathogens, suggesting distinct colonization and pathogenic patterns. To evaluate functional differences, AGS cell co-culture models were established to explore their pro-tumorigenic effects. H. pylori predominantly exerted tumor-promoting effects through bacterial cell-associated mechanisms, whereas S. anginosus exerted stronger pro-tumorigenic effects via its metabolites. In particular, transcriptomic analysis revealed that proliferation-associated genes, including DEK and RTF1, were significantly upregulated by 21.9-fold and 19.2-fold, respectively, in cells treated with Streptococcus anginosus metabolite (SAM). Metabolomic profiling of SAM identified increased levels of spermidine and polyamine-related metabolites. Among these, N-acetylcadaverine, N-acetyltyrosine, N-acetyltryptophan, and urocanic acid were experimentally validated to significantly promote AGS cell proliferation. Collectively, these findings demonstrate that H. pylori and S. anginosus drive gastric tumorigenesis through contact-dependent and metabolite-mediated mechanisms, respectively, highlighting bacterial metabolites as emerging contributors to gastric cancer progression.IMPORTANCEThe gastric microbiota plays a critical role in gastrointestinal health and disease. However, the ecological interactions between Helicobacter pylori and non-H. pylori bacteria remain poorly understood. Among established bacterial pathogens linked to gastric carcinogenesis, H. pylori and Streptococcus anginosus are recognized as major contributors. In this study, we systematically evaluated infection patterns and potential associations between these two pathogens using public metagenomic data sets and qPCR analysis of clinical samples (feces and gastric fluid) from multicenter cohorts. We found no significant association between their infection statuses (P > 0.05), indicating independent colonization patterns and likely differences in their pathogenic mechanisms within the human host. Complementary in vitro and cellular analyses further showed that H. pylori primarily acts through direct mucosal colonization and virulence factors, whereas S. anginosus influences host responses mainly via its metabolic products. These findings demonstrate that H. pylori and S. anginosus operate through distinct colonization strategies and pathogenic pathways. They underscore the importance of accounting for mechanistic heterogeneity in gastric microbiome research and provide a conceptual framework for future investigations into microbe-driven pathogenesis of gastric disease.},
}
RevDate: 2026-07-31
High-resolution taxonomic profiling and metatranscriptomics identify microbial, biochemical, host, and ecological factors in peri-implant disease.
mSystems [Epub ahead of print].
UNLABELLED: Biofilm-associated diseases like peri-implant mucositis (PIM) and peri-implantitis (PI) are significant clinical challenges affecting millions of dental implant patients globally. Although studies have described the role of microbial, host, or environmental factors in disease development, their complex interplay, particularly during dysbiosis, remains poorly understood. This cross-sectional study characterized the microbiome composition and metatranscriptomes of 125 peri-implant biofilms from 48 individuals, uncovering molecular signatures linked to peri-implant health (PIH), PIM, and PI. Distinct variations were observed in biofilm amount, microbial composition and activity, phage populations, and host response. Biofilms were categorized into four community types (CTs) based on the bacterial transcriptional activity: one linked to PIH, one to PI, and two to PIM. PIH and PIM were primarily characterized by aerotolerant taxa with increased anabolic processes, while PI was dominated by obligate anaerobes with complex biofilm morphology. PIM samples, relative to PIH, were characterized by biofilm expansion with minimal functional changes, except for the Neisseria-rich PIM subtype showing higher pyruvate and lipoic acid metabolism. The phagome mirrored the bacterial compositional variations across disease states. Furthermore, human transcriptome responses varied, indicating increased keratinization in PIH, enhanced expression of ribosome components in PIM, and inflammatory signaling and hypoxia in PI. Additionally, we identified complex species-enzyme, phage-bacterium, and host-microbe associations within the peri-implant ecosystem. Our integrative multi-omics approach provides a comprehensive view of microbial, biochemical, host, and ecological factors associated with dysbiosis, offering novel insights into peri-implant disease dynamics.
IMPORTANCE: Peri-implant mucositis and peri-implantitis are highly prevalent inflammatory conditions that compromise the long-term survival and success of dental implants, yet their underlying biological mechanisms are largely unresolved. The full-length 16S rRNA gene amplicon sequencing (full-16S) allows for high-resolution taxonomic profiling of peri-implant biofilms, thereby advancing our understanding of microbial composition across health and peri-implant diseases. The integration of metatranscriptomics, furthermore, captures actively transcribed genes within the biofilm and offers direct insights into microbial community functions and the broader molecular context of peri-implant dysbiosis. DNA- and RNA-derived abundances were strongly correlated, with only a few microbial classes showing moderate diagnosis-related differences after DNA-based normalization of transcriptional activity. In this study, we integrated full-16S with metatranscriptomic profiling to simultaneously assess microbial taxonomy, functional activity, phage dynamics, and host gene expression in peri-implant biofilms. Importantly, we provide a systems-level view and report previously undescribed associations between different molecular signatures in the peri-implant ecosystem.
Additional Links: PMID-42535857
Publisher:
PubMed:
Citation:
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@article {pmid42535857,
year = {2026},
author = {Szafrański, SP and Joshi, AA and Steglich, M and Yang, I and Qu, T and Behrens, W and Muthukumarasamy, U and Melidis, D and Schaefer-Dreyer, P and Grischke, J and Hegermann, J and Nejdl, W and Häussler, S and Stiesch, M},
title = {High-resolution taxonomic profiling and metatranscriptomics identify microbial, biochemical, host, and ecological factors in peri-implant disease.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0075425},
doi = {10.1128/msystems.00754-25},
pmid = {42535857},
issn = {2379-5077},
abstract = {UNLABELLED: Biofilm-associated diseases like peri-implant mucositis (PIM) and peri-implantitis (PI) are significant clinical challenges affecting millions of dental implant patients globally. Although studies have described the role of microbial, host, or environmental factors in disease development, their complex interplay, particularly during dysbiosis, remains poorly understood. This cross-sectional study characterized the microbiome composition and metatranscriptomes of 125 peri-implant biofilms from 48 individuals, uncovering molecular signatures linked to peri-implant health (PIH), PIM, and PI. Distinct variations were observed in biofilm amount, microbial composition and activity, phage populations, and host response. Biofilms were categorized into four community types (CTs) based on the bacterial transcriptional activity: one linked to PIH, one to PI, and two to PIM. PIH and PIM were primarily characterized by aerotolerant taxa with increased anabolic processes, while PI was dominated by obligate anaerobes with complex biofilm morphology. PIM samples, relative to PIH, were characterized by biofilm expansion with minimal functional changes, except for the Neisseria-rich PIM subtype showing higher pyruvate and lipoic acid metabolism. The phagome mirrored the bacterial compositional variations across disease states. Furthermore, human transcriptome responses varied, indicating increased keratinization in PIH, enhanced expression of ribosome components in PIM, and inflammatory signaling and hypoxia in PI. Additionally, we identified complex species-enzyme, phage-bacterium, and host-microbe associations within the peri-implant ecosystem. Our integrative multi-omics approach provides a comprehensive view of microbial, biochemical, host, and ecological factors associated with dysbiosis, offering novel insights into peri-implant disease dynamics.
IMPORTANCE: Peri-implant mucositis and peri-implantitis are highly prevalent inflammatory conditions that compromise the long-term survival and success of dental implants, yet their underlying biological mechanisms are largely unresolved. The full-length 16S rRNA gene amplicon sequencing (full-16S) allows for high-resolution taxonomic profiling of peri-implant biofilms, thereby advancing our understanding of microbial composition across health and peri-implant diseases. The integration of metatranscriptomics, furthermore, captures actively transcribed genes within the biofilm and offers direct insights into microbial community functions and the broader molecular context of peri-implant dysbiosis. DNA- and RNA-derived abundances were strongly correlated, with only a few microbial classes showing moderate diagnosis-related differences after DNA-based normalization of transcriptional activity. In this study, we integrated full-16S with metatranscriptomic profiling to simultaneously assess microbial taxonomy, functional activity, phage dynamics, and host gene expression in peri-implant biofilms. Importantly, we provide a systems-level view and report previously undescribed associations between different molecular signatures in the peri-implant ecosystem.},
}
RevDate: 2026-07-31
Transmission of Xanthomonas campestris pv. incanae and Associated Microbiome in Matthiola incana Seed.
Phytopathology [Epub ahead of print].
Xanthomonas campestris pv. incanae (Xci) is known to cause systemic infections in the stem of Matthiola incana. Prior research observed that the pathogen can invade the vascular system and extend into the seed peduncles of infected plants, suggesting a likely mean for internal contamination of the seeds. However, this and other potential pathways of seed infection and seed-to-seed transmission, have not been sufficiently investigated. Using both culture-based and metagenomic approaches, we evaluated the potential for and efficiency of seed infection by Xci after vascular and floral inoculation of the mother plants, as well as the possibility for seed-to-seed transmission. We also explored the diversity of the M. incana seed microbiome in response to inoculation with Xci. Results showed that the vascular system was a viable and highly efficient pathway of seed infection by Xci, unlike the floral organs, and that seed infection by the vascular pathway negatively impacted seed germination. We also demonstrated that seed-to-seed transmission of Xci occurred at an epidemiologically significant degree. The primary difference among microbiomes of seeds harvested from inoculated and non-inoculated plants was the presence of Xci, which had extremely high relative and absolute abundance in infested seeds. Additionally, minor effects of inoculation treatment, seed infection pathway, and the interaction between the two were observed for overall seed microbial community composition and diversity. These findings pave the way to future exploration of the seed microbiome in M. incana.
Additional Links: PMID-42535886
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@article {pmid42535886,
year = {2026},
author = {Eckles, AE and Poelstra, JW and Toth, HN and McKenzie, ZA and Jacobs, JM and Peduto Hand, F},
title = {Transmission of Xanthomonas campestris pv. incanae and Associated Microbiome in Matthiola incana Seed.},
journal = {Phytopathology},
volume = {},
number = {},
pages = {},
doi = {10.1094/PHYTO-03-26-0074-FI},
pmid = {42535886},
issn = {0031-949X},
abstract = {Xanthomonas campestris pv. incanae (Xci) is known to cause systemic infections in the stem of Matthiola incana. Prior research observed that the pathogen can invade the vascular system and extend into the seed peduncles of infected plants, suggesting a likely mean for internal contamination of the seeds. However, this and other potential pathways of seed infection and seed-to-seed transmission, have not been sufficiently investigated. Using both culture-based and metagenomic approaches, we evaluated the potential for and efficiency of seed infection by Xci after vascular and floral inoculation of the mother plants, as well as the possibility for seed-to-seed transmission. We also explored the diversity of the M. incana seed microbiome in response to inoculation with Xci. Results showed that the vascular system was a viable and highly efficient pathway of seed infection by Xci, unlike the floral organs, and that seed infection by the vascular pathway negatively impacted seed germination. We also demonstrated that seed-to-seed transmission of Xci occurred at an epidemiologically significant degree. The primary difference among microbiomes of seeds harvested from inoculated and non-inoculated plants was the presence of Xci, which had extremely high relative and absolute abundance in infested seeds. Additionally, minor effects of inoculation treatment, seed infection pathway, and the interaction between the two were observed for overall seed microbial community composition and diversity. These findings pave the way to future exploration of the seed microbiome in M. incana.},
}
RevDate: 2026-07-31
Correction: Early-life gut microbiome-metabolome development trajectories in Chinese infants: a decentralized real-world evidence study.
Correction for 'Early-life gut microbiome-metabolome development trajectories in Chinese infants: a decentralized real-world evidence study' by Wanying Zhong et al., Food Funct., 2026, 17, 6596-6607, https://doi.org/10.1039/D6FO02082H.
Additional Links: PMID-42535945
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@article {pmid42535945,
year = {2026},
author = {Zhong, W and Zhu, Z and Zeng, Z and Wu, J and Xie, X and Li, X and Lv, Q and Li, D and Liu, M and Ward, G and Knol, J and Wopereis, H and Guyard, C and Xia, J and Han, L and Wang, B and Li, Y and Roeselers, G and Gong, S},
title = {Correction: Early-life gut microbiome-metabolome development trajectories in Chinese infants: a decentralized real-world evidence study.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d6fo90062c},
pmid = {42535945},
issn = {2042-650X},
abstract = {Correction for 'Early-life gut microbiome-metabolome development trajectories in Chinese infants: a decentralized real-world evidence study' by Wanying Zhong et al., Food Funct., 2026, 17, 6596-6607, https://doi.org/10.1039/D6FO02082H.},
}
RevDate: 2026-07-31
Experimental evidence for early bacterial inheritance in the giant kelp, Macrocystis pyrifera.
FEMS microbiology ecology pii:8748416 [Epub ahead of print].
Bacteria associated with macroalgae influence the development, health, and ecological interactions of their hosts. Although vertical transmission of bacterial symbionts has been proposed in some algal species, evidence remains limited. In this study, we combined 16S rRNA gene amplicon sequencing, fluorescence in situ hybridization (FISH), and transmission electron microscopy (TEM) to assess bacterial presence and localization throughout early developmental stages of the brown macroalga Macrocystis pyrifera. Amplicon sequencing detected bacterial taxa in reproductive sori, released spores, and gametophytes, even under sterile conditions and using pasteurized, filtered seawater. Certain bacterial taxa, including Balneola alkaliphila and Marinoscillum luteum, were recurrently detected across multiple developmental stages. FISH imaging showed bacterial signal associated with host tissues across life stages, distinguishable from algal autofluorescence, while TEM observations revealed structures consistent with intracellular bacterial cells within the cytoplasm of gametophyte cells and embedded in sporangial cuticles. Together, these observations suggest that bacteria are associated with both internal and external reproductive tissues, pointing to multiple potential transmission routes. Altogether, our findings provide evidence consistent with early-stage bacterial inheritance in M. pyrifera, contributing to the growing evidence that macroalgal holobionts are assembled, at least in part, through vertical transmission of symbionts.
Additional Links: PMID-42535965
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@article {pmid42535965,
year = {2026},
author = {Usandizaga, S and Beltrán, J and Rodríguez-Valdecantos, G and Parada-Pozo, G and Guillemin, ML and Faugeron, S and Trefault, N and Camus, C},
title = {Experimental evidence for early bacterial inheritance in the giant kelp, Macrocystis pyrifera.},
journal = {FEMS microbiology ecology},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsec/fiag089},
pmid = {42535965},
issn = {1574-6941},
abstract = {Bacteria associated with macroalgae influence the development, health, and ecological interactions of their hosts. Although vertical transmission of bacterial symbionts has been proposed in some algal species, evidence remains limited. In this study, we combined 16S rRNA gene amplicon sequencing, fluorescence in situ hybridization (FISH), and transmission electron microscopy (TEM) to assess bacterial presence and localization throughout early developmental stages of the brown macroalga Macrocystis pyrifera. Amplicon sequencing detected bacterial taxa in reproductive sori, released spores, and gametophytes, even under sterile conditions and using pasteurized, filtered seawater. Certain bacterial taxa, including Balneola alkaliphila and Marinoscillum luteum, were recurrently detected across multiple developmental stages. FISH imaging showed bacterial signal associated with host tissues across life stages, distinguishable from algal autofluorescence, while TEM observations revealed structures consistent with intracellular bacterial cells within the cytoplasm of gametophyte cells and embedded in sporangial cuticles. Together, these observations suggest that bacteria are associated with both internal and external reproductive tissues, pointing to multiple potential transmission routes. Altogether, our findings provide evidence consistent with early-stage bacterial inheritance in M. pyrifera, contributing to the growing evidence that macroalgal holobionts are assembled, at least in part, through vertical transmission of symbionts.},
}
RevDate: 2026-07-31
Alteration of subgingival microbiome in patients with type 2 diabetes induced by diabetes treatment.
Journal of diabetes investigation [Epub ahead of print].
AIMS/INTRODUCTION: Diabetes and periodontal disease, a bacterial infection involving the oral microbiome, have a bidirectional relationship. However, the relationship between poor glycemic control and the oral microbiome remains unclear. The aim of this study was to assess the direct effect of intensive glycemic control on the oral microbiome in patients with type 2 diabetes mellitus (T2DM).
MATERIALS AND METHODS: Twenty-nine patients with T2DM and 29 controls were enrolled in this study. Patients underwent a 2-week intensive glycemic control regimen. We collected subgingival dental plaque and conducted full-length 16S ribosomal RNA gene sequencing to identify bacterial species. The focus was on the subgingival microbiome, particularly 29 species of oral bacteria related to periodontal disease, and the characteristics of the diabetic cohort. Periodontal inflammation was quantified using the periodontal inflamed surface area (PISA).
RESULTS: Prior to diabetes treatment, the relative abundance of Porphyromonas gingivalis (P = 0.018), Tannerella forsythia (P < 0.001), Fusobacterium nucleatum (P = 0.041), and Prevotella intermedia (P < 0.001), known for their high pathogenicity in periodontal disease, was higher in the diabetes group than in the control group. The bacterial species whose relative abundance changed significantly before and after treatment differed between the PISA improved and non-improved groups in patients with diabetes.
CONCLUSIONS: Oral bacteria changed pre- and post-diabetes treatment, correlating with improvements in PISA.
Additional Links: PMID-42536059
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PubMed:
Citation:
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@article {pmid42536059,
year = {2026},
author = {Inoue, M and Sakanaka, A and Katakami, N and Nishizawa, H and Omori, K and Taya, N and Ishikawa, A and Mayumi, S and Takeuchi, H and Amano, A and Takeshita, T and Fukusaki, E and Shimomura, I and Kuboniwa, M},
title = {Alteration of subgingival microbiome in patients with type 2 diabetes induced by diabetes treatment.},
journal = {Journal of diabetes investigation},
volume = {},
number = {},
pages = {},
doi = {10.1111/jdi.70408},
pmid = {42536059},
issn = {2040-1124},
support = {JP22ym0126809//Japan Agency for Medical Research and Development/ ; 22H03300//Japan Society for the Promotion of Science/ ; 22K19622//Japan Society for the Promotion of Science/ ; 21K18281//Japan Society for the Promotion of Science/ ; 20K18827//Japan Society for the Promotion of Science/ ; JP23KJ15250//Japan Society for the Promotion of Science/ ; 25K02837//Japan Society for the Promotion of Science/ ; },
abstract = {AIMS/INTRODUCTION: Diabetes and periodontal disease, a bacterial infection involving the oral microbiome, have a bidirectional relationship. However, the relationship between poor glycemic control and the oral microbiome remains unclear. The aim of this study was to assess the direct effect of intensive glycemic control on the oral microbiome in patients with type 2 diabetes mellitus (T2DM).
MATERIALS AND METHODS: Twenty-nine patients with T2DM and 29 controls were enrolled in this study. Patients underwent a 2-week intensive glycemic control regimen. We collected subgingival dental plaque and conducted full-length 16S ribosomal RNA gene sequencing to identify bacterial species. The focus was on the subgingival microbiome, particularly 29 species of oral bacteria related to periodontal disease, and the characteristics of the diabetic cohort. Periodontal inflammation was quantified using the periodontal inflamed surface area (PISA).
RESULTS: Prior to diabetes treatment, the relative abundance of Porphyromonas gingivalis (P = 0.018), Tannerella forsythia (P < 0.001), Fusobacterium nucleatum (P = 0.041), and Prevotella intermedia (P < 0.001), known for their high pathogenicity in periodontal disease, was higher in the diabetes group than in the control group. The bacterial species whose relative abundance changed significantly before and after treatment differed between the PISA improved and non-improved groups in patients with diabetes.
CONCLUSIONS: Oral bacteria changed pre- and post-diabetes treatment, correlating with improvements in PISA.},
}
RevDate: 2026-07-31
An innovative organoid model to screen for bacteria and their metabolites that protect against inflammation-induced colonic barrier disruption.
mSphere [Epub ahead of print].
Organoids provide a useful model system to study interactions between gut microbes and the activity of host tissues, including gastrointestinal (GI) barrier function. However, most organoid models have limited capacity to mimic the physiological hypoxia experienced by the colonic epithelium in vivo. While oxygen is required to support respiration in the host cells, many gut microbes are anaerobes that require anoxic conditions to grow. Using an innovative anaerobe co-culture system that maintains constant oxygen concentrations on the basolateral side of colonic epithelial monolayers and anoxic conditions on the luminal side, we demonstrate that colonic monolayers derived from a primary human cell line behaved more like in vivo epithelia when cultivated in the co-culture system than when cultured under ambient oxygen concentrations. We then identified interactions between the colonic epithelium and a strain of Bifidobacterium adolescentis-an oxygen-sensitive species that is prevalent and abundant in the adult gut microbiome. Co-culturing colonic monolayers with Bifidobacterium adolescentis U269-1 in the anoxic apical chamber mitigated loss of the barrier function in monolayers exposed to inflammatory cytokines. We identified indole lactic acid (ILA) as one metabolite from B. adolescentis that provides dose-dependent protection against inflammatory cytokines. Oral administration of ILA was well tolerated in mice and provided protection against immunotherapy-induced (anti-CTLA4) colitis in female, but not male mice. Together, we demonstrated the utility of the co-culture system for screening microbes and their metabolites for interactions with the colonic epithelium, as well as advancing our understanding of interactions between bifidobacteria and host barrier function.IMPORTANCEThe present study yielded strong evidence for the beneficial effects of B. adolescentis on the maintenance of colonic barrier function in an asymmetric oxygen system that mimics the colonic environment. The bifidobacterial metabolite indole lactic acid was implicated in this protection both in vitro and in a mouse model. We also refined and scaled the co-culture system to a 96-well plate format to provide the capacity for higher-throughput screening of microbes and microbial metabolites under physiologically relevant conditions.
Additional Links: PMID-42536076
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PubMed:
Citation:
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@article {pmid42536076,
year = {2026},
author = {Cady, N and Meyer, SR and Kim, K and Lo, BC and So, N and Chen, GY and Rosshart, SP and Shah, YM and Núñez, G and Sexton, JZ and Schmidt, TM},
title = {An innovative organoid model to screen for bacteria and their metabolites that protect against inflammation-induced colonic barrier disruption.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0092625},
doi = {10.1128/msphere.00926-25},
pmid = {42536076},
issn = {2379-5042},
abstract = {Organoids provide a useful model system to study interactions between gut microbes and the activity of host tissues, including gastrointestinal (GI) barrier function. However, most organoid models have limited capacity to mimic the physiological hypoxia experienced by the colonic epithelium in vivo. While oxygen is required to support respiration in the host cells, many gut microbes are anaerobes that require anoxic conditions to grow. Using an innovative anaerobe co-culture system that maintains constant oxygen concentrations on the basolateral side of colonic epithelial monolayers and anoxic conditions on the luminal side, we demonstrate that colonic monolayers derived from a primary human cell line behaved more like in vivo epithelia when cultivated in the co-culture system than when cultured under ambient oxygen concentrations. We then identified interactions between the colonic epithelium and a strain of Bifidobacterium adolescentis-an oxygen-sensitive species that is prevalent and abundant in the adult gut microbiome. Co-culturing colonic monolayers with Bifidobacterium adolescentis U269-1 in the anoxic apical chamber mitigated loss of the barrier function in monolayers exposed to inflammatory cytokines. We identified indole lactic acid (ILA) as one metabolite from B. adolescentis that provides dose-dependent protection against inflammatory cytokines. Oral administration of ILA was well tolerated in mice and provided protection against immunotherapy-induced (anti-CTLA4) colitis in female, but not male mice. Together, we demonstrated the utility of the co-culture system for screening microbes and their metabolites for interactions with the colonic epithelium, as well as advancing our understanding of interactions between bifidobacteria and host barrier function.IMPORTANCEThe present study yielded strong evidence for the beneficial effects of B. adolescentis on the maintenance of colonic barrier function in an asymmetric oxygen system that mimics the colonic environment. The bifidobacterial metabolite indole lactic acid was implicated in this protection both in vitro and in a mouse model. We also refined and scaled the co-culture system to a 96-well plate format to provide the capacity for higher-throughput screening of microbes and microbial metabolites under physiologically relevant conditions.},
}
RevDate: 2026-07-31
CmpDate: 2026-07-31
Effect of gut bacterial extracellular vesicles on angiogenic potential and vascular integrity: positive and negative aspects.
Inflammation research : official journal of the European Histamine Research Society ... [et al.], 75(1):.
Extracellular vesicles (EVs) are intercellular mediators in prokaryotic and eukaryotic systems that have the potential to regulate various physiological and pathological processes in recipient cells. Among them, bacterial extracellular vesicles (BEVs), including Gram-negative outer membrane vesicles (OMVs) and Gram-positive membrane vesicles (MVs) produced by the gut microbiota, have special roles in humans and animals. Due to their nanoscale dimensions and distinct molecular payloads, BEVs can cross biological barriers, including the vascular endothelium, to reach distant target tissues and affect various pathophysiological processes. Dysbiosis and compromised epithelial barriers facilitate the systemic dissemination of gut microbiota-derived BEVs, increasing the risk of diseases such as atherosclerosis and cardiovascular disease. Importantly, while this review emphasizes symbiotic intestinal BEVs, evidence from oral and pathogenic bacteria has also been integrated as indirect mechanistic sources to shed more light on BEV-induced endothelial dysfunction and altered angiogenesis. Here, we aimed to highlight the impact of BEVs on the vascular compartment, focusing on endothelial cells (ECs) in terms of molecular and cellular events. Understanding the underlying mechanisms will enable us to develop sophisticated engineered BEVs to control and inhibit certain pathological conditions.
Additional Links: PMID-42536162
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@article {pmid42536162,
year = {2026},
author = {Chegeni, SA and Yalameha, B and Rashidi, S and Javani, G and Seddighi, N and Bagheri, HS and Khalifezadeh, M and Roozbahani, G and Molaaghaee-Rouzbahani, S and Rahbarghazi, R},
title = {Effect of gut bacterial extracellular vesicles on angiogenic potential and vascular integrity: positive and negative aspects.},
journal = {Inflammation research : official journal of the European Histamine Research Society ... [et al.]},
volume = {75},
number = {1},
pages = {},
pmid = {42536162},
issn = {1420-908X},
support = {IR.TBZMED.VCR.REC.1404.100//Tabriz University of Medical Sciences/ ; },
mesh = {Humans ; Animals ; *Extracellular Vesicles/physiology ; *Gastrointestinal Microbiome ; *Angiogenesis ; *Bacteria ; Endothelial Cells/physiology ; Endothelium, Vascular ; Neovascularization, Physiologic ; },
abstract = {Extracellular vesicles (EVs) are intercellular mediators in prokaryotic and eukaryotic systems that have the potential to regulate various physiological and pathological processes in recipient cells. Among them, bacterial extracellular vesicles (BEVs), including Gram-negative outer membrane vesicles (OMVs) and Gram-positive membrane vesicles (MVs) produced by the gut microbiota, have special roles in humans and animals. Due to their nanoscale dimensions and distinct molecular payloads, BEVs can cross biological barriers, including the vascular endothelium, to reach distant target tissues and affect various pathophysiological processes. Dysbiosis and compromised epithelial barriers facilitate the systemic dissemination of gut microbiota-derived BEVs, increasing the risk of diseases such as atherosclerosis and cardiovascular disease. Importantly, while this review emphasizes symbiotic intestinal BEVs, evidence from oral and pathogenic bacteria has also been integrated as indirect mechanistic sources to shed more light on BEV-induced endothelial dysfunction and altered angiogenesis. Here, we aimed to highlight the impact of BEVs on the vascular compartment, focusing on endothelial cells (ECs) in terms of molecular and cellular events. Understanding the underlying mechanisms will enable us to develop sophisticated engineered BEVs to control and inhibit certain pathological conditions.},
}
MeSH Terms:
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Humans
Animals
*Extracellular Vesicles/physiology
*Gastrointestinal Microbiome
*Angiogenesis
*Bacteria
Endothelial Cells/physiology
Endothelium, Vascular
Neovascularization, Physiologic
RevDate: 2026-07-31
CmpDate: 2026-07-31
Cover trees associations shape bacterial diversity in coffee production systems.
Antonie van Leeuwenhoek, 119(9):.
Traditional coffee agroforestry systems often involve shade trees, which play a crucial role in maintaining soil fertility and biodiversity. In contrast, monoculture systems negatively influence soil chemistry, microbial diversity, and overall soil health over time. Although the use of cover trees such as mango (Mangifera indica L.) and banana (Musa paradisiaca, var. Cavendish.) has been shown to have beneficial effects on the soil chemical properties, little is known about their influence on microbial communities associated with coffee production systems. The main objective of this study was to identify the bacteria inhabiting roots and soil of three coffee management systems via partial 16S rRNA sequencing, and to assess how coffee-shade tree associations, with different soil and plant parameters, influence the bacterial ecosystem. Results revealed that the association between coffee and shade trees increased alpha diversity, with the highest diversity found in the agroforestry systems. The dominant bacterial genera found in most of the samples, i.e., Kribbella, Nonomuraea, Nitrospira, Sphingobium and Neobacillus were strongly correlated with key soil chemical properties, including nitrogen content, organic matter, and available phosphorus. These correlations suggest that tree cover strategies exert beneficial effects on the bacterial microbiome. Moreover, the overall bacterial community structure was different when comparing coffee monoculture system and shade-associated systems. Our findings highlight that traditional coffee agroforestry practices involving shade trees foster more diverse bacterial communities, thereby contributing to healthier soils and more sustainable coffee production.
Additional Links: PMID-42536199
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@article {pmid42536199,
year = {2026},
author = {Chávez-Tinoco, M and Senés-Guerrero, C and Verduzco Garibay, M and Carrillo-González, R and González-Chávez, MDCA},
title = {Cover trees associations shape bacterial diversity in coffee production systems.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {9},
pages = {},
pmid = {42536199},
issn = {1572-9699},
mesh = {*Soil Microbiology ; *Bacteria/classification/genetics/isolation & purification ; RNA, Ribosomal, 16S/genetics ; Biodiversity ; *Trees/microbiology ; *Musa/microbiology ; Soil/chemistry ; *Coffee ; Plant Roots/microbiology ; *Mangifera/microbiology ; Phylogeny ; Coffea ; DNA, Bacterial/genetics ; Agriculture/methods ; Microbiota ; },
abstract = {Traditional coffee agroforestry systems often involve shade trees, which play a crucial role in maintaining soil fertility and biodiversity. In contrast, monoculture systems negatively influence soil chemistry, microbial diversity, and overall soil health over time. Although the use of cover trees such as mango (Mangifera indica L.) and banana (Musa paradisiaca, var. Cavendish.) has been shown to have beneficial effects on the soil chemical properties, little is known about their influence on microbial communities associated with coffee production systems. The main objective of this study was to identify the bacteria inhabiting roots and soil of three coffee management systems via partial 16S rRNA sequencing, and to assess how coffee-shade tree associations, with different soil and plant parameters, influence the bacterial ecosystem. Results revealed that the association between coffee and shade trees increased alpha diversity, with the highest diversity found in the agroforestry systems. The dominant bacterial genera found in most of the samples, i.e., Kribbella, Nonomuraea, Nitrospira, Sphingobium and Neobacillus were strongly correlated with key soil chemical properties, including nitrogen content, organic matter, and available phosphorus. These correlations suggest that tree cover strategies exert beneficial effects on the bacterial microbiome. Moreover, the overall bacterial community structure was different when comparing coffee monoculture system and shade-associated systems. Our findings highlight that traditional coffee agroforestry practices involving shade trees foster more diverse bacterial communities, thereby contributing to healthier soils and more sustainable coffee production.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Soil Microbiology
*Bacteria/classification/genetics/isolation & purification
RNA, Ribosomal, 16S/genetics
Biodiversity
*Trees/microbiology
*Musa/microbiology
Soil/chemistry
*Coffee
Plant Roots/microbiology
*Mangifera/microbiology
Phylogeny
Coffea
DNA, Bacterial/genetics
Agriculture/methods
Microbiota
RevDate: 2026-07-31
Decoding multifactorial stress responses in plants: lessons from omics integration.
Journal of experimental botany pii:8748560 [Epub ahead of print].
Plants in natural and agricultural environments are continuously exposed to multiple simultaneous abiotic stresses whose combined effects markedly differ from those of individual stresses. Despite this, our mechanistic understanding of plant stress biology still largely relies on reductionist frameworks based on single or pairwise interactions. Here, we argue that plant responses to increasing stress complexity are fundamentally non-additive and involve emergent molecular, metabolic, and physiological states that require a shift towards integrative and predictive approaches. We synthesize recent advances showing how signaling and metabolic networks are rewired under multifactorial stress combination (MFSC), leading to nonlinear behaviors and context-dependent regulation. We highlight the central role of multi-omics integration in uncovering system-level responses and discuss how emerging computational frameworks, including machine learning, can transform high-dimensional datasets into predictive models linking molecular states to plant performance. We further evaluate the limitations of current experimental systems, emphasizing the gap between controlled-environment studies and field conditions, where stress dynamics, microbiome interactions, and genotype × environment complexity shape plant responses. Together, we propose a roadmap towards a predictive science of plant resilience under MFSC, with direct implications for crop improvement in the context of climate change.
Additional Links: PMID-42536708
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PubMed:
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@article {pmid42536708,
year = {2026},
author = {Molinero-Domingo, L and S Pascual, L and Rivero, RM and Mittler, R and I Zandalinas, S},
title = {Decoding multifactorial stress responses in plants: lessons from omics integration.},
journal = {Journal of experimental botany},
volume = {},
number = {},
pages = {},
doi = {10.1093/jxb/erag389},
pmid = {42536708},
issn = {1460-2431},
abstract = {Plants in natural and agricultural environments are continuously exposed to multiple simultaneous abiotic stresses whose combined effects markedly differ from those of individual stresses. Despite this, our mechanistic understanding of plant stress biology still largely relies on reductionist frameworks based on single or pairwise interactions. Here, we argue that plant responses to increasing stress complexity are fundamentally non-additive and involve emergent molecular, metabolic, and physiological states that require a shift towards integrative and predictive approaches. We synthesize recent advances showing how signaling and metabolic networks are rewired under multifactorial stress combination (MFSC), leading to nonlinear behaviors and context-dependent regulation. We highlight the central role of multi-omics integration in uncovering system-level responses and discuss how emerging computational frameworks, including machine learning, can transform high-dimensional datasets into predictive models linking molecular states to plant performance. We further evaluate the limitations of current experimental systems, emphasizing the gap between controlled-environment studies and field conditions, where stress dynamics, microbiome interactions, and genotype × environment complexity shape plant responses. Together, we propose a roadmap towards a predictive science of plant resilience under MFSC, with direct implications for crop improvement in the context of climate change.},
}
RevDate: 2026-07-31
AI-2 type quorum-sensing signal enhances mercury resistance and adsorption in thermotolerant Bacillus subtilis.
Journal of hazardous materials, 515:143148 pii:S0304-3894(26)02128-X [Epub ahead of print].
Heavy metal contamination in coastal sediments threatens marine microbes and ecological health. Elucidating microbial community synergistic resistance mechanisms is essential for developing novel bioremediation strategies. Microorganisms are known to regulate population-level adaptation to environmental stress through quorum-sensing signals, yet the role of autoinducer-2 (AI-2) in mercury (Hg) resistance and immobilization remains poorly understood. Here, we isolated a thermotolerant Bacillus subtilis strain from coastal sediments and demonstrated that Hg stress selectively activated luxS-associated AI-2 production. AI-2 addition enhanced bacterial survival under combined Hg and heat stress by reducing intracellular reactive oxygen species, increasing antioxidant enzyme activities, promoting biofilm formation, and strengthening Hg adsorption. Sediment microcosm validation further showed that the B. subtilis + AI-2 treatment reduced soluble Hg by 29.6% after 24 h and increased the biomass-associated Hg fraction. These results reveal an AI-2-associated microbial strategy that links intracellular detoxification with extracellular Hg immobilization. While further genetic validation is needed to establish its causal role, this mechanism provides mechanistic insight for microbiome-assisted mercury remediation in thermally dynamic coastal sediments.
Additional Links: PMID-42537292
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PubMed:
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@article {pmid42537292,
year = {2026},
author = {Han, S and Mo, Q and Wen, X and Wang, X and Wang, X and Yu, Y and Yang, Y and Yang, C and Cai, Z and Zhou, J},
title = {AI-2 type quorum-sensing signal enhances mercury resistance and adsorption in thermotolerant Bacillus subtilis.},
journal = {Journal of hazardous materials},
volume = {515},
number = {},
pages = {143148},
doi = {10.1016/j.jhazmat.2026.143148},
pmid = {42537292},
issn = {1873-3336},
abstract = {Heavy metal contamination in coastal sediments threatens marine microbes and ecological health. Elucidating microbial community synergistic resistance mechanisms is essential for developing novel bioremediation strategies. Microorganisms are known to regulate population-level adaptation to environmental stress through quorum-sensing signals, yet the role of autoinducer-2 (AI-2) in mercury (Hg) resistance and immobilization remains poorly understood. Here, we isolated a thermotolerant Bacillus subtilis strain from coastal sediments and demonstrated that Hg stress selectively activated luxS-associated AI-2 production. AI-2 addition enhanced bacterial survival under combined Hg and heat stress by reducing intracellular reactive oxygen species, increasing antioxidant enzyme activities, promoting biofilm formation, and strengthening Hg adsorption. Sediment microcosm validation further showed that the B. subtilis + AI-2 treatment reduced soluble Hg by 29.6% after 24 h and increased the biomass-associated Hg fraction. These results reveal an AI-2-associated microbial strategy that links intracellular detoxification with extracellular Hg immobilization. While further genetic validation is needed to establish its causal role, this mechanism provides mechanistic insight for microbiome-assisted mercury remediation in thermally dynamic coastal sediments.},
}
RevDate: 2026-07-31
Changes in dysbiosis and gene expression in the gut of wharf roach (Ligia spp.) fed with expanded polystyrene.
Marine pollution bulletin, 233(Pt 1):120200 pii:S0025-326X(26)00987-2 [Epub ahead of print].
The East Asian region, with its intensive human and fishery activity, suffers from serious marine plastic pollution along its coastlines. Wharf roaches (Ligia spp.) on the coast of western Japan frequently ingest expanded polystyrene (EPS) and excrete it as microplastic in their feces, yet the effects on their gut remain unclear. Under controlled laboratory exposure, we examined both the host gut transcriptome, and the gut microbiome of wharf roaches fed EPS versus a fasted control group. DESeq2 and PyDESeq2 yielded a high-confidence set of 25 differentially expressed genes, among which xenobiotic-metabolism enzymes-a cytochrome P450, a UDP-glucuronosyltransferase, and a sulfotransferase-were up-regulated in the EPS-fed group. In contrast, the overall gut microbial community structure was unchanged: neither alpha nor beta diversity differed significantly between groups in any domain. At the taxon level, a few low-abundance archaeal and viral taxa, including the archaea Methanospirillum, Halalkalicoccus, and Desulfurococcus, and T4-like viruses, were detected in all EPS samples but were below the detection limit in all controls. Because the comparison used a fasted control, the extent to which these responses are specific to EPS exposure remains to be established. Building on previous field studies identifying wharf roaches as bioindicators of coastal EPS pollution, this study highlights the wharf roach as a tractable model for investigating the gut-level effects of plastic ingestion.
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@article {pmid42537413,
year = {2026},
author = {Lee, S and Miyamoto, H and Takai, Y and Suda, W and Ohno, H and Shimasaki, Y and Oshima, Y},
title = {Changes in dysbiosis and gene expression in the gut of wharf roach (Ligia spp.) fed with expanded polystyrene.},
journal = {Marine pollution bulletin},
volume = {233},
number = {Pt 1},
pages = {120200},
doi = {10.1016/j.marpolbul.2026.120200},
pmid = {42537413},
issn = {1879-3363},
abstract = {The East Asian region, with its intensive human and fishery activity, suffers from serious marine plastic pollution along its coastlines. Wharf roaches (Ligia spp.) on the coast of western Japan frequently ingest expanded polystyrene (EPS) and excrete it as microplastic in their feces, yet the effects on their gut remain unclear. Under controlled laboratory exposure, we examined both the host gut transcriptome, and the gut microbiome of wharf roaches fed EPS versus a fasted control group. DESeq2 and PyDESeq2 yielded a high-confidence set of 25 differentially expressed genes, among which xenobiotic-metabolism enzymes-a cytochrome P450, a UDP-glucuronosyltransferase, and a sulfotransferase-were up-regulated in the EPS-fed group. In contrast, the overall gut microbial community structure was unchanged: neither alpha nor beta diversity differed significantly between groups in any domain. At the taxon level, a few low-abundance archaeal and viral taxa, including the archaea Methanospirillum, Halalkalicoccus, and Desulfurococcus, and T4-like viruses, were detected in all EPS samples but were below the detection limit in all controls. Because the comparison used a fasted control, the extent to which these responses are specific to EPS exposure remains to be established. Building on previous field studies identifying wharf roaches as bioindicators of coastal EPS pollution, this study highlights the wharf roach as a tractable model for investigating the gut-level effects of plastic ingestion.},
}
RevDate: 2026-07-31
Near-infrared spectroscopy with chemometric analysis distinguishes genitourinary syndrome of menopause in vaginal samples.
European journal of obstetrics, gynecology, and reproductive biology, 325:115336 pii:S0301-2115(26)00404-5 [Epub ahead of print].
BACKGROUND: Genitourinary syndrome of menopause (GSM) is a prevalent condition characterized by estrogen deficiency-induced vulvovaginal and urinary symptoms, yet lacks objective diagnostic biomarkers.
OBJECTIVE: This study aimed to investigate whether near-infrared (NIR) spectroscopy combined with multivariate chemometrics analysis of vaginal samples could serve as a quantitative diagnostic tool for GSM.
DESIGN: We applied NIR spectroscopy combined with multivariate chemometric analysis to vaginal samples from 81 postmenopausal women (50 GSM cases, 31 controls), assessing vaginal health via the Vaginal Health Index (VHI).
RESULTS: Women with GSM had significantly lower total VHI scores. GSM samples exhibited distinct spectral signatures related to tissue hydration, lipids, and proteins. Classification models using genetic and successive projections algorithms coupled with linear discriminant analysis achieved 100% accuracy in independent validation.
CONCLUSION: For the first time, this study demonstrated that NIR spectroscopy with chemometrics enables non-invasive, objective discrimination of GSM, supporting a shift from subjective symptom assessment toward quantitative molecular phenotyping. This study offers a novel perspective on the spectral differences associated with GSM. This approach holds promise for point-of-care diagnostics and monitoring therapeutic response, pending further validation. These findings should be regarded as hypothesis-generating, derived from a single-center pilot cohort, and require confirmation in larger, multicenter, prospective studies incorporating microbiome analysis before clinical implementation.
Additional Links: PMID-42537619
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@article {pmid42537619,
year = {2026},
author = {da Silva Figueiredo Vidal, I and de Souza, ATB and Silva, LG and de Andrade Santana, LH and de Morais Filho, JR and Câmara, ABF and Cobucci, RN and de Lima, KMG and de Oliveira Crispim, JC},
title = {Near-infrared spectroscopy with chemometric analysis distinguishes genitourinary syndrome of menopause in vaginal samples.},
journal = {European journal of obstetrics, gynecology, and reproductive biology},
volume = {325},
number = {},
pages = {115336},
doi = {10.1016/j.ejogrb.2026.115336},
pmid = {42537619},
issn = {1872-7654},
abstract = {BACKGROUND: Genitourinary syndrome of menopause (GSM) is a prevalent condition characterized by estrogen deficiency-induced vulvovaginal and urinary symptoms, yet lacks objective diagnostic biomarkers.
OBJECTIVE: This study aimed to investigate whether near-infrared (NIR) spectroscopy combined with multivariate chemometrics analysis of vaginal samples could serve as a quantitative diagnostic tool for GSM.
DESIGN: We applied NIR spectroscopy combined with multivariate chemometric analysis to vaginal samples from 81 postmenopausal women (50 GSM cases, 31 controls), assessing vaginal health via the Vaginal Health Index (VHI).
RESULTS: Women with GSM had significantly lower total VHI scores. GSM samples exhibited distinct spectral signatures related to tissue hydration, lipids, and proteins. Classification models using genetic and successive projections algorithms coupled with linear discriminant analysis achieved 100% accuracy in independent validation.
CONCLUSION: For the first time, this study demonstrated that NIR spectroscopy with chemometrics enables non-invasive, objective discrimination of GSM, supporting a shift from subjective symptom assessment toward quantitative molecular phenotyping. This study offers a novel perspective on the spectral differences associated with GSM. This approach holds promise for point-of-care diagnostics and monitoring therapeutic response, pending further validation. These findings should be regarded as hypothesis-generating, derived from a single-center pilot cohort, and require confirmation in larger, multicenter, prospective studies incorporating microbiome analysis before clinical implementation.},
}
RevDate: 2026-07-31
Early-life immune imprinting by a B. infantis-HMO synbiotic shapes infant immune signatures and protects against experimental respiratory disease.
Cell reports. Medicine pii:S2666-3791(26)00352-6 [Epub ahead of print].
Early microbial colonization influences immune development, with lower abundance of human milk oligosaccharide (HMO)-utilizing bifidobacteria linked to immune-related disorder risk. Here, we demonstrate that synbiotic supplementation with Bifidobacterium infantis (LMG 11588) and a blend of six structurally diverse HMOs plus Bifidobacterium lactis (CNCM I-3446) altered gut microbiome composition, changed systemic immune cell-networks, and reduced persistence of a T helper 2 (Th2) bias in formula-fed infants, following a pattern observed in breastfed infants. In preclinical models, synbiotic reduces lower respiratory tract infection (LRI) severity and aberrant type-2 immune responses and confers lasting immune benefits into adulthood. These effects are associated with changes in the circulating metabolome, including increased 12(S)-hydroxyheptadecatrienoic acid (12-HHT), which correlates with improved infection outcomes and phenocopies synbiotic-mediated protection when administered orally. Together, these findings indicate that infant-type synbiotic supplementation during a critical early-life window can imprint immune function and promote disease tolerance.
Additional Links: PMID-42537648
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@article {pmid42537648,
year = {2026},
author = {Rashid, RB and Chung, CK and Namubiru, P and Ahmed, T and , and Howard, DR and Sebina, I and Wilkins, T and Rana, MS and Morrow, JP and Creek, DJ and Moll, JM and Vidal, K and Fumero, C and Lavalle, L and Maes, D and Hays, NP and Silva-Zolezzi, I and Forbes-Blom, E and Sprenger, N and Picaud, JC and Phipps, S and Noti, M},
title = {Early-life immune imprinting by a B. infantis-HMO synbiotic shapes infant immune signatures and protects against experimental respiratory disease.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {102935},
doi = {10.1016/j.xcrm.2026.102935},
pmid = {42537648},
issn = {2666-3791},
abstract = {Early microbial colonization influences immune development, with lower abundance of human milk oligosaccharide (HMO)-utilizing bifidobacteria linked to immune-related disorder risk. Here, we demonstrate that synbiotic supplementation with Bifidobacterium infantis (LMG 11588) and a blend of six structurally diverse HMOs plus Bifidobacterium lactis (CNCM I-3446) altered gut microbiome composition, changed systemic immune cell-networks, and reduced persistence of a T helper 2 (Th2) bias in formula-fed infants, following a pattern observed in breastfed infants. In preclinical models, synbiotic reduces lower respiratory tract infection (LRI) severity and aberrant type-2 immune responses and confers lasting immune benefits into adulthood. These effects are associated with changes in the circulating metabolome, including increased 12(S)-hydroxyheptadecatrienoic acid (12-HHT), which correlates with improved infection outcomes and phenocopies synbiotic-mediated protection when administered orally. Together, these findings indicate that infant-type synbiotic supplementation during a critical early-life window can imprint immune function and promote disease tolerance.},
}
RevDate: 2026-07-31
Industrial additive and dietary fiber inulin induces tumor-selective necrotic death via mitochondrial lipid peroxidation involving MYC and YAP.
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association pii:S0278-6915(26)00383-2 [Epub ahead of print].
Inulin as a prebiotic fiber and an industrial additive, has been shown to regulate gut and small intestinal microbiome for health, but non-microbiota-dependent cellular pathways remain unclear. Here we aim to determine how the natural polysaccharide inulin reshapes metabolic stress responses especially in colon cancer cells. In tumor cells treated by inulin, oxidized lipids accumulated in the perimitochondrial region and were accompanied by mitochondrial fragmentation, Golgi dispersion, endoplasmic reticulum (ER) disorganization, lysosomal remodeling, increased mitochondrially encoded cytochrome c oxidase II (MTCO2), and nuclear p21, indicating organelle stress coupled to metabolic reprogramming. Non-malignant cells showed elevated lipid peroxidation but limited necrotic death, consistent with greater metabolic tolerance. YAP/MYC inhibition increased inulin sensitivity. Importantly, ataxia telangiectasia and Rad3-related (ATR) supported stress adaptation, particularly in normal cells. Additionally, inulin decreased nuclear active MYC and YAP and enhanced nuclear androgen receptor (AR). Network pharmacology identified inulin against colon cancer by AR-related hub gene PTGS2 (prostaglandin G/H synthase-2) and validated by a synergistic combination with progesterone. Thus, inulin triggers tumor-selective metabolic stress and disrupts adaptive MYC/YAP, providing a rationale for metabolism-based precision cancer therapy.
Additional Links: PMID-42537713
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@article {pmid42537713,
year = {2026},
author = {Li, M and Kablan, A and Toktau, G and Ahmad, A and Meng, L and Li, Z and Zuo, Z and Gemingbai, S and Otebay, A and Satiyeva, A and Xie, Y},
title = {Industrial additive and dietary fiber inulin induces tumor-selective necrotic death via mitochondrial lipid peroxidation involving MYC and YAP.},
journal = {Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association},
volume = {},
number = {},
pages = {116309},
doi = {10.1016/j.fct.2026.116309},
pmid = {42537713},
issn = {1873-6351},
abstract = {Inulin as a prebiotic fiber and an industrial additive, has been shown to regulate gut and small intestinal microbiome for health, but non-microbiota-dependent cellular pathways remain unclear. Here we aim to determine how the natural polysaccharide inulin reshapes metabolic stress responses especially in colon cancer cells. In tumor cells treated by inulin, oxidized lipids accumulated in the perimitochondrial region and were accompanied by mitochondrial fragmentation, Golgi dispersion, endoplasmic reticulum (ER) disorganization, lysosomal remodeling, increased mitochondrially encoded cytochrome c oxidase II (MTCO2), and nuclear p21, indicating organelle stress coupled to metabolic reprogramming. Non-malignant cells showed elevated lipid peroxidation but limited necrotic death, consistent with greater metabolic tolerance. YAP/MYC inhibition increased inulin sensitivity. Importantly, ataxia telangiectasia and Rad3-related (ATR) supported stress adaptation, particularly in normal cells. Additionally, inulin decreased nuclear active MYC and YAP and enhanced nuclear androgen receptor (AR). Network pharmacology identified inulin against colon cancer by AR-related hub gene PTGS2 (prostaglandin G/H synthase-2) and validated by a synergistic combination with progesterone. Thus, inulin triggers tumor-selective metabolic stress and disrupts adaptive MYC/YAP, providing a rationale for metabolism-based precision cancer therapy.},
}
RevDate: 2026-07-31
Beyond the parasite: reframing cutaneous leishmaniasis as a host-microbiome-vector ecosystem.
International journal of pharmaceutics pii:S0378-5173(26)00698-8 [Epub ahead of print].
Disease outcomes of cutaneous leishmaniasis (CL) result from dynamic interactions between host immunity, Leishmania parasites and the host-sandfly microbiomes. Current treatments focus on parasite elimination but are limited by toxicity, drug resistance, side effects and poor wound healing. These challenges highlight the need for multi-targeted interventions by transforming CL treatment from a single-infection model to an integrated host-microbe-parasite model. This review features advances in host-microbe-parasite-vector-based strategies for CL treatment, including emerging engineering and synthetic biology approaches. We also discuss the growing role of computational and artificial intelligence (AI)-driven frameworks in guiding the design of novel therapeutics and enhancing the efficacy of existing treatments. Climate change through rising temperatures, altered precipitation, and extended suitable habitats, is likely to increase the risk and geographic range of CL in many parts of the world. By integrating these engineering platforms with AI-guided approaches, this review outlines a systems-level strategy for developing next-generation therapies aimed at reducing the global burden of CL.
Additional Links: PMID-42537823
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PubMed:
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@article {pmid42537823,
year = {2026},
author = {Laetitia Huët, MA and Bhaw-Luximon, A},
title = {Beyond the parasite: reframing cutaneous leishmaniasis as a host-microbiome-vector ecosystem.},
journal = {International journal of pharmaceutics},
volume = {},
number = {},
pages = {127250},
doi = {10.1016/j.ijpharm.2026.127250},
pmid = {42537823},
issn = {1873-3476},
abstract = {Disease outcomes of cutaneous leishmaniasis (CL) result from dynamic interactions between host immunity, Leishmania parasites and the host-sandfly microbiomes. Current treatments focus on parasite elimination but are limited by toxicity, drug resistance, side effects and poor wound healing. These challenges highlight the need for multi-targeted interventions by transforming CL treatment from a single-infection model to an integrated host-microbe-parasite model. This review features advances in host-microbe-parasite-vector-based strategies for CL treatment, including emerging engineering and synthetic biology approaches. We also discuss the growing role of computational and artificial intelligence (AI)-driven frameworks in guiding the design of novel therapeutics and enhancing the efficacy of existing treatments. Climate change through rising temperatures, altered precipitation, and extended suitable habitats, is likely to increase the risk and geographic range of CL in many parts of the world. By integrating these engineering platforms with AI-guided approaches, this review outlines a systems-level strategy for developing next-generation therapies aimed at reducing the global burden of CL.},
}
RevDate: 2026-07-31
CmpDate: 2026-07-31
Probiotics for Primary or Secondary Prevention of Clostridioides difficile Infection.
Gastroenterology clinics of North America, 55(3):433-445.
Clostridioides difficile infection (CDI) is a leading cause of hospital-acquired infectious diarrhea, often triggered by disruption of the gut microbiota. Recurrence is common after antibiotic treatment, prompting interest in microbial therapies such as probiotics. While some studies suggest probiotics may help prevent initial or recurrent CDI episodes, overall evidence remains inconsistent. Data on prebiotics and synbiotics are even more limited. Although generally safe, probiotics may delay restoration of the normal microbiome, which is key to preventing recurrence. Current guidelines vary from cautious support to discouragement of their use, leaving the role of these therapies in CDI management uncertain and investigational.
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@article {pmid42538087,
year = {2026},
author = {Kaiser-Powers, T and Weingarden, AR},
title = {Probiotics for Primary or Secondary Prevention of Clostridioides difficile Infection.},
journal = {Gastroenterology clinics of North America},
volume = {55},
number = {3},
pages = {433-445},
doi = {10.1016/j.gtc.2026.05.004},
pmid = {42538087},
issn = {1558-1942},
mesh = {Humans ; *Probiotics/therapeutic use ; *Clostridium Infections/prevention & control ; *Secondary Prevention/methods ; Clostridioides difficile ; Primary Prevention/methods ; Prebiotics ; Anti-Bacterial Agents/therapeutic use ; Synbiotics ; },
abstract = {Clostridioides difficile infection (CDI) is a leading cause of hospital-acquired infectious diarrhea, often triggered by disruption of the gut microbiota. Recurrence is common after antibiotic treatment, prompting interest in microbial therapies such as probiotics. While some studies suggest probiotics may help prevent initial or recurrent CDI episodes, overall evidence remains inconsistent. Data on prebiotics and synbiotics are even more limited. Although generally safe, probiotics may delay restoration of the normal microbiome, which is key to preventing recurrence. Current guidelines vary from cautious support to discouragement of their use, leaving the role of these therapies in CDI management uncertain and investigational.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Probiotics/therapeutic use
*Clostridium Infections/prevention & control
*Secondary Prevention/methods
Clostridioides difficile
Primary Prevention/methods
Prebiotics
Anti-Bacterial Agents/therapeutic use
Synbiotics
RevDate: 2026-07-31
CmpDate: 2026-07-31
Non-Fecal Microbiota Transplantation Strategies for Treatment of Recurrent Clostridioides difficile Infection.
Gastroenterology clinics of North America, 55(3):493-501.
Clostridioides difficile infection (CDI) is a leading healthcare-associated illness with significant recurrence rates and clinical burden. Recurrent CDI (rCDI) arises from microbiota disruption, often exacerbated by antibiotic therapy. Current treatment strategies include fidaxomicin and vancomycin taper regimens, with adjunctive options such as rifaximin in select cases. Preventive approaches focus on environmental decontamination and microbiome preservation. Emerging therapies, including live biotherapeutics, non-toxigenic strains, and microbiome-protective agents, show promise in reducing recurrence. Dietary interventions that enhance microbial diversity may also support recovery. Together, these strategies highlight a shift toward microbiome-centered management of rCDI.
Additional Links: PMID-42538092
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@article {pmid42538092,
year = {2026},
author = {Adamopoulos, A and Stollman, N},
title = {Non-Fecal Microbiota Transplantation Strategies for Treatment of Recurrent Clostridioides difficile Infection.},
journal = {Gastroenterology clinics of North America},
volume = {55},
number = {3},
pages = {493-501},
doi = {10.1016/j.gtc.2026.05.009},
pmid = {42538092},
issn = {1558-1942},
mesh = {Humans ; *Clostridium Infections/therapy/microbiology ; Anti-Bacterial Agents/therapeutic use ; Recurrence ; Clostridioides difficile ; Fidaxomicin/therapeutic use ; Vancomycin/therapeutic use ; *Gastrointestinal Microbiome ; Fecal Microbiota Transplantation ; Secondary Prevention ; Microbiota ; },
abstract = {Clostridioides difficile infection (CDI) is a leading healthcare-associated illness with significant recurrence rates and clinical burden. Recurrent CDI (rCDI) arises from microbiota disruption, often exacerbated by antibiotic therapy. Current treatment strategies include fidaxomicin and vancomycin taper regimens, with adjunctive options such as rifaximin in select cases. Preventive approaches focus on environmental decontamination and microbiome preservation. Emerging therapies, including live biotherapeutics, non-toxigenic strains, and microbiome-protective agents, show promise in reducing recurrence. Dietary interventions that enhance microbial diversity may also support recovery. Together, these strategies highlight a shift toward microbiome-centered management of rCDI.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Clostridium Infections/therapy/microbiology
Anti-Bacterial Agents/therapeutic use
Recurrence
Clostridioides difficile
Fidaxomicin/therapeutic use
Vancomycin/therapeutic use
*Gastrointestinal Microbiome
Fecal Microbiota Transplantation
Secondary Prevention
Microbiota
RevDate: 2026-07-31
CmpDate: 2026-07-31
Food and Drug Administration-Approved Fecal Microbiota-Based Therapies for Recurrent Clostridioides difficile Infection.
Gastroenterology clinics of North America, 55(3):503-516.
Recurrent Clostridioides difficile infection remains common despite optimized antibiotic therapy. Two Food and Drug Administration-approved donor-derived fecal microbiota-based products, fecal microbiota, live-jslm (Rebyota / RBL) and fecal microbiota spores, live-brpk (Vowst / VOS) reduce recurrence when administered after completion of standard antibiotics. This review summarizes the clinical development programs supporting these products, including pivotal randomized trials, open-label extensions, durability data, safety outcomes, and emerging real-world evidence. We also discuss patient selection, timing after antibiotics, diagnostic considerations, and practical implementation. These therapies represent standardized, evidence-based approaches to restoring colonization resistance and preventing recurrent infection in appropriately selected adults.
Additional Links: PMID-42538093
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@article {pmid42538093,
year = {2026},
author = {Berry, P and Allegretti, JR and Khanna, S},
title = {Food and Drug Administration-Approved Fecal Microbiota-Based Therapies for Recurrent Clostridioides difficile Infection.},
journal = {Gastroenterology clinics of North America},
volume = {55},
number = {3},
pages = {503-516},
doi = {10.1016/j.gtc.2026.05.010},
pmid = {42538093},
issn = {1558-1942},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Clostridium Infections/therapy ; Recurrence ; United States ; Clostridioides difficile ; Anti-Bacterial Agents/therapeutic use ; United States Food and Drug Administration ; Secondary Prevention/methods ; },
abstract = {Recurrent Clostridioides difficile infection remains common despite optimized antibiotic therapy. Two Food and Drug Administration-approved donor-derived fecal microbiota-based products, fecal microbiota, live-jslm (Rebyota / RBL) and fecal microbiota spores, live-brpk (Vowst / VOS) reduce recurrence when administered after completion of standard antibiotics. This review summarizes the clinical development programs supporting these products, including pivotal randomized trials, open-label extensions, durability data, safety outcomes, and emerging real-world evidence. We also discuss patient selection, timing after antibiotics, diagnostic considerations, and practical implementation. These therapies represent standardized, evidence-based approaches to restoring colonization resistance and preventing recurrent infection in appropriately selected adults.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Fecal Microbiota Transplantation/methods
*Clostridium Infections/therapy
Recurrence
United States
Clostridioides difficile
Anti-Bacterial Agents/therapeutic use
United States Food and Drug Administration
Secondary Prevention/methods
RevDate: 2026-07-29
The Methicillin-Resistant S pseudintermedius Crisis: Are We Out of Options to Treat the Most Common Canine Pathogen?.
The Veterinary clinics of North America. Small animal practice pii:S0195-5616(26)00085-9 [Epub ahead of print].
S pseudintermedius is a leading cause of canine pyoderma and an important pathogen in small animal skin, soft tissue, otic, wound, and postoperative infections. The emergence of methicillin-resistant S pseudintermedius (MRSP) has made recurrent infections more difficult to manage by combining multidrug resistance, biofilm-associated persistence, treatment failure, and repeated antimicrobial exposure. This article reviews MRSP emergence and epidemiology, mechanisms of resistance and recurrence, and the limitations of current treatment options. It discusses emerging therapeutic strategies, including phage-based therapies, microbiome-directed interventions, immune modulation, nanomaterials, photodynamic therapy, and antimicrobial peptides, that serve as adjuncts to standard care and reduce reliance on systemic antimicrobials.
Additional Links: PMID-42527298
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@article {pmid42527298,
year = {2026},
author = {Pluta, DH and Gilbertie, JM},
title = {The Methicillin-Resistant S pseudintermedius Crisis: Are We Out of Options to Treat the Most Common Canine Pathogen?.},
journal = {The Veterinary clinics of North America. Small animal practice},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cvsm.2026.06.004},
pmid = {42527298},
issn = {1878-1306},
abstract = {S pseudintermedius is a leading cause of canine pyoderma and an important pathogen in small animal skin, soft tissue, otic, wound, and postoperative infections. The emergence of methicillin-resistant S pseudintermedius (MRSP) has made recurrent infections more difficult to manage by combining multidrug resistance, biofilm-associated persistence, treatment failure, and repeated antimicrobial exposure. This article reviews MRSP emergence and epidemiology, mechanisms of resistance and recurrence, and the limitations of current treatment options. It discusses emerging therapeutic strategies, including phage-based therapies, microbiome-directed interventions, immune modulation, nanomaterials, photodynamic therapy, and antimicrobial peptides, that serve as adjuncts to standard care and reduce reliance on systemic antimicrobials.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Clostridium innocuum Bacteremia: Case Report and Systematic Review.
South Dakota medicine : the journal of the South Dakota State Medical Association, 79(6):271-273.
Clostridium innocuum is an anaerobic gram-positive spore-forming bacteria, a commensal member of the human gut microbiome. We encountered a case of bacteremia with this organism as a complication of a foot ulcer in a middle-aged patient with diabetes, end-stage renal disease, and malnutrition. A systematic review of the limited number of previously reported cases of C. innocuum bacteremia is presented, along with a brief narrative review the organism's association with other diseases, ranging from diarrhea and local infections to modulating inflammatory bowel disease and kidney disease.
Additional Links: PMID-42527363
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@article {pmid42527363,
year = {2026},
author = {de Matos-Konrad, C and Chima, N and Huntington, MK},
title = {Clostridium innocuum Bacteremia: Case Report and Systematic Review.},
journal = {South Dakota medicine : the journal of the South Dakota State Medical Association},
volume = {79},
number = {6},
pages = {271-273},
pmid = {42527363},
issn = {0038-3317},
mesh = {Humans ; *Clostridium Infections/diagnosis/drug therapy/microbiology ; *Bacteremia/microbiology/drug therapy/diagnosis ; *Clostridium/isolation & purification ; Middle Aged ; Anti-Bacterial Agents/therapeutic use ; *Diabetic Foot/complications ; Male ; Kidney Failure, Chronic/complications ; },
abstract = {Clostridium innocuum is an anaerobic gram-positive spore-forming bacteria, a commensal member of the human gut microbiome. We encountered a case of bacteremia with this organism as a complication of a foot ulcer in a middle-aged patient with diabetes, end-stage renal disease, and malnutrition. A systematic review of the limited number of previously reported cases of C. innocuum bacteremia is presented, along with a brief narrative review the organism's association with other diseases, ranging from diarrhea and local infections to modulating inflammatory bowel disease and kidney disease.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Clostridium Infections/diagnosis/drug therapy/microbiology
*Bacteremia/microbiology/drug therapy/diagnosis
*Clostridium/isolation & purification
Middle Aged
Anti-Bacterial Agents/therapeutic use
*Diabetic Foot/complications
Male
Kidney Failure, Chronic/complications
RevDate: 2026-07-29
Sex-specific modulation of lung function and transcriptome in neonate mice exposed to thirdhand electronic-cigarette aerosols.
Pediatric research [Epub ahead of print].
BACKGROUND: Vaping is increasingly prevalent among young adults at age for starting families. Thirdhand e-cigarette aerosols (THEA) are persistent residues that adhere to indoor surfaces and can resuspend in air. Since lung development continues after birth, infants from homes with adults who vape, are vulnerable to THEA exposures.
METHODS: Neonate mice were exposed to THEA with nicotine or nicotine + tobacco-flavoring from terrycloth and carpet for the first 21 days of life. We assessed broncho-alveolar lavage cytology, lung morphometry, gene expression, and intestinal microbiomes at 21 days. At 10 weeks, we evaluated lung function.
RESULTS: We showed that exposures to THEA during alveologenesis, a critical window of lung development, induced sex-specific alterations in pulmonary inflammatory and developmental trajectories. Females exhibited acute pulmonary neutrophilic inflammation with a resolving cytokine profile. In contrast, males exhibited upregulation of genes associated with pulmonary inflammation and epithelial mesenchymal transition, plus delayed lung development, leading to lung dysfunction in adulthood. Male gut microbiomes showed reduced abundance of taxa associated with xenobiotic biotransformation, suggesting host-microbial detoxification capacity as a target of THEA exposure.
CONCLUSION: Low-level of THEA exposures in early life can alter lung inflammation, structure, and function, increasing susceptibility to respiratory dysfunction later in life.
IMPACT: Early-life exposures to nicotine and carbonyls from thirdhand e-cigarette aerosols (THEA) may induce alterations in lung alveologenesis and augment susceptibility to lung conditions later in life. Using a preclinical model of pediatric airways, we showed that THEA exposures caused neutrophilic inflammation in neonate female mice. In neonate male mice, THEA exposures led to alterations in lung structure, gene expression, and gut microbiome dysbiosis. Adult male mice exposed to THEA as neonates exhibited decline in lung function characteristic of obstructive pulmonary physiology.
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@article {pmid42527537,
year = {2026},
author = {Zaman, A and Cook, T and Mabou, DB and Schexnayder, M and Xiao, R and Perveen, Z and Penn, AL and Noël, A},
title = {Sex-specific modulation of lung function and transcriptome in neonate mice exposed to thirdhand electronic-cigarette aerosols.},
journal = {Pediatric research},
volume = {},
number = {},
pages = {},
pmid = {42527537},
issn = {1530-0447},
abstract = {BACKGROUND: Vaping is increasingly prevalent among young adults at age for starting families. Thirdhand e-cigarette aerosols (THEA) are persistent residues that adhere to indoor surfaces and can resuspend in air. Since lung development continues after birth, infants from homes with adults who vape, are vulnerable to THEA exposures.
METHODS: Neonate mice were exposed to THEA with nicotine or nicotine + tobacco-flavoring from terrycloth and carpet for the first 21 days of life. We assessed broncho-alveolar lavage cytology, lung morphometry, gene expression, and intestinal microbiomes at 21 days. At 10 weeks, we evaluated lung function.
RESULTS: We showed that exposures to THEA during alveologenesis, a critical window of lung development, induced sex-specific alterations in pulmonary inflammatory and developmental trajectories. Females exhibited acute pulmonary neutrophilic inflammation with a resolving cytokine profile. In contrast, males exhibited upregulation of genes associated with pulmonary inflammation and epithelial mesenchymal transition, plus delayed lung development, leading to lung dysfunction in adulthood. Male gut microbiomes showed reduced abundance of taxa associated with xenobiotic biotransformation, suggesting host-microbial detoxification capacity as a target of THEA exposure.
CONCLUSION: Low-level of THEA exposures in early life can alter lung inflammation, structure, and function, increasing susceptibility to respiratory dysfunction later in life.
IMPACT: Early-life exposures to nicotine and carbonyls from thirdhand e-cigarette aerosols (THEA) may induce alterations in lung alveologenesis and augment susceptibility to lung conditions later in life. Using a preclinical model of pediatric airways, we showed that THEA exposures caused neutrophilic inflammation in neonate female mice. In neonate male mice, THEA exposures led to alterations in lung structure, gene expression, and gut microbiome dysbiosis. Adult male mice exposed to THEA as neonates exhibited decline in lung function characteristic of obstructive pulmonary physiology.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Gut microbiota restricts intestinal lipid uptake via modulation of bile phosphatidylcholine metabolism in mice.
Nature microbiology, 11(8):2349-2364.
The gut microbiota influences host metabolism, but the mechanisms of lipid uptake from food remain mysterious. Here we used stable isotope-labelled tracers in gnotobiotic mouse models, which revealed that host uptake of dietary lipids depends on microbial colonization. Systemic lipid metabolism modelling predicted that the gut microbiota restricts intestinal lipid absorption, and labelled lipid administration verified that the gut contents of microbiota-colonized mice contained up to 12-fold more lipids than those of germ-free animals. A combination of lipidomics and proteomics showed that gut microbes trigger Myd88 signalling, leading to a downregulation of hepatic Cyp7b1 activity and increased taurocholate production. Taurocholate stimulates phospholipase A1 activity in bile, causing the degradation of phosphatidylcholine that is essential for luminal micelle formation and lipid uptake. A diverse microbiome was associated with lower phosphatidylcholine content. This previously unrecognized host-gut microbiota interplay via enzymes in bile could provide future targets to modulate dietary lipid absorption.
Additional Links: PMID-42527633
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Citation:
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@article {pmid42527633,
year = {2026},
author = {Brunner, S and Plagge, J and Zimmermann-Kogadeeva, M and Höring, M and Liebisch, G and Basic, M and Bolsega, S and Janssen, KP and Slack, E and von Gamm, S and Viehof-Beckmann, A and Clavel, T and Zimmermann, M and Heeren, J and Giansanti, P and Weiss, AS and Hermeling, S and Dupont, A and Ullrich, AL and Jokisch, F and Seeliger, C and Bleich, A and Hidrobo, M and Stecher, B and Coleman, OI and Moresi, C and Greter, G and Arnoldini, M and Scheiber, J and Matysik, S and Klingenspor, M and Küster, B and Haller, D and Burkhardt, R and Kuipers, F and Ecker, J},
title = {Gut microbiota restricts intestinal lipid uptake via modulation of bile phosphatidylcholine metabolism in mice.},
journal = {Nature microbiology},
volume = {11},
number = {8},
pages = {2349-2364},
pmid = {42527633},
issn = {2058-5276},
support = {395357507-SFB 1371, P13//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 446175916//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; INST 95/1650-1 FUGG//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 395357507-SFB 1371//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 279971426//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; },
mesh = {Animals ; *Phosphatidylcholines/metabolism ; Mice ; *Bile/metabolism ; *Lipid Metabolism ; *Gastrointestinal Microbiome/physiology ; Germ-Free Life ; Taurocholic Acid/metabolism ; Mice, Inbred C57BL ; Liver/metabolism ; Male ; Intestinal Absorption ; Intestinal Mucosa/metabolism ; },
abstract = {The gut microbiota influences host metabolism, but the mechanisms of lipid uptake from food remain mysterious. Here we used stable isotope-labelled tracers in gnotobiotic mouse models, which revealed that host uptake of dietary lipids depends on microbial colonization. Systemic lipid metabolism modelling predicted that the gut microbiota restricts intestinal lipid absorption, and labelled lipid administration verified that the gut contents of microbiota-colonized mice contained up to 12-fold more lipids than those of germ-free animals. A combination of lipidomics and proteomics showed that gut microbes trigger Myd88 signalling, leading to a downregulation of hepatic Cyp7b1 activity and increased taurocholate production. Taurocholate stimulates phospholipase A1 activity in bile, causing the degradation of phosphatidylcholine that is essential for luminal micelle formation and lipid uptake. A diverse microbiome was associated with lower phosphatidylcholine content. This previously unrecognized host-gut microbiota interplay via enzymes in bile could provide future targets to modulate dietary lipid absorption.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Phosphatidylcholines/metabolism
Mice
*Bile/metabolism
*Lipid Metabolism
*Gastrointestinal Microbiome/physiology
Germ-Free Life
Taurocholic Acid/metabolism
Mice, Inbred C57BL
Liver/metabolism
Male
Intestinal Absorption
Intestinal Mucosa/metabolism
RevDate: 2026-07-29
Short-chain fatty acids.
Nature metabolism [Epub ahead of print].
Short-chain fatty acids (SCFAs), principally acetate, propionate and butyrate, are produced by the gut microbiota through the fermentation of non-digestible carbohydrates. Beyond serving as energy substrates, SCFAs act as signalling molecules that influence metabolism, immune function and physiological homeostasis across multiple organ systems. This Review consolidates the fragmented literature on SCFAs and provides an overview of their production, metabolism and physiological actions. We discuss the microbial and dietary determinants of SCFA production, including the roles of the gut microbiome, cross-feeding interactions and dietary carbohydrates. We then examine the mechanisms through which SCFAs exert their effects, focusing on receptor-mediated signalling, epigenetic regulation and tissue-specific physiological functions. Finally, we evaluate the current evidence linking SCFAs to metabolic health and disease and consider the translational potential of targeting SCFA pathways through dietary and therapeutic approaches. At a time when inadequate dietary fibre intake is a growing public health concern, this Review highlights the physiological importance of SCFAs and their potential role in metabolic health and disease prevention.
Additional Links: PMID-42527661
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@article {pmid42527661,
year = {2026},
author = {Dagbasi, A and Cai, M and Hirdaramani, A and Hanyaloglu, A and Morrison, DJ and Frost, G},
title = {Short-chain fatty acids.},
journal = {Nature metabolism},
volume = {},
number = {},
pages = {},
pmid = {42527661},
issn = {2522-5812},
support = {BB/N016947/1//RCUK | Biotechnology and Biological Sciences Research Council (BBSRC)/ ; },
abstract = {Short-chain fatty acids (SCFAs), principally acetate, propionate and butyrate, are produced by the gut microbiota through the fermentation of non-digestible carbohydrates. Beyond serving as energy substrates, SCFAs act as signalling molecules that influence metabolism, immune function and physiological homeostasis across multiple organ systems. This Review consolidates the fragmented literature on SCFAs and provides an overview of their production, metabolism and physiological actions. We discuss the microbial and dietary determinants of SCFA production, including the roles of the gut microbiome, cross-feeding interactions and dietary carbohydrates. We then examine the mechanisms through which SCFAs exert their effects, focusing on receptor-mediated signalling, epigenetic regulation and tissue-specific physiological functions. Finally, we evaluate the current evidence linking SCFAs to metabolic health and disease and consider the translational potential of targeting SCFA pathways through dietary and therapeutic approaches. At a time when inadequate dietary fibre intake is a growing public health concern, this Review highlights the physiological importance of SCFAs and their potential role in metabolic health and disease prevention.},
}
RevDate: 2026-07-29
Impact of labor before delivery on necrotizing enterocolitis in very low birth weight infants.
Journal of neonatal-perinatal medicine [Epub ahead of print].
BackgroundNecrotizing Enterocolitis (NEC) is multifactorial, and the gut microbiome may contribute. Neonatal gut colonization differs by delivery mode; while delivery mode has not been linked to NEC in prior studies, the impact of labor prior to delivery is unknown. Our objective was to investigate the impact of labor prior to delivery on NEC incidence in very low birth weight (VLBW, <1500 g) infants.MethodsWe performed a single-center retrospective cohort study of VLBW infants 23 0/7-34 6/7 weeks gestation born at our center between 03/25/2012 and 12/31/2023. Infants with congenital anomalies or who died prior to admission were excluded. Labor was defined as uterine contractions with cervical dilation or effacement. When cervical exam was undocumented, labor was determined by presence of regular contractions >1 h before delivery. Multivariable logistic regression evaluated the association between labor before delivery and NEC after adjusting for baseline differences.ResultsAmong 1,951 infants, 1,175 (60.2%) were exposed to labor before delivery. Groups differed by gestational age, birth weight, chorioamnionitis, maternal diabetes, multiple gestation, and small for gestational age. Exposure to labor had lower odds of NEC (odds ratio [OR] = 0.606, 95% confidence interval [CI]: 0.407-0.902, p = 0.01), compared to those unexposed. This association remained significant after adjustment (adjusted OR = 0.614, 95% CI: 0.384-0.983, p = 0.04). There was no difference in surgical NEC.ConclusionsLabor prior to delivery was associated with lower odds of NEC in this VLBW cohort, highlighting the potential importance of perinatal microbial exposures and suggesting new avenues for NEC risk stratification and prevention.
Additional Links: PMID-42527892
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@article {pmid42527892,
year = {2026},
author = {Dhawan, N and Yasrebi, S and Hagan, J and Brasher, MI and Patil, MS},
title = {Impact of labor before delivery on necrotizing enterocolitis in very low birth weight infants.},
journal = {Journal of neonatal-perinatal medicine},
volume = {},
number = {},
pages = {19345798261475330},
doi = {10.1177/19345798261475330},
pmid = {42527892},
issn = {1878-4429},
abstract = {BackgroundNecrotizing Enterocolitis (NEC) is multifactorial, and the gut microbiome may contribute. Neonatal gut colonization differs by delivery mode; while delivery mode has not been linked to NEC in prior studies, the impact of labor prior to delivery is unknown. Our objective was to investigate the impact of labor prior to delivery on NEC incidence in very low birth weight (VLBW, <1500 g) infants.MethodsWe performed a single-center retrospective cohort study of VLBW infants 23 0/7-34 6/7 weeks gestation born at our center between 03/25/2012 and 12/31/2023. Infants with congenital anomalies or who died prior to admission were excluded. Labor was defined as uterine contractions with cervical dilation or effacement. When cervical exam was undocumented, labor was determined by presence of regular contractions >1 h before delivery. Multivariable logistic regression evaluated the association between labor before delivery and NEC after adjusting for baseline differences.ResultsAmong 1,951 infants, 1,175 (60.2%) were exposed to labor before delivery. Groups differed by gestational age, birth weight, chorioamnionitis, maternal diabetes, multiple gestation, and small for gestational age. Exposure to labor had lower odds of NEC (odds ratio [OR] = 0.606, 95% confidence interval [CI]: 0.407-0.902, p = 0.01), compared to those unexposed. This association remained significant after adjustment (adjusted OR = 0.614, 95% CI: 0.384-0.983, p = 0.04). There was no difference in surgical NEC.ConclusionsLabor prior to delivery was associated with lower odds of NEC in this VLBW cohort, highlighting the potential importance of perinatal microbial exposures and suggesting new avenues for NEC risk stratification and prevention.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-30
Astrovirus infection alters gut microbial communities in a widespread neotropical bat across human-modified landscapes.
BMC microbiology, 26(1):.
Astroviruses are becoming a growing concern in public and veterinary health. In humans, astrovirus infections can cause severe diarrhea and may lead to neuropathological encephalitis, whereas in wildlife, these enteropathogenic viral infections often lack overt symptoms and thus remain unnoticed. Yet their close interaction with the host's gastrointestinal microbiome might drive cascading effects with disadvantages for host health. Bats harbor many zoonotic viruses without showing signs of disease, and many species move freely along the gradient from pristine to agricultural landscapes. To better understand the impact of astrovirus (AstV) infection under a One Health framework, we investigated the gut microbiome of naturally AstV-infected Seba's short-tailed bats (Carollia perspicillata, n = 234) inhabiting old-growth lowland forests or forest fragments embedded in an agricultural matrix in Panama. AstV prevalence was higher in forest fragments. We observed that AstV infection is associated with a shift in microbial beta but not alpha diversity, which points towards the replacement of common gut microbial taxa when infected. Indeed, potentially beneficial bacteria, such as Lactococcus, decreased in abundance, whereas potentially pathogenic bacteria from the Helicobacter genus increased in AstV-positive bats. Two Helicobacter haplotypes closely related to avian Helicobacter species were identified. We conclude that even though the impact of infection on the microbiome was not amplified in forest fragments, the higher infection likelihood in landscapes altered by humans implies more frequent or prolonged health repercussions for bats.
Additional Links: PMID-42527911
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Citation:
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@article {pmid42527911,
year = {2026},
author = {Brändel, SD and Melville, DW and Wilhelm, K and Corman, VM and Page, R and Drosten, C and Tschapka, M and Sommer, S and Wasimuddin, },
title = {Astrovirus infection alters gut microbial communities in a widespread neotropical bat across human-modified landscapes.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {},
pmid = {42527911},
issn = {1471-2180},
mesh = {Animals ; *Chiroptera/microbiology/virology ; *Astroviridae Infections/veterinary/virology/epidemiology ; *Gastrointestinal Microbiome ; *Bacteria/classification/genetics/isolation & purification ; Panama ; *Astroviridae/isolation & purification ; Humans ; RNA, Ribosomal, 16S/genetics ; Forests ; Sequence Analysis, DNA ; Feces/microbiology/virology ; Phylogeny ; Biodiversity ; },
abstract = {Astroviruses are becoming a growing concern in public and veterinary health. In humans, astrovirus infections can cause severe diarrhea and may lead to neuropathological encephalitis, whereas in wildlife, these enteropathogenic viral infections often lack overt symptoms and thus remain unnoticed. Yet their close interaction with the host's gastrointestinal microbiome might drive cascading effects with disadvantages for host health. Bats harbor many zoonotic viruses without showing signs of disease, and many species move freely along the gradient from pristine to agricultural landscapes. To better understand the impact of astrovirus (AstV) infection under a One Health framework, we investigated the gut microbiome of naturally AstV-infected Seba's short-tailed bats (Carollia perspicillata, n = 234) inhabiting old-growth lowland forests or forest fragments embedded in an agricultural matrix in Panama. AstV prevalence was higher in forest fragments. We observed that AstV infection is associated with a shift in microbial beta but not alpha diversity, which points towards the replacement of common gut microbial taxa when infected. Indeed, potentially beneficial bacteria, such as Lactococcus, decreased in abundance, whereas potentially pathogenic bacteria from the Helicobacter genus increased in AstV-positive bats. Two Helicobacter haplotypes closely related to avian Helicobacter species were identified. We conclude that even though the impact of infection on the microbiome was not amplified in forest fragments, the higher infection likelihood in landscapes altered by humans implies more frequent or prolonged health repercussions for bats.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Chiroptera/microbiology/virology
*Astroviridae Infections/veterinary/virology/epidemiology
*Gastrointestinal Microbiome
*Bacteria/classification/genetics/isolation & purification
Panama
*Astroviridae/isolation & purification
Humans
RNA, Ribosomal, 16S/genetics
Forests
Sequence Analysis, DNA
Feces/microbiology/virology
Phylogeny
Biodiversity
RevDate: 2026-07-30
Rhizosphere Engineering by Root Exudates: High-Yielding Alfalfa Recruits Functional PGPR to Sustain Soil Nutrient Availability Under Long-Term Cultivation.
Plant, cell & environment [Epub ahead of print].
Soil nutrient transformation capacity is a critical determinant of sustainable productivity in perennial cropping systems; however, the extent to which high-yielding crops actively regulate rhizosphere microbial assembly to maintain nutrient availability remains poorly understood. We investigated whether root exudates from high-yielding alfalfa (Medicago sativa L.) selectively recruit plant growth-promoting rhizobacteria (PGPR) to enhance nutrient transformation. In an 8-year continuous alfalfa system (2018-2025), high-yielding cultivars increased soil organic carbon by 8.64%, total nitrogen by 6.01%, and moderately labile phosphorus fractions by 1.62%. Rhizobox experiments demonstrated that root exudates enhanced growth only with an active microbiome. High-yielding alfalfa enriched PGPR communities, specifically Ensifer, Pseudomonas, and Bacillus. Isolated strains exhibited N fixation, P solubilisation, and IAA production. Metabolomic profiling revealed that exudates were enriched in specific sugars and amino acids. Maltopentaose, maltotetraose, taurine, N-acetyl-L-leucine, and asparagine functioned as chemoattractants, stimulating PGPR proliferation and biofilm formation. These findings demonstrate that root exudate-mediated, targeted recruitment of functional PGPR enhances N fixation and P transformation, thereby supporting sustained high alfalfa productivity. This study demonstrates a key rhizosphere mechanism underlying the long-term sustainability of high-yielding perennial legume systems and provides a mechanistic basis for microbiome-informed sustainable alfalfa production and management.
Additional Links: PMID-42528084
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PubMed:
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@article {pmid42528084,
year = {2026},
author = {Sun, Y and Wei, K and Yang, K and Hui, J and Xia, D and Wang, X and Cartmill, AD and López, IF and Ma, C and Zhang, Q},
title = {Rhizosphere Engineering by Root Exudates: High-Yielding Alfalfa Recruits Functional PGPR to Sustain Soil Nutrient Availability Under Long-Term Cultivation.},
journal = {Plant, cell & environment},
volume = {},
number = {},
pages = {},
doi = {10.1111/pce.70631},
pmid = {42528084},
issn = {1365-3040},
support = {2023B02031//Xinjiang Uygur Autonomous Region Key R&D Task Special Project/ ; 2026DB001//Science and Technology Program of XPCC/ ; 32260347//National Natural Science Foundation of China/ ; //T. R. Ellett Agricultural Research Trust/ ; },
abstract = {Soil nutrient transformation capacity is a critical determinant of sustainable productivity in perennial cropping systems; however, the extent to which high-yielding crops actively regulate rhizosphere microbial assembly to maintain nutrient availability remains poorly understood. We investigated whether root exudates from high-yielding alfalfa (Medicago sativa L.) selectively recruit plant growth-promoting rhizobacteria (PGPR) to enhance nutrient transformation. In an 8-year continuous alfalfa system (2018-2025), high-yielding cultivars increased soil organic carbon by 8.64%, total nitrogen by 6.01%, and moderately labile phosphorus fractions by 1.62%. Rhizobox experiments demonstrated that root exudates enhanced growth only with an active microbiome. High-yielding alfalfa enriched PGPR communities, specifically Ensifer, Pseudomonas, and Bacillus. Isolated strains exhibited N fixation, P solubilisation, and IAA production. Metabolomic profiling revealed that exudates were enriched in specific sugars and amino acids. Maltopentaose, maltotetraose, taurine, N-acetyl-L-leucine, and asparagine functioned as chemoattractants, stimulating PGPR proliferation and biofilm formation. These findings demonstrate that root exudate-mediated, targeted recruitment of functional PGPR enhances N fixation and P transformation, thereby supporting sustained high alfalfa productivity. This study demonstrates a key rhizosphere mechanism underlying the long-term sustainability of high-yielding perennial legume systems and provides a mechanistic basis for microbiome-informed sustainable alfalfa production and management.},
}
RevDate: 2026-07-30
Comparison of the effects of four commercially available prescription diet regimens on the fecal microbiome in healthy cats.
The Journal of veterinary medical science [Epub ahead of print].
Diet significantly influences the gut microbiota, with variations in macronutrient content (proteins, fats, and carbohydrates) and the presence of non-digestible carbohydrates, such as fiber, playing crucial roles in shaping microbial composition. This study investigated the effects of four commercial prescription diets (low-carbohydrate, weight-loss, high soluble fiber, and renal) on the fecal microbiome of five healthy domestic cats using a 4×4 Latin square design. Fecal samples were analyzed using Illumina sequencing of the bacterial 16S rRNA gene to assess bacterial community structure and diversity. Results showed that cats fed the renal diet (low protein, high carbohydrate, high fat) were associated with higher relative abundances of the phylum Actinobacteria, particularly Bifidobacterium. The low-carbohydrate diet was associated with higher relative abundances of Adlercreutzia, Collinsella, and Slackia. The high-soluble fiber diet was associated with a higher relative proportion of Streptococcaceae. In contrast, the renal diet was associated with lower relative abundances of Blautia and Erysipelotrichaceae. No significant differences were observed in alpha-diversity indices among diets, whereas beta-diversity analysis showed significant differences in microbial community composition among dietary groups. These findings suggest that dietary composition may influence the fecal microbiome in healthy cats. However, given the exploratory design and compositional nature of the sequencing data, these findings should be interpreted cautiously and considered hypothesis-generating.
Additional Links: PMID-42528237
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PubMed:
Citation:
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@article {pmid42528237,
year = {2026},
author = {Komiya, T and Koyama, K and Akiyama, R and Oda, H and Gokita, K and Sako, T and Mori, A},
title = {Comparison of the effects of four commercially available prescription diet regimens on the fecal microbiome in healthy cats.},
journal = {The Journal of veterinary medical science},
volume = {},
number = {},
pages = {},
doi = {10.1292/jvms.24-0494},
pmid = {42528237},
issn = {1347-7439},
abstract = {Diet significantly influences the gut microbiota, with variations in macronutrient content (proteins, fats, and carbohydrates) and the presence of non-digestible carbohydrates, such as fiber, playing crucial roles in shaping microbial composition. This study investigated the effects of four commercial prescription diets (low-carbohydrate, weight-loss, high soluble fiber, and renal) on the fecal microbiome of five healthy domestic cats using a 4×4 Latin square design. Fecal samples were analyzed using Illumina sequencing of the bacterial 16S rRNA gene to assess bacterial community structure and diversity. Results showed that cats fed the renal diet (low protein, high carbohydrate, high fat) were associated with higher relative abundances of the phylum Actinobacteria, particularly Bifidobacterium. The low-carbohydrate diet was associated with higher relative abundances of Adlercreutzia, Collinsella, and Slackia. The high-soluble fiber diet was associated with a higher relative proportion of Streptococcaceae. In contrast, the renal diet was associated with lower relative abundances of Blautia and Erysipelotrichaceae. No significant differences were observed in alpha-diversity indices among diets, whereas beta-diversity analysis showed significant differences in microbial community composition among dietary groups. These findings suggest that dietary composition may influence the fecal microbiome in healthy cats. However, given the exploratory design and compositional nature of the sequencing data, these findings should be interpreted cautiously and considered hypothesis-generating.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Biomarkers From the Microbiome to Predict ALD Progression and Its Severity: A Comprehensive Review.
Mediators of inflammation, 2026(1):e7244952.
Alcohol use is a major global health issue, causing about 3.3 million deaths each year, or roughly 5.9% of all deaths worldwide. Alcohol-related liver disease develops in stages: steatosis, steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. If alcohol consumption is discontinued at early stages, alcohol-related fatty liver disease can be reversed; however, continued exposure leads to progressive liver injury and increased mortality risk. Current diagnostic tools lack sufficient sensitivity and specificity to detect early-stage disease or accurately assess disease progression. This highlights the need for reliable and mechanistically relevant biomarkers for early diagnosis and staging. This review examines alterations in gut microbiota across different stages of alcohol-associated liver disease and evaluates gut microbiota-associated biomarkers, including microbial metabolites, in the context of their potential diagnostic and prognostic utility. In addition, the review discusses the limitations of existing biomarkers and highlights the emerging role of microbiome-derived signals in reflecting disease mechanisms. These findings suggest that gut microbiota-related biomarkers may provide a promising but still evolving approach for improving early detection and understanding disease progression in alcohol-associated liver disease.
Additional Links: PMID-42528288
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@article {pmid42528288,
year = {2026},
author = {Mishra, S and Solanki, H and Mandal, P},
title = {Biomarkers From the Microbiome to Predict ALD Progression and Its Severity: A Comprehensive Review.},
journal = {Mediators of inflammation},
volume = {2026},
number = {1},
pages = {e7244952},
pmid = {42528288},
issn = {1466-1861},
mesh = {Humans ; *Biomarkers/metabolism ; Disease Progression ; *Gastrointestinal Microbiome/physiology ; *Microbiota ; *Liver Diseases, Alcoholic/metabolism/microbiology ; Animals ; },
abstract = {Alcohol use is a major global health issue, causing about 3.3 million deaths each year, or roughly 5.9% of all deaths worldwide. Alcohol-related liver disease develops in stages: steatosis, steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. If alcohol consumption is discontinued at early stages, alcohol-related fatty liver disease can be reversed; however, continued exposure leads to progressive liver injury and increased mortality risk. Current diagnostic tools lack sufficient sensitivity and specificity to detect early-stage disease or accurately assess disease progression. This highlights the need for reliable and mechanistically relevant biomarkers for early diagnosis and staging. This review examines alterations in gut microbiota across different stages of alcohol-associated liver disease and evaluates gut microbiota-associated biomarkers, including microbial metabolites, in the context of their potential diagnostic and prognostic utility. In addition, the review discusses the limitations of existing biomarkers and highlights the emerging role of microbiome-derived signals in reflecting disease mechanisms. These findings suggest that gut microbiota-related biomarkers may provide a promising but still evolving approach for improving early detection and understanding disease progression in alcohol-associated liver disease.},
}
MeSH Terms:
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Humans
*Biomarkers/metabolism
Disease Progression
*Gastrointestinal Microbiome/physiology
*Microbiota
*Liver Diseases, Alcoholic/metabolism/microbiology
Animals
RevDate: 2026-07-30
CmpDate: 2026-07-30
Multivariate functional linear discriminant analysis with feature selection: an application to inflammatory bowel disease classification.
Biostatistics (Oxford, England), 27(1):.
Inflammatory Bowel Disease (IBD), including Crohn's Disease (CD) and Ulcerative Colitis (UC), presents significant public health challenges due to its complex etiology. Motivated by the IBD study of the Integrative Human Microbiome Project, our objective is to identify microbial pathways that distinguish between CD, UC, and non-IBD over time. Most current research relies on simplistic analyses that examine 1 variable or time point at a time, or address binary classification problems, limiting our understanding of the dynamic interactions within the microbiome over time. To address these limitations, we develop a novel functional data analysis approach for discriminant analysis of multivariate functional data that can effectively handle multiple high-dimensional predictors, sparse time points, and categorical outcomes. Our method seeks linear combinations of functions (ie discriminant functions) that maximize separation between 2 or more classes over time. We impose a sparsity-inducing penalty when estimating the discriminant functions, allowing us to identify relevant discriminating variables over time. Applications of our method to the motivating data identified microbial features related to mucin degradation, amino acid metabolism, and peptidoglycan recognition, which are implicated in the progression and development of IBD. Furthermore, our method highlighted the role of multiple vitamin B deficiencies in the context of IBD. By moving beyond traditional analytical frameworks, our innovative approach holds the potential for uncovering clinically meaningful discoveries in IBD research.
Additional Links: PMID-42528381
PubMed:
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@article {pmid42528381,
year = {2026},
author = {Liu, L and Wang, G and Safo, SE},
title = {Multivariate functional linear discriminant analysis with feature selection: an application to inflammatory bowel disease classification.},
journal = {Biostatistics (Oxford, England)},
volume = {27},
number = {1},
pages = {},
pmid = {42528381},
issn = {1468-4357},
support = {/NH/NIH HHS/United States ; },
mesh = {Humans ; Discriminant Analysis ; *Inflammatory Bowel Diseases/classification/microbiology ; Multivariate Analysis ; Colitis, Ulcerative/microbiology/classification ; },
abstract = {Inflammatory Bowel Disease (IBD), including Crohn's Disease (CD) and Ulcerative Colitis (UC), presents significant public health challenges due to its complex etiology. Motivated by the IBD study of the Integrative Human Microbiome Project, our objective is to identify microbial pathways that distinguish between CD, UC, and non-IBD over time. Most current research relies on simplistic analyses that examine 1 variable or time point at a time, or address binary classification problems, limiting our understanding of the dynamic interactions within the microbiome over time. To address these limitations, we develop a novel functional data analysis approach for discriminant analysis of multivariate functional data that can effectively handle multiple high-dimensional predictors, sparse time points, and categorical outcomes. Our method seeks linear combinations of functions (ie discriminant functions) that maximize separation between 2 or more classes over time. We impose a sparsity-inducing penalty when estimating the discriminant functions, allowing us to identify relevant discriminating variables over time. Applications of our method to the motivating data identified microbial features related to mucin degradation, amino acid metabolism, and peptidoglycan recognition, which are implicated in the progression and development of IBD. Furthermore, our method highlighted the role of multiple vitamin B deficiencies in the context of IBD. By moving beyond traditional analytical frameworks, our innovative approach holds the potential for uncovering clinically meaningful discoveries in IBD research.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Discriminant Analysis
*Inflammatory Bowel Diseases/classification/microbiology
Multivariate Analysis
Colitis, Ulcerative/microbiology/classification
RevDate: 2026-07-30
CmpDate: 2026-07-30
Coexist or eliminate? Antibody-based functional silencing versus eradication in gut microbiome- targeted therapy.
Frontiers in immunology, 17:1903103.
BACKGROUND: Dominant anti-infective strategies equate therapeutic success with pathogen eradication, yet in the gut most clinically relevant "pathogens" are pathobionts that cause disease only under specific ecological conditions. Antibiotics resolve infection but decimate commensal communities and select for resistance.
SCOPE AND APPROACH: We review antibody-based interventions, native mucosal antibodies (IgA, IgM), monoclonal antibodies, and immunoglobulin Y (IgY), as mechanistic test cases for a functional silencing paradigm, in which pathobiont virulence is attenuated through non-bactericidal mechanisms while preserving community architecture.
KEY FINDINGS: Drawing on randomized trial data (bezlotoxumab in Clostridioides difficile recurrence prevention, MODIFY I/II, n = 2,655), preclinical and early clinical IgY studies in enteric infections, and long-term IgY deployment in aquaculture, we find that functional silencing delivers durable benefit when disease is driven by discrete virulence factors. However, evolutionary risks, including phase variation, conformational switching, and the theoretical framework of "imperfect immunity", identify conditions under which retained pathobionts may re-emerge as threats.
CONCLUSIONS: Eradication and functional silencing are best understood as complementary strategies whose optimal deployment depends on host immune status, barrier integrity, and the nature of pathobiont virulence. Defining the boundary between safe coexistence and evolutionary rebound constitutes the field's central unresolved challenge.
Additional Links: PMID-42528616
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Citation:
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@article {pmid42528616,
year = {2026},
author = {El-Kafrawy, SA and Abbas, AT and El-Kafrawy, AS and El-Daly, MM and Azhar, EI},
title = {Coexist or eliminate? Antibody-based functional silencing versus eradication in gut microbiome- targeted therapy.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1903103},
pmid = {42528616},
issn = {1664-3224},
mesh = {Humans ; Animals ; *Gastrointestinal Microbiome/immunology/drug effects ; *Antibodies, Monoclonal/therapeutic use ; Clostridioides difficile/immunology ; Immunoglobulins/immunology/therapeutic use ; *Clostridium Infections/immunology/microbiology/therapy ; },
abstract = {BACKGROUND: Dominant anti-infective strategies equate therapeutic success with pathogen eradication, yet in the gut most clinically relevant "pathogens" are pathobionts that cause disease only under specific ecological conditions. Antibiotics resolve infection but decimate commensal communities and select for resistance.
SCOPE AND APPROACH: We review antibody-based interventions, native mucosal antibodies (IgA, IgM), monoclonal antibodies, and immunoglobulin Y (IgY), as mechanistic test cases for a functional silencing paradigm, in which pathobiont virulence is attenuated through non-bactericidal mechanisms while preserving community architecture.
KEY FINDINGS: Drawing on randomized trial data (bezlotoxumab in Clostridioides difficile recurrence prevention, MODIFY I/II, n = 2,655), preclinical and early clinical IgY studies in enteric infections, and long-term IgY deployment in aquaculture, we find that functional silencing delivers durable benefit when disease is driven by discrete virulence factors. However, evolutionary risks, including phase variation, conformational switching, and the theoretical framework of "imperfect immunity", identify conditions under which retained pathobionts may re-emerge as threats.
CONCLUSIONS: Eradication and functional silencing are best understood as complementary strategies whose optimal deployment depends on host immune status, barrier integrity, and the nature of pathobiont virulence. Defining the boundary between safe coexistence and evolutionary rebound constitutes the field's central unresolved challenge.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Animals
*Gastrointestinal Microbiome/immunology/drug effects
*Antibodies, Monoclonal/therapeutic use
Clostridioides difficile/immunology
Immunoglobulins/immunology/therapeutic use
*Clostridium Infections/immunology/microbiology/therapy
RevDate: 2026-07-30
CmpDate: 2026-07-30
Microbial dysbiosis and wound healing in diabetic foot ulcers: a mini review with a note on the role of artificial intelligence.
Frontiers in cellular and infection microbiology, 16:1891884.
Diabetic foot ulcers (DFUs) are a serious diabetes-related complication characterized by high rates of amputation and mortality. Emerging evidence suggests that DFUs are not simply the result of infection, but also involve microbiome dysbiosis, which impairs healing. Systemically, disturbances to the gut microbiota via the gut-skin axis promote systemic inflammation and metabolic dysfunction. Locally, skin microbial diversity is significantly reduced, allowing opportunistic pathogens such as Staphylococcus aureus and Pseudomonas aeruginosa to form resilient biofilms. These biofilms resist antibiotics and host immunity, while microbial virulence factors exacerbate tissue damage and disrupt the healing cascade. This synergy between host pathology and dysbiosis perpetuates chronic ulceration. Novel therapeutic strategies therefore aim to modulate this aberrant ecology by shifting from broad-spectrum eradication to targeted restoration. Promising approaches include probiotics, phage therapy, traditional Chinese medicine, and faecal microbiota transplantation, which seek to recalibrate the microbiome and promote healing. However, translation into clinical practice requires more robust evidence from large-scale trials. Future perspectives point towards personalized microbial medicine, integrating multi-omics data and artificial intelligence to match interventions with specific microbial ecotypes, which may reduce the global burden of DFUs.
Additional Links: PMID-42528685
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Citation:
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@article {pmid42528685,
year = {2026},
author = {Yu, X and Liu, Q and Huang, Y and Wang, Q and Wang, Y and Zhao, G},
title = {Microbial dysbiosis and wound healing in diabetic foot ulcers: a mini review with a note on the role of artificial intelligence.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1891884},
pmid = {42528685},
issn = {2235-2988},
mesh = {Humans ; *Diabetic Foot/microbiology/therapy ; *Dysbiosis/microbiology/therapy ; *Wound Healing ; *Artificial Intelligence ; Biofilms/growth & development ; Probiotics/therapeutic use ; Gastrointestinal Microbiome ; Animals ; Skin Microbiome ; },
abstract = {Diabetic foot ulcers (DFUs) are a serious diabetes-related complication characterized by high rates of amputation and mortality. Emerging evidence suggests that DFUs are not simply the result of infection, but also involve microbiome dysbiosis, which impairs healing. Systemically, disturbances to the gut microbiota via the gut-skin axis promote systemic inflammation and metabolic dysfunction. Locally, skin microbial diversity is significantly reduced, allowing opportunistic pathogens such as Staphylococcus aureus and Pseudomonas aeruginosa to form resilient biofilms. These biofilms resist antibiotics and host immunity, while microbial virulence factors exacerbate tissue damage and disrupt the healing cascade. This synergy between host pathology and dysbiosis perpetuates chronic ulceration. Novel therapeutic strategies therefore aim to modulate this aberrant ecology by shifting from broad-spectrum eradication to targeted restoration. Promising approaches include probiotics, phage therapy, traditional Chinese medicine, and faecal microbiota transplantation, which seek to recalibrate the microbiome and promote healing. However, translation into clinical practice requires more robust evidence from large-scale trials. Future perspectives point towards personalized microbial medicine, integrating multi-omics data and artificial intelligence to match interventions with specific microbial ecotypes, which may reduce the global burden of DFUs.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Diabetic Foot/microbiology/therapy
*Dysbiosis/microbiology/therapy
*Wound Healing
*Artificial Intelligence
Biofilms/growth & development
Probiotics/therapeutic use
Gastrointestinal Microbiome
Animals
Skin Microbiome
RevDate: 2026-07-30
CmpDate: 2026-07-30
Ecological and functional roles of plant microbiomes in environmental detoxification.
Frontiers in microbiology, 17:1883316.
Plant-associated microbiomes play a crucial role in environmental detoxification by influencing the degradation, immobilization, and resistance to toxins in polluted settings. The ecological and functional activity of endogenous microbial communities, such as rhizobacteria and endophytic microorganisms, is not well studied when examining contaminants and their environments, despite the fact that plant-mediated bioremediation has garnered a lot of research attention. The majority of previously published research focuses on a single biodegradation route or solitary plant-microbe interactions. Our knowledge of how the microbiome's composition, functional diversity, and ecological stability of microbial communities work together to produce detoxifying results in practical applications is currently lacking. To advance understanding of how plant microbiomes cooperatively mediate environmental detoxification through metabolic interactions, adaptive responses, and host-microbiome communication, this review integrates insights from microbial ecology and functional microbiology. Its primary objective is to synthesize current knowledge on key microbial functions, including metal sequestration, xenobiotic degradation, redox regulation, and modulation of plant responses to biotic stress, while linking these functions to ecological processes such as host specificity, niche specialization, and community assembly. A distinctive aspect of this review is its ecosystem-level perspective, which shifts the focus from individual microbial taxa to the functional resilience of microbial communities in determining detoxification efficiency. The information provided in this review has a scope to provide framework to develop ecologically-sustaining, microbiome-based strategies for the detoxification of the environment and for conducting future bioremediation research.
Additional Links: PMID-42528698
PubMed:
Citation:
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@article {pmid42528698,
year = {2026},
author = {Selim, S and Adhikary, K and Sarkar, R and Ganguly, K and Misra, A and Kashmiry, AA and Alshareef, SA and Alkhatib, SN and Hagagy, N and Maiti, R},
title = {Ecological and functional roles of plant microbiomes in environmental detoxification.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1883316},
pmid = {42528698},
issn = {1664-302X},
abstract = {Plant-associated microbiomes play a crucial role in environmental detoxification by influencing the degradation, immobilization, and resistance to toxins in polluted settings. The ecological and functional activity of endogenous microbial communities, such as rhizobacteria and endophytic microorganisms, is not well studied when examining contaminants and their environments, despite the fact that plant-mediated bioremediation has garnered a lot of research attention. The majority of previously published research focuses on a single biodegradation route or solitary plant-microbe interactions. Our knowledge of how the microbiome's composition, functional diversity, and ecological stability of microbial communities work together to produce detoxifying results in practical applications is currently lacking. To advance understanding of how plant microbiomes cooperatively mediate environmental detoxification through metabolic interactions, adaptive responses, and host-microbiome communication, this review integrates insights from microbial ecology and functional microbiology. Its primary objective is to synthesize current knowledge on key microbial functions, including metal sequestration, xenobiotic degradation, redox regulation, and modulation of plant responses to biotic stress, while linking these functions to ecological processes such as host specificity, niche specialization, and community assembly. A distinctive aspect of this review is its ecosystem-level perspective, which shifts the focus from individual microbial taxa to the functional resilience of microbial communities in determining detoxification efficiency. The information provided in this review has a scope to provide framework to develop ecologically-sustaining, microbiome-based strategies for the detoxification of the environment and for conducting future bioremediation research.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Decoding the gut-adipose-ovary axis in polycystic ovary syndrome: from metabolic dysregulation to oncological risk modulation.
Frontiers in microbiology, 17:1882127.
Polycystic ovary syndrome (PCOS) is traditionally managed as a localized reproductive disorder, but emerging evidence redefines it as a systemic metabolic-endocrine continuum with profound long-term health implications. This review comprehensively synthesizes the pathogenic role of the nutrition-mediated "gut-adipose-ovary axis" in bridging PCOS-associated metabolic dysfunction with an elevated risk of gynecological malignancies. Aberrant nutritional intake acts as the primary environmental catalyst, driving gut microbiota dysbiosis and metabolic endotoxemia. These gut-derived signals provoke visceral adipose tissue dysfunction, initiating a self-reinforcing cascade of systemic insulin resistance, hyperandrogenism, and chronic low-grade inflammation. Crucially, the convergence of these systemic insults continuously remodels the localized ovarian microenvironment. By sustaining proliferative signaling, forcing metabolic reprogramming, and fostering immune evasion, these convergent insults may contribute to a permissive pre-neoplastic microenvironment in susceptible patients with PCOS. To dismantle this pathogenic network, we outline a multi-dimensional therapeutic framework that integrates precision nutrition, microbiome modulation, and targeted pharmacological agents. Ultimately, this systems-biology perspective mandates a paradigm shift in clinical practice: moving beyond empirical symptom palliation toward proactive, risk-stratified interventions that interrupt the disease continuum and reduce long-term oncological risk in appropriately stratified women with PCOS.
Additional Links: PMID-42528754
PubMed:
Citation:
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@article {pmid42528754,
year = {2026},
author = {Guo, L and Lu, J and Liu, L and Zhang, M and Yu, N and Lu, L and Yang, T and Zhou, J and Hou, B and Chen, Y and Geng, Y},
title = {Decoding the gut-adipose-ovary axis in polycystic ovary syndrome: from metabolic dysregulation to oncological risk modulation.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1882127},
pmid = {42528754},
issn = {1664-302X},
abstract = {Polycystic ovary syndrome (PCOS) is traditionally managed as a localized reproductive disorder, but emerging evidence redefines it as a systemic metabolic-endocrine continuum with profound long-term health implications. This review comprehensively synthesizes the pathogenic role of the nutrition-mediated "gut-adipose-ovary axis" in bridging PCOS-associated metabolic dysfunction with an elevated risk of gynecological malignancies. Aberrant nutritional intake acts as the primary environmental catalyst, driving gut microbiota dysbiosis and metabolic endotoxemia. These gut-derived signals provoke visceral adipose tissue dysfunction, initiating a self-reinforcing cascade of systemic insulin resistance, hyperandrogenism, and chronic low-grade inflammation. Crucially, the convergence of these systemic insults continuously remodels the localized ovarian microenvironment. By sustaining proliferative signaling, forcing metabolic reprogramming, and fostering immune evasion, these convergent insults may contribute to a permissive pre-neoplastic microenvironment in susceptible patients with PCOS. To dismantle this pathogenic network, we outline a multi-dimensional therapeutic framework that integrates precision nutrition, microbiome modulation, and targeted pharmacological agents. Ultimately, this systems-biology perspective mandates a paradigm shift in clinical practice: moving beyond empirical symptom palliation toward proactive, risk-stratified interventions that interrupt the disease continuum and reduce long-term oncological risk in appropriately stratified women with PCOS.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Trained immunity in chronic rhinosinusitis: epigenetic reprogramming of innate immune memory as a driver of mucosal inflammation and recurrence.
Frontiers in immunology, 17:1822395.
Chronic rhinosinusitis (CRS) is a highly prevalent and debilitating inflammatory condition of the upper airway, affecting 5-28% of the global population and imposing a substantial socioeconomic burden. Despite major advances in endoscopic sinus surgery, pharmacological management, and targeted biologic therapies, long-term disease recurrence following treatment remains an unresolved clinical challenge. Current pathophysiological frameworks centered on adaptive type 2 immunity, eosinophilic inflammation, and pathogen persistence fail to fully account for the chronification and therapy resistance of CRS. Emerging evidence positions trained immunity (the epigenetic and metabolic reprogramming of innate immune cells enabling non-antigen-specific functional memory) as a fundamental and previously underappreciated mechanism driving CRS recurrence. Persistent sinonasal microbial colonizers, including Staphylococcus aureus biofilms and fungal components, along with viral pathogens and dysbiotic microbiome communities, function as potent epigenetic training stimuli that reprogram sinonasal macrophages, group 2 innate lymphoid cells (ILC2s), and epithelial progenitor cells. The recent identification of a TLR4+ trained ILC2 subset in nasal polyp tissue, sustained by AP-1-driven chromatin remodeling at the Tlr4 locus, exemplifies the cellular specificity of this phenomenon. Concurrently, nasal basal stem cells acquire heritable pro-inflammatory chromatin states following type 2 cytokine exposure, encoding an epithelial inflammatory memory that perpetuates mucosal dysfunction independent of ongoing stimulation. This review systematically examines the microbial triggers, epigenetic mechanisms, key cellular mediators, and therapeutic implications of trained immunity in CRS, proposing a new framework for disease-modifying strategies targeting the sinonasal epigenetic inflammatory landscape.
Additional Links: PMID-42528773
PubMed:
Citation:
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@article {pmid42528773,
year = {2026},
author = {Huang, GJ and Li, LJ and Li, PS and Fan, ZJ and Lu, BQ},
title = {Trained immunity in chronic rhinosinusitis: epigenetic reprogramming of innate immune memory as a driver of mucosal inflammation and recurrence.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1822395},
pmid = {42528773},
issn = {1664-3224},
mesh = {Humans ; *Rhinosinusitis/immunology/genetics ; *Trained Immunity ; *Immunity, Innate ; Chronic Disease ; *Immunologic Memory ; *Epigenesis, Genetic ; Animals ; Recurrence ; Inflammation/immunology ; *Nasal Mucosa/immunology ; Immunity, Mucosal ; },
abstract = {Chronic rhinosinusitis (CRS) is a highly prevalent and debilitating inflammatory condition of the upper airway, affecting 5-28% of the global population and imposing a substantial socioeconomic burden. Despite major advances in endoscopic sinus surgery, pharmacological management, and targeted biologic therapies, long-term disease recurrence following treatment remains an unresolved clinical challenge. Current pathophysiological frameworks centered on adaptive type 2 immunity, eosinophilic inflammation, and pathogen persistence fail to fully account for the chronification and therapy resistance of CRS. Emerging evidence positions trained immunity (the epigenetic and metabolic reprogramming of innate immune cells enabling non-antigen-specific functional memory) as a fundamental and previously underappreciated mechanism driving CRS recurrence. Persistent sinonasal microbial colonizers, including Staphylococcus aureus biofilms and fungal components, along with viral pathogens and dysbiotic microbiome communities, function as potent epigenetic training stimuli that reprogram sinonasal macrophages, group 2 innate lymphoid cells (ILC2s), and epithelial progenitor cells. The recent identification of a TLR4+ trained ILC2 subset in nasal polyp tissue, sustained by AP-1-driven chromatin remodeling at the Tlr4 locus, exemplifies the cellular specificity of this phenomenon. Concurrently, nasal basal stem cells acquire heritable pro-inflammatory chromatin states following type 2 cytokine exposure, encoding an epithelial inflammatory memory that perpetuates mucosal dysfunction independent of ongoing stimulation. This review systematically examines the microbial triggers, epigenetic mechanisms, key cellular mediators, and therapeutic implications of trained immunity in CRS, proposing a new framework for disease-modifying strategies targeting the sinonasal epigenetic inflammatory landscape.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Rhinosinusitis/immunology/genetics
*Trained Immunity
*Immunity, Innate
Chronic Disease
*Immunologic Memory
*Epigenesis, Genetic
Animals
Recurrence
Inflammation/immunology
*Nasal Mucosa/immunology
Immunity, Mucosal
RevDate: 2026-07-30
CmpDate: 2026-07-30
The diet-microbiota-inflammation axis and colorectal cancer.
Frontiers in oncology, 16:1895753.
BACKGROUND: Colorectal cancer (CRC) is still one of the leading causes of cancer morbidity and mortality worldwide. There is increasing evidence that diet, gut microbiota, microbial metabolites and chronic inflammation are important factors in colorectal carcinogenesis and may provide novel opportunities for prevention, diagnosis and treatment.
AIM: To provide a comprehensive review of the current evidence on the role of diet, nutrition, microbial metabolism and chronic inflammation in CRC, with emphasis on emerging translational applications including microbiome-based biomarkers and microbiota-targeted therapeutic strategies.
METHODS: A literature search was performed with PubMed, Scopus and the Cochrane Library. Relevant studies on diet-microbiota interactions, microbial metabolites, inflammatory mechanisms, colorectal carcinogenesis, microbiome-derived biomarkers, and microbiota-targeted interventions were identified and reviewed. Preclinical and clinical studies and high quality reviews and meta-analyses were considered.
RESULTS: Dietary patterns have been shown to have a major impact on the composition and function of the gut microbiota. Rich-fiber diets and short-chain fatty acids (SCFAs) production seem protective against CRC, while western dietary patterns, ultra-processed foods and dysbiosis-associated metabolites promote a pro-inflammatory environment associated with carcinogenesis. Some microorganisms such as Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis and pks-positive Escherichia coli have been associated with CRC by inflammatory, genotoxic and immune-modulatory mechanisms. Recent advances in sequencing technologies and multi-omics approaches have enabled the identification of microbial signatures with potential diagnostic and prognostic value. Moreover, microbiota-targeted interventions such as probiotics, prebiotics, postbiotics, faecal microbiota transplantation, and next-generation microbial therapies have yielded promising preclinical and early clinical results.
CONCLUSIONS: The diet-microbiota-inflammation axis is a key player in colorectal carcinogenesis and a promising target for translational research. Microbiome-based biomarkers and microbiota-targeted therapies may have a role in future precision prevention and personalised management strategies of colorectal cancer despite significant challenges in terms of causation, standardisation and translation into clinical practice.
Additional Links: PMID-42528838
PubMed:
Citation:
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@article {pmid42528838,
year = {2026},
author = {Kossenas, K and Damaskos, C and Garmpis, N},
title = {The diet-microbiota-inflammation axis and colorectal cancer.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1895753},
pmid = {42528838},
issn = {2234-943X},
abstract = {BACKGROUND: Colorectal cancer (CRC) is still one of the leading causes of cancer morbidity and mortality worldwide. There is increasing evidence that diet, gut microbiota, microbial metabolites and chronic inflammation are important factors in colorectal carcinogenesis and may provide novel opportunities for prevention, diagnosis and treatment.
AIM: To provide a comprehensive review of the current evidence on the role of diet, nutrition, microbial metabolism and chronic inflammation in CRC, with emphasis on emerging translational applications including microbiome-based biomarkers and microbiota-targeted therapeutic strategies.
METHODS: A literature search was performed with PubMed, Scopus and the Cochrane Library. Relevant studies on diet-microbiota interactions, microbial metabolites, inflammatory mechanisms, colorectal carcinogenesis, microbiome-derived biomarkers, and microbiota-targeted interventions were identified and reviewed. Preclinical and clinical studies and high quality reviews and meta-analyses were considered.
RESULTS: Dietary patterns have been shown to have a major impact on the composition and function of the gut microbiota. Rich-fiber diets and short-chain fatty acids (SCFAs) production seem protective against CRC, while western dietary patterns, ultra-processed foods and dysbiosis-associated metabolites promote a pro-inflammatory environment associated with carcinogenesis. Some microorganisms such as Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis and pks-positive Escherichia coli have been associated with CRC by inflammatory, genotoxic and immune-modulatory mechanisms. Recent advances in sequencing technologies and multi-omics approaches have enabled the identification of microbial signatures with potential diagnostic and prognostic value. Moreover, microbiota-targeted interventions such as probiotics, prebiotics, postbiotics, faecal microbiota transplantation, and next-generation microbial therapies have yielded promising preclinical and early clinical results.
CONCLUSIONS: The diet-microbiota-inflammation axis is a key player in colorectal carcinogenesis and a promising target for translational research. Microbiome-based biomarkers and microbiota-targeted therapies may have a role in future precision prevention and personalised management strategies of colorectal cancer despite significant challenges in terms of causation, standardisation and translation into clinical practice.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Integrated metagenomic and metabolomic insights into microbial metabolic reprogramming in the rhizosphere of the invasive plant Praxelis clematidea under low-temperature stress.
Frontiers in microbiology, 17:1852122.
A primary factor preventing the spread of the invasive plant Praxelis clematidea to higher latitudes and altitudes is the low-temperature stress induced by global climate change. The present study investigated the impact of low-temperature stress on the rhizosphere soil micro-ecosystem of P. clematidea, with the aim of examining its adaptive micro-ecological mechanisms via a comprehensive multi-omics approach. The rhizosphere soils of plants were compared under low-temperature (LT, 5 °C) or normal-temperature (HT, 25 °C) treatments. Using soil physicochemical analysis, enzyme activity assay, metagenomics, and non-targeted metabolomics, we observed that LT stress did not significantly alter microbial alpha diversity but strongly shifted the community structure. This change enriched cold-tolerant bacterial taxa, including Nocardiopsis, Sphingobium and Azoarcus. The LT stress was associated with altered carbon and nitrogen cycling, as indicated by increased soil urease activity but decreased alkaline phosphatase and catalase activities. The nitrate-N and ammonium-N levels increased, but total nitrogen, total organic carbon, and organic matter were reduced. Additionally, metagenomic study revealed overexpression of major microbial carbon metabolism genes (e.g., TCA cycle and glycolysis) and downregulation of nitrogen assimilation genes (e.g., glnA and NasA). Furthermore, metabolomics indicated a rise in carbohydrates and vitamins, along with a notable accumulation of stress-resistant secondary metabolites such as phenolic acids, flavonoids, and terpenes in the rhizosphere soils under LT stress. Correlation analysis indicated strong positive associations between the enriched cold-tolerant genera and these stress-resistant metabolites (e.g., costunolide and choline sulfate). Functional enrichment analysis suggested a metabolic reprogramming signature coupled with low-temperature treatment. Finally, this integrated multi-omics study reveals that P. clematidea is associated with an altered rhizosphere microbiome, differential functional gene abundance, and reorganized metabolic networks under low-temperature conditions. These findings offer a vital micro-ecological elucidation for P. clematidea effective colonization and propagation in novel, colder habitats.
Additional Links: PMID-42528952
PubMed:
Citation:
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@article {pmid42528952,
year = {2026},
author = {Liu, X and Cheng, W and Li, C and Dessie, W and Qi, C and Ayaz, M and Xu, X},
title = {Integrated metagenomic and metabolomic insights into microbial metabolic reprogramming in the rhizosphere of the invasive plant Praxelis clematidea under low-temperature stress.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1852122},
pmid = {42528952},
issn = {1664-302X},
abstract = {A primary factor preventing the spread of the invasive plant Praxelis clematidea to higher latitudes and altitudes is the low-temperature stress induced by global climate change. The present study investigated the impact of low-temperature stress on the rhizosphere soil micro-ecosystem of P. clematidea, with the aim of examining its adaptive micro-ecological mechanisms via a comprehensive multi-omics approach. The rhizosphere soils of plants were compared under low-temperature (LT, 5 °C) or normal-temperature (HT, 25 °C) treatments. Using soil physicochemical analysis, enzyme activity assay, metagenomics, and non-targeted metabolomics, we observed that LT stress did not significantly alter microbial alpha diversity but strongly shifted the community structure. This change enriched cold-tolerant bacterial taxa, including Nocardiopsis, Sphingobium and Azoarcus. The LT stress was associated with altered carbon and nitrogen cycling, as indicated by increased soil urease activity but decreased alkaline phosphatase and catalase activities. The nitrate-N and ammonium-N levels increased, but total nitrogen, total organic carbon, and organic matter were reduced. Additionally, metagenomic study revealed overexpression of major microbial carbon metabolism genes (e.g., TCA cycle and glycolysis) and downregulation of nitrogen assimilation genes (e.g., glnA and NasA). Furthermore, metabolomics indicated a rise in carbohydrates and vitamins, along with a notable accumulation of stress-resistant secondary metabolites such as phenolic acids, flavonoids, and terpenes in the rhizosphere soils under LT stress. Correlation analysis indicated strong positive associations between the enriched cold-tolerant genera and these stress-resistant metabolites (e.g., costunolide and choline sulfate). Functional enrichment analysis suggested a metabolic reprogramming signature coupled with low-temperature treatment. Finally, this integrated multi-omics study reveals that P. clematidea is associated with an altered rhizosphere microbiome, differential functional gene abundance, and reorganized metabolic networks under low-temperature conditions. These findings offer a vital micro-ecological elucidation for P. clematidea effective colonization and propagation in novel, colder habitats.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Microbiota-directed therapies for atopic dermatitis: a three-tier framework for inflammation control, immune modulation, and microbiome restoration.
Frontiers in immunology, 17:1873455.
The pathogenesis of atopic dermatitis (AD) involves cutaneous barrier dysfunction, immune dysregulation, and microbiota imbalance. Although microbiota-directed therapeutic approaches have garnered increasing attention, current evidence is heterogeneous, encompassing probiotics, postbiotics, microbial metabolites, local microbial interventions, antimicrobials and ecological modulation strategies. This narrative review does not aim to provide clinical guidelines, but rather seeks to synthesise existing evidence within a three-tier conceptual framework. This framework classifies interventions into three categories: those primarily addressing local inflammation and barrier-associated microbiota dysbiosis; those exerting systemic immunomodulation via gut-derived microbial signals; and those modulating the skin microbiota ecology. It should be noted that human clinical data are still limited and heterogeneous, and much mechanistic insight is derived from preclinical research. By clarifying mechanistic layers and evidentiary gaps, this framework may facilitate future research to evaluate the sequencing or combination of anti-inflammatory therapy, barrier restoration, and microbiota ecological modulation.
Additional Links: PMID-42529037
PubMed:
Citation:
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@article {pmid42529037,
year = {2026},
author = {Zhao, Y and Gao, Q and Li, G and Zhou, Q and Yang, F and Zhu, X},
title = {Microbiota-directed therapies for atopic dermatitis: a three-tier framework for inflammation control, immune modulation, and microbiome restoration.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1873455},
pmid = {42529037},
issn = {1664-3224},
mesh = {Humans ; *Dermatitis, Atopic/therapy/immunology/microbiology ; Skin Microbiome ; Animals ; *Immunomodulation ; Inflammation/therapy/immunology ; Probiotics/therapeutic use ; *Microbiota/immunology ; Dysbiosis/immunology/therapy ; *Gastrointestinal Microbiome/immunology ; Skin/microbiology/immunology ; },
abstract = {The pathogenesis of atopic dermatitis (AD) involves cutaneous barrier dysfunction, immune dysregulation, and microbiota imbalance. Although microbiota-directed therapeutic approaches have garnered increasing attention, current evidence is heterogeneous, encompassing probiotics, postbiotics, microbial metabolites, local microbial interventions, antimicrobials and ecological modulation strategies. This narrative review does not aim to provide clinical guidelines, but rather seeks to synthesise existing evidence within a three-tier conceptual framework. This framework classifies interventions into three categories: those primarily addressing local inflammation and barrier-associated microbiota dysbiosis; those exerting systemic immunomodulation via gut-derived microbial signals; and those modulating the skin microbiota ecology. It should be noted that human clinical data are still limited and heterogeneous, and much mechanistic insight is derived from preclinical research. By clarifying mechanistic layers and evidentiary gaps, this framework may facilitate future research to evaluate the sequencing or combination of anti-inflammatory therapy, barrier restoration, and microbiota ecological modulation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Dermatitis, Atopic/therapy/immunology/microbiology
Skin Microbiome
Animals
*Immunomodulation
Inflammation/therapy/immunology
Probiotics/therapeutic use
*Microbiota/immunology
Dysbiosis/immunology/therapy
*Gastrointestinal Microbiome/immunology
Skin/microbiology/immunology
RevDate: 2026-07-30
CmpDate: 2026-07-30
Shotgun metagenomic analysis reveals taxonomic and functional alterations in the gut microbiome across prodromal and symptomatic Lewy body disease.
Frontiers in microbiomes, 5:1834726.
BACKGROUND: Lewy body disease (LBD) is a progressive neurodegenerative a-synucleinopathy, whereas isolated REM sleep behavior disorder (iRBD) is recognized as a prodromal stage of LBD. Although growing evidence implicates the gut-brain axis in neurodegeneration, the taxonomic and functional roles of the gut microbiome across the prodromal-to-symptomatic LBD continuum remain poorly defined.
METHODS: Here, we performed shotgun metagenomic sequencing on stool samples from 25 patients with LBD (10 mild cognitive impairment due to LBD [MCI-LB] and 15 dementia with Lewy bodies [DLB]), 10 individuals with iRBD, and their household matched cohabitant controls to characterize disease-associated microbial alterations while minimizing environmental confounding.
RESULTS: Despite no significant differences in global microbial diversity, we identified convergent shifts in microbial taxa, metabolic pathways, and gene families across disease stages. Both LBD and iRBD showed increased abundance of microbial taxa potentially associated with gut barrier disruption, as well as higher abundance of functional pathways related to lipopolysaccharide biosynthesis. LBD showed lower abundance of pathways related to complex carbohydrate fermentation, and both groups showed lower abundance of pathways associated with neurotransmitter-related metabolism. In particular, pathways and gene families associated with starch degradation were reduced in LBD, and those associated with histidine-to-glutamate/ GABA metabolism were reduced in both groups.
DISCUSSION: These exploratory findings represent the first high-resolution, shotgun metagenomic characterization of gut microbiome alterations across the LBD continuum, highlighting functional patterns that may serve as candidate markers of disease progression in future longitudinal and mechanistic studies.
Additional Links: PMID-42529077
PubMed:
Citation:
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@article {pmid42529077,
year = {2026},
author = {Zhao, X and McCarter, SJ and Gupta, VK and Grant, KM and St Louis, EK and Kantarci, K and Savica, R and Hill, M and Vuong, HE and Staley, C and Boeve, BF and Ross, OA and Teigen, LM and Sung, J},
title = {Shotgun metagenomic analysis reveals taxonomic and functional alterations in the gut microbiome across prodromal and symptomatic Lewy body disease.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1834726},
pmid = {42529077},
issn = {2813-4338},
abstract = {BACKGROUND: Lewy body disease (LBD) is a progressive neurodegenerative a-synucleinopathy, whereas isolated REM sleep behavior disorder (iRBD) is recognized as a prodromal stage of LBD. Although growing evidence implicates the gut-brain axis in neurodegeneration, the taxonomic and functional roles of the gut microbiome across the prodromal-to-symptomatic LBD continuum remain poorly defined.
METHODS: Here, we performed shotgun metagenomic sequencing on stool samples from 25 patients with LBD (10 mild cognitive impairment due to LBD [MCI-LB] and 15 dementia with Lewy bodies [DLB]), 10 individuals with iRBD, and their household matched cohabitant controls to characterize disease-associated microbial alterations while minimizing environmental confounding.
RESULTS: Despite no significant differences in global microbial diversity, we identified convergent shifts in microbial taxa, metabolic pathways, and gene families across disease stages. Both LBD and iRBD showed increased abundance of microbial taxa potentially associated with gut barrier disruption, as well as higher abundance of functional pathways related to lipopolysaccharide biosynthesis. LBD showed lower abundance of pathways related to complex carbohydrate fermentation, and both groups showed lower abundance of pathways associated with neurotransmitter-related metabolism. In particular, pathways and gene families associated with starch degradation were reduced in LBD, and those associated with histidine-to-glutamate/ GABA metabolism were reduced in both groups.
DISCUSSION: These exploratory findings represent the first high-resolution, shotgun metagenomic characterization of gut microbiome alterations across the LBD continuum, highlighting functional patterns that may serve as candidate markers of disease progression in future longitudinal and mechanistic studies.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Dose Titration of Plant-Based Flavonoid Blend Supplementation on Performance, Digestibility, Gut Microbiome, Blood Biomarkers, and Meat Quality of Growing Rabbits.
Food science & nutrition, 14(8):e72156.
Rabbit meat is increasingly valued for its high nutritional quality, driving growing interest in enhancing its production through phytobiotics like plant-based flavonoid blend (PFB). So, this study looked at how a PFB at different doses influences the performance, digestibility, gut microbiota, blood biomarkers, liver health, and meat quality of growing rabbits. Sixty rabbits (body weight 552.63 ± 13.44 g) were assigned at random to five dietary groups, having twelve replicates per group. The rabbits were fed a basal diet as a total mixed ration having 17.02% crude protein and 11.60 MJ metabolizable energy/kg dry matter (DM), supplemented with PFB (g/kg diet) at 0.0 (control), 0.20, 0.40, 0.60, and 0.80. Following a 2 weeks adjustment period, the feeding trial was conducted for 5 weeks. When the trial was over, rabbits were sacrificed to collect digesta, blood, and meat samples for further analysis. Supplementation with PFB at 0.60 g/kg diet (range: 0.50-0.70 g/kg) showed a better final body weight (p = 0.01), weight gain (p < 0.001), and feed conversion ratio (p < 0.001), while significantly improving DM, nitrogen-free extract (p < 0.001), and ether extract (p = 0.02) digestibility. Besides, supplementation with PFB presented a linear reduction in Escherichia coli (p = 0.003), accompanied by linear improvement in Lactobacillus spp. (p < 0.001) and serum high density lipoprotein-cholesterol (HDL-C; p = 0.001). Broken-line analysis indicated optimal PFB supplementation levels of 0.60, 0.47, and 0.60 g/kg diet for E. coli, Lactobacillus spp., and HDL-C, respectively. However, feed intake, serum triglycerides, other cholesterols, total protein, albumin, globulin, and uric acid remained unchanged across the groups. Furthermore, supplementation with PFB with an estimated breakpoint of 0.55 g PFB/kg of diet effectively (p ≤ 0.02) reduced serum liver enzymes (aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase) indicating better liver health. In addition, PFB supplementation linearly reduced meat ether extract content and improved meat redness (p < 0.001), with optimal responses at 0.58 and 0.60 g/kg diet, respectively, while having no impacts on meat protein, ash, lightness, or yellowness. Therefore, dietary inclusion of PFB at 0.55 g-0.60 g per kg diet optimized growth performance through enhanced weight gain, feed efficiency, and nutrient digestibility, while favorably modulating cecum microbiome, serum cholesterol, liver enzyme activities, and ameliorated meat quality.
Additional Links: PMID-42529078
PubMed:
Citation:
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@article {pmid42529078,
year = {2026},
author = {Rahman, MA and Hasan, MM and Hashem, MA and Siddique, MP and Chowdhury, R},
title = {Dose Titration of Plant-Based Flavonoid Blend Supplementation on Performance, Digestibility, Gut Microbiome, Blood Biomarkers, and Meat Quality of Growing Rabbits.},
journal = {Food science & nutrition},
volume = {14},
number = {8},
pages = {e72156},
pmid = {42529078},
issn = {2048-7177},
abstract = {Rabbit meat is increasingly valued for its high nutritional quality, driving growing interest in enhancing its production through phytobiotics like plant-based flavonoid blend (PFB). So, this study looked at how a PFB at different doses influences the performance, digestibility, gut microbiota, blood biomarkers, liver health, and meat quality of growing rabbits. Sixty rabbits (body weight 552.63 ± 13.44 g) were assigned at random to five dietary groups, having twelve replicates per group. The rabbits were fed a basal diet as a total mixed ration having 17.02% crude protein and 11.60 MJ metabolizable energy/kg dry matter (DM), supplemented with PFB (g/kg diet) at 0.0 (control), 0.20, 0.40, 0.60, and 0.80. Following a 2 weeks adjustment period, the feeding trial was conducted for 5 weeks. When the trial was over, rabbits were sacrificed to collect digesta, blood, and meat samples for further analysis. Supplementation with PFB at 0.60 g/kg diet (range: 0.50-0.70 g/kg) showed a better final body weight (p = 0.01), weight gain (p < 0.001), and feed conversion ratio (p < 0.001), while significantly improving DM, nitrogen-free extract (p < 0.001), and ether extract (p = 0.02) digestibility. Besides, supplementation with PFB presented a linear reduction in Escherichia coli (p = 0.003), accompanied by linear improvement in Lactobacillus spp. (p < 0.001) and serum high density lipoprotein-cholesterol (HDL-C; p = 0.001). Broken-line analysis indicated optimal PFB supplementation levels of 0.60, 0.47, and 0.60 g/kg diet for E. coli, Lactobacillus spp., and HDL-C, respectively. However, feed intake, serum triglycerides, other cholesterols, total protein, albumin, globulin, and uric acid remained unchanged across the groups. Furthermore, supplementation with PFB with an estimated breakpoint of 0.55 g PFB/kg of diet effectively (p ≤ 0.02) reduced serum liver enzymes (aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase) indicating better liver health. In addition, PFB supplementation linearly reduced meat ether extract content and improved meat redness (p < 0.001), with optimal responses at 0.58 and 0.60 g/kg diet, respectively, while having no impacts on meat protein, ash, lightness, or yellowness. Therefore, dietary inclusion of PFB at 0.55 g-0.60 g per kg diet optimized growth performance through enhanced weight gain, feed efficiency, and nutrient digestibility, while favorably modulating cecum microbiome, serum cholesterol, liver enzyme activities, and ameliorated meat quality.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Diversity and taxonomic differences in the oral microbiota of stroke patients: a systematic review and meta-analysis.
Frontiers in microbiology, 17:1874193.
BACKGROUND: In recent years, a growing body of evidence suggests that stroke may be associated with an imbalance in the oral microbiome. To further elucidate this potential link, this study aims to systematically compare differences in the oral microbiome between stroke patients and healthy individuals.
OBJECTIVE: To systematically evaluate the differences in oral microbiota diversity and taxonomic composition between stroke patients and healthy controls.
METHOD: From the date each database was established up to 20 February 2026, we conducted searches in CNKI, Wanfang, PubMed, Embase, SinoMed, Web of Science, the Cochrane Library and grey literature databases, with the aim of identifying studies reporting on the oral microbiota of stroke patients and healthy individuals. The Newcastle-Ottawa Scale (NOS) was used to assess the risk of bias in the included studies, and meta-analysis was performed using RevMan 5.4 software. The pooled effect size was calculated as the standardized mean difference (SMD) and a parallel Z-test was conducted; heterogeneity was assessed using Cochran's Q test and the I[2] statistic.
RESULT: This meta-analysis of 11 studies (746 stroke patients, 552 controls) showed upward trends in Observed species (SMD = 0.39, 95% CI: 0.05-0.72, I[2] = 84%) and Shannon (SMD = 0.31, 95% CI: 0.02-0.61, I[2] = 82%) indices, though these findings were not robust in sensitivity analyses. Chao1 and Simpson showed no significant differences. Eight of nine β-diversity studies reported significant differences between groups. Meta-analysis showed higher Bacteroidota (SMD = 0.36, 95% CI: 0.18-0.54, 3 studies; I[2] = 44%). Higher abundances of Firmicutes, Spirochaetes, and several genera were suggested by descriptive synthesis but should be considered exploratory.
CONCLUSION: The oral microbiota of stroke patients exhibits characteristic changes, which may provide preliminary clues for understanding post-stroke oral microbial alterations and offer a theoretical basis for oral care, but require validation in prospective studies.
Unique Identifier: CRD420251235256, https://www.crd.york.ac.uk/PROSPERO/view/CRD420251235256.
Additional Links: PMID-42529147
PubMed:
Citation:
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@article {pmid42529147,
year = {2026},
author = {Chen, Y and Tian, Y and Jin, Y and Wu, X and Li, X and Du, W and Li, W and Li, J},
title = {Diversity and taxonomic differences in the oral microbiota of stroke patients: a systematic review and meta-analysis.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1874193},
pmid = {42529147},
issn = {1664-302X},
abstract = {BACKGROUND: In recent years, a growing body of evidence suggests that stroke may be associated with an imbalance in the oral microbiome. To further elucidate this potential link, this study aims to systematically compare differences in the oral microbiome between stroke patients and healthy individuals.
OBJECTIVE: To systematically evaluate the differences in oral microbiota diversity and taxonomic composition between stroke patients and healthy controls.
METHOD: From the date each database was established up to 20 February 2026, we conducted searches in CNKI, Wanfang, PubMed, Embase, SinoMed, Web of Science, the Cochrane Library and grey literature databases, with the aim of identifying studies reporting on the oral microbiota of stroke patients and healthy individuals. The Newcastle-Ottawa Scale (NOS) was used to assess the risk of bias in the included studies, and meta-analysis was performed using RevMan 5.4 software. The pooled effect size was calculated as the standardized mean difference (SMD) and a parallel Z-test was conducted; heterogeneity was assessed using Cochran's Q test and the I[2] statistic.
RESULT: This meta-analysis of 11 studies (746 stroke patients, 552 controls) showed upward trends in Observed species (SMD = 0.39, 95% CI: 0.05-0.72, I[2] = 84%) and Shannon (SMD = 0.31, 95% CI: 0.02-0.61, I[2] = 82%) indices, though these findings were not robust in sensitivity analyses. Chao1 and Simpson showed no significant differences. Eight of nine β-diversity studies reported significant differences between groups. Meta-analysis showed higher Bacteroidota (SMD = 0.36, 95% CI: 0.18-0.54, 3 studies; I[2] = 44%). Higher abundances of Firmicutes, Spirochaetes, and several genera were suggested by descriptive synthesis but should be considered exploratory.
CONCLUSION: The oral microbiota of stroke patients exhibits characteristic changes, which may provide preliminary clues for understanding post-stroke oral microbial alterations and offer a theoretical basis for oral care, but require validation in prospective studies.
Unique Identifier: CRD420251235256, https://www.crd.york.ac.uk/PROSPERO/view/CRD420251235256.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Gut microbiota and intestinal permeability in rheumatoid arthritis: pathogenic mechanisms.
Frontiers in immunology, 17:1887782.
Rheumatoid arthritis is a chronic systemic autoimmune disease in which the earliest breaks in immune tolerance may arise at mucosal surfaces before the clinical onset of synovitis. Among these sites, the gut has emerged as a particularly compelling candidate because it integrates microbial, epithelial, metabolic, and immune pathways with the potential to shape systemic inflammation. In this review, we examine the biological foundations of the gut-joint axis in rheumatoid arthritis, focusing on intestinal barrier structure, microbiome alterations, mucosal immune crosstalk, and mechanisms of barrier dysfunction. Current human evidence links rheumatoid arthritis to heterogeneous shifts in gut microbial composition, depletion of beneficial metabolite-producing commensals, altered immune-metabolic signaling, and biomarker patterns consistent with epithelial injury and microbial-product translocation. At the same time, available data do not support the existence of a single, universal microbial or permeability signature that defines the disease across populations. Recent longitudinal studies further challenge the concept of stable, long-standing dysbiosis and instead suggest a late, transient phase of ecological instability arising close to symptom onset. Experimental models provide stronger mechanistic support, showing that dysbiotic microbial communities, impaired barrier integrity, and strain-specific host-microbe interactions can promote T helper 17-skewed immunity and aggravate arthritis. Collectively, these findings support a context-dependent contribution of the gut to rheumatoid arthritis pathogenesis while underscoring the need for longitudinal, strain-resolved, and multi-omic human studies to clarify causality, refine disease models, and identify clinically meaningful windows for intervention.
Additional Links: PMID-42529164
PubMed:
Citation:
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@article {pmid42529164,
year = {2026},
author = {Bilski, J and Schramm-Luc, AI and Szczepanik, M and Pierzchalski, P and Krawczyk, A and Luc, K},
title = {Gut microbiota and intestinal permeability in rheumatoid arthritis: pathogenic mechanisms.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1887782},
pmid = {42529164},
issn = {1664-3224},
mesh = {Humans ; *Arthritis, Rheumatoid/immunology/microbiology/metabolism ; Intestinal Barrier Function ; *Gastrointestinal Microbiome/immunology ; Animals ; Dysbiosis/immunology ; *Intestinal Mucosa/immunology/microbiology/metabolism ; Permeability ; },
abstract = {Rheumatoid arthritis is a chronic systemic autoimmune disease in which the earliest breaks in immune tolerance may arise at mucosal surfaces before the clinical onset of synovitis. Among these sites, the gut has emerged as a particularly compelling candidate because it integrates microbial, epithelial, metabolic, and immune pathways with the potential to shape systemic inflammation. In this review, we examine the biological foundations of the gut-joint axis in rheumatoid arthritis, focusing on intestinal barrier structure, microbiome alterations, mucosal immune crosstalk, and mechanisms of barrier dysfunction. Current human evidence links rheumatoid arthritis to heterogeneous shifts in gut microbial composition, depletion of beneficial metabolite-producing commensals, altered immune-metabolic signaling, and biomarker patterns consistent with epithelial injury and microbial-product translocation. At the same time, available data do not support the existence of a single, universal microbial or permeability signature that defines the disease across populations. Recent longitudinal studies further challenge the concept of stable, long-standing dysbiosis and instead suggest a late, transient phase of ecological instability arising close to symptom onset. Experimental models provide stronger mechanistic support, showing that dysbiotic microbial communities, impaired barrier integrity, and strain-specific host-microbe interactions can promote T helper 17-skewed immunity and aggravate arthritis. Collectively, these findings support a context-dependent contribution of the gut to rheumatoid arthritis pathogenesis while underscoring the need for longitudinal, strain-resolved, and multi-omic human studies to clarify causality, refine disease models, and identify clinically meaningful windows for intervention.},
}
MeSH Terms:
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Humans
*Arthritis, Rheumatoid/immunology/microbiology/metabolism
Intestinal Barrier Function
*Gastrointestinal Microbiome/immunology
Animals
Dysbiosis/immunology
*Intestinal Mucosa/immunology/microbiology/metabolism
Permeability
RevDate: 2026-07-30
CmpDate: 2026-07-30
Beyond scarring: immune-epithelial crosstalk in wound-induced hair follicle neogenesis.
Frontiers in immunology, 17:1872547.
Wound-induced hair follicle neogenesis (WIHN) represents a remarkable regenerative phenomenon observed in adult mammalian skin (predominantly studied in mice), in which large full-thickness wounds bypass fibrotic scarring to generate fully functional de novo hair follicles. This process reflects the context-dependent reactivation of embryonic morphogenetic programs, driven by a coordinated tripartite immune-microbial-epithelial axis (defined here as the integrated multi-directional signaling network among localized immune cells, epithelial stem cells, and the skin microbiota/fibroblasts). Mechanistically, γδ T cells initiate dermal fibroblast reprogramming through an FGF9-Wnt feed-forward loop, while macrophages promote AKT/β-catenin signaling in Lgr5[+] epithelial stem cells via TNF-α-driven non-canonical pathways. Regulatory T cells (Tregs) further support follicular morphogenesis by delivering Jagged1/Notch signals. In parallel, the skin microbiota acts as a key amplifier of regeneration, modulating the wound microenvironment through the IL-1β/MyD88 signaling axis. Taken together, WIHN illustrates the remarkable functional plasticity of immune signaling, which can be repurposed from host defense to orchestrating tissue regeneration. By elucidating this dynamic murine skin-immune dialogue, this mini-review provides a conceptual framework for speculative precision immunomodulatory therapies and emerging translational approaches-such as laser-assisted tissue remodeling-aimed at treating inflammatory and scarring alopecia, as well as achieving scarless and functionally restorative wound healing.
Additional Links: PMID-42529170
PubMed:
Citation:
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@article {pmid42529170,
year = {2026},
author = {Ma, YM and Shen, W and Xie, XL and Tang, SL and Wu, Y and Zhong, HJ and Yan, Q and Sun, H},
title = {Beyond scarring: immune-epithelial crosstalk in wound-induced hair follicle neogenesis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1872547},
pmid = {42529170},
issn = {1664-3224},
mesh = {Animals ; *Hair Follicle/immunology ; Humans ; *Wound Healing/immunology ; *Cicatrix/immunology ; Signal Transduction ; Regeneration/immunology ; Skin Microbiome ; Skin/immunology ; *Epithelial Cells/immunology/metabolism ; },
abstract = {Wound-induced hair follicle neogenesis (WIHN) represents a remarkable regenerative phenomenon observed in adult mammalian skin (predominantly studied in mice), in which large full-thickness wounds bypass fibrotic scarring to generate fully functional de novo hair follicles. This process reflects the context-dependent reactivation of embryonic morphogenetic programs, driven by a coordinated tripartite immune-microbial-epithelial axis (defined here as the integrated multi-directional signaling network among localized immune cells, epithelial stem cells, and the skin microbiota/fibroblasts). Mechanistically, γδ T cells initiate dermal fibroblast reprogramming through an FGF9-Wnt feed-forward loop, while macrophages promote AKT/β-catenin signaling in Lgr5[+] epithelial stem cells via TNF-α-driven non-canonical pathways. Regulatory T cells (Tregs) further support follicular morphogenesis by delivering Jagged1/Notch signals. In parallel, the skin microbiota acts as a key amplifier of regeneration, modulating the wound microenvironment through the IL-1β/MyD88 signaling axis. Taken together, WIHN illustrates the remarkable functional plasticity of immune signaling, which can be repurposed from host defense to orchestrating tissue regeneration. By elucidating this dynamic murine skin-immune dialogue, this mini-review provides a conceptual framework for speculative precision immunomodulatory therapies and emerging translational approaches-such as laser-assisted tissue remodeling-aimed at treating inflammatory and scarring alopecia, as well as achieving scarless and functionally restorative wound healing.},
}
MeSH Terms:
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hide MeSH Terms
Animals
*Hair Follicle/immunology
Humans
*Wound Healing/immunology
*Cicatrix/immunology
Signal Transduction
Regeneration/immunology
Skin Microbiome
Skin/immunology
*Epithelial Cells/immunology/metabolism
RevDate: 2026-07-30
CmpDate: 2026-07-30
Correlation of preoperative gut microbiota and postoperative delirium in patients undergoing minimally invasive direct coronary artery bypass grafting.
Frontiers in microbiology, 17:1854098.
BACKGROUND: Postoperative delirium (POD) is a common complication after cardiac surgery, but the role of preoperative gut microbiota, especially the mycobiome, in POD susceptibility remains unclear. This study investigated the association between preoperative gut bacterome and mycobiome profiles and POD in elderly patients undergoing minimally invasive direct coronary artery bypass grafting (MIDCABG).
METHODS: Preoperative fecal samples from 31 elderly patients scheduled for MIDCABG were analyzed via 16S rRNA and ITS high-throughput sequencing. POD was assessed twice daily using the 3D-CAM scale. Patients were divided into delirium (M, n = 7) and control (C, n = 24) groups. Microbial diversity, composition, and bacteria-fungi correlations were systematically evaluated.
RESULTS: POD incidence was 22.58%. No baseline differences were observed between groups. Group M exhibited significantly lower gut microbiome health index and higher microbial dysbiosis index at both bacterome and mycobiome levels. Alpha/beta diversity did not differ significantly. LEfSe revealed bacterial enrichment of Clostridium and Intestinibacter in Group M, and Bifidobacterium in Group C. Fungally, Aspergillus and Basidiomycota predominated in Group M, while Saccharomyces and Ascomycota were enriched in Group C. candida showed the highest abundance in Group M and was a key node in the fungal co-occurrence network. Correlation analysis revealed positive associations between bacterial genera (Klebsiella, Enterococcus, Roseburia) and fungal taxa (Wickerhamomyces, Pichia, Geotrichum), suggesting ecological interactions potentially linked to POD.
CONCLUSION: Preoperative dysbiosis of gut bacterome and mycobiome is associated with POD in elderly MIDCABG patients. Several bacterial and fungal taxa, including Clostridium, Intestinibacter, Aspergillus, Saccharomyces, and Candida, were identified as candidate microbial biomarkers associated with POD and may contribute to future microbiota-based risk stratification strategies.
Additional Links: PMID-42529203
PubMed:
Citation:
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@article {pmid42529203,
year = {2026},
author = {Hu, R and Fang, Y and Han, P and Han, Y and Wang, J and Liu, H and Shi, Y and Li, Z and Zhang, L},
title = {Correlation of preoperative gut microbiota and postoperative delirium in patients undergoing minimally invasive direct coronary artery bypass grafting.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1854098},
pmid = {42529203},
issn = {1664-302X},
abstract = {BACKGROUND: Postoperative delirium (POD) is a common complication after cardiac surgery, but the role of preoperative gut microbiota, especially the mycobiome, in POD susceptibility remains unclear. This study investigated the association between preoperative gut bacterome and mycobiome profiles and POD in elderly patients undergoing minimally invasive direct coronary artery bypass grafting (MIDCABG).
METHODS: Preoperative fecal samples from 31 elderly patients scheduled for MIDCABG were analyzed via 16S rRNA and ITS high-throughput sequencing. POD was assessed twice daily using the 3D-CAM scale. Patients were divided into delirium (M, n = 7) and control (C, n = 24) groups. Microbial diversity, composition, and bacteria-fungi correlations were systematically evaluated.
RESULTS: POD incidence was 22.58%. No baseline differences were observed between groups. Group M exhibited significantly lower gut microbiome health index and higher microbial dysbiosis index at both bacterome and mycobiome levels. Alpha/beta diversity did not differ significantly. LEfSe revealed bacterial enrichment of Clostridium and Intestinibacter in Group M, and Bifidobacterium in Group C. Fungally, Aspergillus and Basidiomycota predominated in Group M, while Saccharomyces and Ascomycota were enriched in Group C. candida showed the highest abundance in Group M and was a key node in the fungal co-occurrence network. Correlation analysis revealed positive associations between bacterial genera (Klebsiella, Enterococcus, Roseburia) and fungal taxa (Wickerhamomyces, Pichia, Geotrichum), suggesting ecological interactions potentially linked to POD.
CONCLUSION: Preoperative dysbiosis of gut bacterome and mycobiome is associated with POD in elderly MIDCABG patients. Several bacterial and fungal taxa, including Clostridium, Intestinibacter, Aspergillus, Saccharomyces, and Candida, were identified as candidate microbial biomarkers associated with POD and may contribute to future microbiota-based risk stratification strategies.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
The forehead and glabella show pronounced Cutibacterium relative abundance differences between acne and healthy groups: a regional facial 16S rRNA gene sequencing study.
Frontiers in microbiology, 17:1853291.
INTRODUCTION: Acne vulgaris is a prevalent chronic inflammatory skin disease, and Cutibacterium overproliferation is a core pathogenic factor, yet findings remain controversial, partly due to single anatomical area sampling bias.
METHODS: We conducted a crosssectional study with anatomically paired sampling across multiple facial anatomical areas in 85 subjects (30 healthy subjects, 55 acne subjects), analyzing 763 samples from 6 facial anatomical areas for 16S rRNA V4 region sequencing and microbial community analysis.
RESULTS: At the whole-face level, acne subjects had a significantly higher relative abundance of Cutibacterium and Staphylococcus compared with healthy subjects. Critically, Cutibacterium enrichment was highly dependent on facial anatomical areas: only the forehead and glabella showed significant intergroup differences, with the forehead showing a 127% higher median relative abundance (adjusted q = 0.043) and the glabella showing a 53% higher median relative abundance (adjusted q = 0.043), while Staphylococcus enrichment was widespread (present in 5 of 6 areas, except the jaw), and Corynebacterium showed no intergroup differences in any facial area, although LEfSe classified it as a health-associated taxon. Tax4Fun-based functional prediction suggested upregulated antimicrobial resistance and adaptation pathways, and downregulated core metabolic pathways, in acne-associated microbiota.
DISCUSSION: This study demonstrates the facial anatomical area specificity of Cutibacterium enrichment, identifies the forehead and glabella as the areas with pronounced relative abundance differences between acne and healthy groups.
Additional Links: PMID-42529208
PubMed:
Citation:
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@article {pmid42529208,
year = {2026},
author = {Zha, W and Li, K and Qian, Y and Zhao, L and Cheung, S and Huang, J and Miao, F and Shen, J and Yu, Y and Hu, X and Wang, H and Lyu, T and Shi, L},
title = {The forehead and glabella show pronounced Cutibacterium relative abundance differences between acne and healthy groups: a regional facial 16S rRNA gene sequencing study.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1853291},
pmid = {42529208},
issn = {1664-302X},
abstract = {INTRODUCTION: Acne vulgaris is a prevalent chronic inflammatory skin disease, and Cutibacterium overproliferation is a core pathogenic factor, yet findings remain controversial, partly due to single anatomical area sampling bias.
METHODS: We conducted a crosssectional study with anatomically paired sampling across multiple facial anatomical areas in 85 subjects (30 healthy subjects, 55 acne subjects), analyzing 763 samples from 6 facial anatomical areas for 16S rRNA V4 region sequencing and microbial community analysis.
RESULTS: At the whole-face level, acne subjects had a significantly higher relative abundance of Cutibacterium and Staphylococcus compared with healthy subjects. Critically, Cutibacterium enrichment was highly dependent on facial anatomical areas: only the forehead and glabella showed significant intergroup differences, with the forehead showing a 127% higher median relative abundance (adjusted q = 0.043) and the glabella showing a 53% higher median relative abundance (adjusted q = 0.043), while Staphylococcus enrichment was widespread (present in 5 of 6 areas, except the jaw), and Corynebacterium showed no intergroup differences in any facial area, although LEfSe classified it as a health-associated taxon. Tax4Fun-based functional prediction suggested upregulated antimicrobial resistance and adaptation pathways, and downregulated core metabolic pathways, in acne-associated microbiota.
DISCUSSION: This study demonstrates the facial anatomical area specificity of Cutibacterium enrichment, identifies the forehead and glabella as the areas with pronounced relative abundance differences between acne and healthy groups.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Rethinking the hepatoprotective potential of vegetarian diets in dysfunction-associated steatotic liver disease/metabolic-associated fatty liver disease: a critical narrative review.
Frontiers in nutrition, 13:1902349.
Dietary intervention is central to the management of metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as metabolic-associated fatty liver disease (MAFLD). Although vegetarian dietary patterns are widely considered hepatoprotective, emerging evidence indicates that certain individuals following non-standardized vegetarian diets may fail to obtain the expected hepatic benefits-a phenomenon termed the "vegetarian hepatoprotection paradox." This critical narrative examines the putative mechanisms underlying this paradox. Excessive intake of high-glycemic carbohydrates and fructose, which is common in some vegetarian diets, may activate hepatic de novo lipogenesis. Furthermore, incomplete plant proteins may contribute to impaired very low-density lipoprotein (VLDL)-mediated lipid export, while an imbalanced n-6:n-3 fatty acid ratio may promote hepatic inflammation. These dietary factors may interact with genetic susceptibility, including patatin-like phospholipase domain-containing protein 3 (PNPLA3) I148M and transmembrane 6 superfamily member 2 (TM6SF2) E167K variants, disrupting hepatic lipid homeostasis. Additionally, gut dysbiosis may propagate metabolic disturbance through chronic inflammation. Accordingly, a shift from the categorical vegetarian labeling toward an emphasis on plant-based dietary quality-reflecting the principle that dietary quality matters more than the vegetarian label itself-may be warranted. This review discusses evidence-based dietary patterns, including the Mediterranean diet, the Green Mediterranean diet, and the Dietary Approaches to Stop Hypertension (DASH) diet, together with chrononutrition strategies. A precision nutrition approach integrating genetic, metabolic, and microbiome characteristics may represent an emerging but still investigational framework for individualized MASLD/MAFLD interventions.
Additional Links: PMID-42529254
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@article {pmid42529254,
year = {2026},
author = {Jiang, W and Yang, Z and Cui, Y and Huang, N and Dong, L and Sun, T and Zhang, B},
title = {Rethinking the hepatoprotective potential of vegetarian diets in dysfunction-associated steatotic liver disease/metabolic-associated fatty liver disease: a critical narrative review.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1902349},
pmid = {42529254},
issn = {2296-861X},
abstract = {Dietary intervention is central to the management of metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as metabolic-associated fatty liver disease (MAFLD). Although vegetarian dietary patterns are widely considered hepatoprotective, emerging evidence indicates that certain individuals following non-standardized vegetarian diets may fail to obtain the expected hepatic benefits-a phenomenon termed the "vegetarian hepatoprotection paradox." This critical narrative examines the putative mechanisms underlying this paradox. Excessive intake of high-glycemic carbohydrates and fructose, which is common in some vegetarian diets, may activate hepatic de novo lipogenesis. Furthermore, incomplete plant proteins may contribute to impaired very low-density lipoprotein (VLDL)-mediated lipid export, while an imbalanced n-6:n-3 fatty acid ratio may promote hepatic inflammation. These dietary factors may interact with genetic susceptibility, including patatin-like phospholipase domain-containing protein 3 (PNPLA3) I148M and transmembrane 6 superfamily member 2 (TM6SF2) E167K variants, disrupting hepatic lipid homeostasis. Additionally, gut dysbiosis may propagate metabolic disturbance through chronic inflammation. Accordingly, a shift from the categorical vegetarian labeling toward an emphasis on plant-based dietary quality-reflecting the principle that dietary quality matters more than the vegetarian label itself-may be warranted. This review discusses evidence-based dietary patterns, including the Mediterranean diet, the Green Mediterranean diet, and the Dietary Approaches to Stop Hypertension (DASH) diet, together with chrononutrition strategies. A precision nutrition approach integrating genetic, metabolic, and microbiome characteristics may represent an emerging but still investigational framework for individualized MASLD/MAFLD interventions.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Dominant Role of Habitat Transformation in Driving the Divergence of Health-Risk Related Microbial Functional Genes in Karst Mountain Parks: A Metagenomic Study.
Ecology and evolution, 16(8):e74112.
The transformation of natural forests into urban parks has had a profound impact on subterranean ecosystems. Nevertheless, the underlying mechanisms by which this land use change affects human health through alterations in soil microbial functional genes remain to be elucidated. Focusing on a karst mountain park in Guiyang, China, we used metagenomic sequencing to compare the abundance and composition of antibiotic resistance genes (ARGs), pathogen-host interaction genes (PHIs), and virulence factor genes (VFs) between remnant forests and artificial green spaces, and examined how plant diversity and soil chemometrics drove their variation. Habitat type emerged as the strongest driver of gene composition. PHIs and VFs were more abundant in remnant forests and positively correlated with native plant diversity, while ARGs were enriched in artificial green spaces. All three gene categories showed positive correlations with soil nitrogen content in artificial green spaces. Remnant forests harbored microbial functions linked to complex plant-microbe interactions, whereas intensive management in artificial green spaces selects for antibiotic resistance and nutrient-adaptive genes. These findings reveal distinct health risks across habitats, suggesting that differentiated park management strategies are needed to mitigate public health risks while maintaining ecological sustainability.
Additional Links: PMID-42529303
PubMed:
Citation:
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@article {pmid42529303,
year = {2026},
author = {Wang, W and Cen, C and Yang, J},
title = {Dominant Role of Habitat Transformation in Driving the Divergence of Health-Risk Related Microbial Functional Genes in Karst Mountain Parks: A Metagenomic Study.},
journal = {Ecology and evolution},
volume = {16},
number = {8},
pages = {e74112},
pmid = {42529303},
issn = {2045-7758},
abstract = {The transformation of natural forests into urban parks has had a profound impact on subterranean ecosystems. Nevertheless, the underlying mechanisms by which this land use change affects human health through alterations in soil microbial functional genes remain to be elucidated. Focusing on a karst mountain park in Guiyang, China, we used metagenomic sequencing to compare the abundance and composition of antibiotic resistance genes (ARGs), pathogen-host interaction genes (PHIs), and virulence factor genes (VFs) between remnant forests and artificial green spaces, and examined how plant diversity and soil chemometrics drove their variation. Habitat type emerged as the strongest driver of gene composition. PHIs and VFs were more abundant in remnant forests and positively correlated with native plant diversity, while ARGs were enriched in artificial green spaces. All three gene categories showed positive correlations with soil nitrogen content in artificial green spaces. Remnant forests harbored microbial functions linked to complex plant-microbe interactions, whereas intensive management in artificial green spaces selects for antibiotic resistance and nutrient-adaptive genes. These findings reveal distinct health risks across habitats, suggesting that differentiated park management strategies are needed to mitigate public health risks while maintaining ecological sustainability.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Integrated microbiomic and proteomic profiling reveals distinct ocular surface molecular and microbial landscapes in dry eye after SMILE surgery.
Frontiers in cellular and infection microbiology, 16:1858069.
OBJECTIVES: The aim of this study is to investigate the microbial and proteomic features of the ocular surface following small incision lenticule extraction (SMILE) surgery and to elucidate their association with the development of postoperative dry eye disease (DED).
METHODS: This study comprised a prospective cohort for baseline assessment and a cross-sectional postoperative assessment. We enrolled two sets of participants: a preoperative cohort (PG) consisting of patients scheduled for SMILE; and a postoperative cohort,consisting of patients who had undergone SMILE. The postoperative cohort was further categorized into non-dry eye group (NDEG) and dry eye group (DEG) groups based on examination. Conjunctival swabs and tear samples were collected for 16S rRNA gene sequencing (V3-V4 region) and label-free quantitative proteomics, respectively.
RESULTS: A total of 52 subjects were included. Microbiome analysis revealed significantly lower α-diversity (Chao1, Shannon) in the DEG than in the PG and/or NDEG (p < 0.05). β-diversity analysis showed significant structural differences between the DEG and both the PG and NDEG. Staphylococcus and Corynebacterium were enriched in the DEG, while commensals such as Clostridia and Bacteroidota showed higher relative abundances in the NDEG. DEG exhibited specific activation of stress pathways (NF-κB signaling, macroautophagy) and a bidirectional dysregulation of the coagulation-complement system, a pattern suggestive of a potential "thromboinflammation"-like state. Weighted gene co-expression network analysis delineated three axes: an overactive "Metabolism-Stress Axis", and impaired "Homeostatic Regulation Axis" and "Orderly Repair Axis" in the DEG.
CONCLUSIONS: In this cross-sectional analysis, the presence of DED after SMILE is associated with a distinct shift in the ocular surface microbiome towards a pro-inflammatory state and a concomitant breakdown of host proteomic homeostasis. The observed correlation between microbial dysbiosis and dysregulation of host pathways, particularly the coagulation-complement system, suggests a potential integrated mechanism for postoperative dry eye. These findings identify candidate biomarkers for risk prediction and new therapeutic targets.
Additional Links: PMID-42529330
PubMed:
Citation:
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@article {pmid42529330,
year = {2026},
author = {Zhang, L and Chen, P and Han, P and Fu, H and Sun, B},
title = {Integrated microbiomic and proteomic profiling reveals distinct ocular surface molecular and microbial landscapes in dry eye after SMILE surgery.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1858069},
pmid = {42529330},
issn = {2235-2988},
mesh = {Humans ; *Dry Eye Syndromes/microbiology/etiology/metabolism ; *Proteomics ; *Microbiota ; Female ; Tears/microbiology/chemistry ; Cross-Sectional Studies ; Male ; RNA, Ribosomal, 16S/genetics ; Prospective Studies ; Adult ; *Bacteria/classification/genetics/isolation & purification ; Conjunctiva/microbiology ; *Proteome/analysis ; Middle Aged ; Multiomics ; *Postoperative Complications/microbiology ; },
abstract = {OBJECTIVES: The aim of this study is to investigate the microbial and proteomic features of the ocular surface following small incision lenticule extraction (SMILE) surgery and to elucidate their association with the development of postoperative dry eye disease (DED).
METHODS: This study comprised a prospective cohort for baseline assessment and a cross-sectional postoperative assessment. We enrolled two sets of participants: a preoperative cohort (PG) consisting of patients scheduled for SMILE; and a postoperative cohort,consisting of patients who had undergone SMILE. The postoperative cohort was further categorized into non-dry eye group (NDEG) and dry eye group (DEG) groups based on examination. Conjunctival swabs and tear samples were collected for 16S rRNA gene sequencing (V3-V4 region) and label-free quantitative proteomics, respectively.
RESULTS: A total of 52 subjects were included. Microbiome analysis revealed significantly lower α-diversity (Chao1, Shannon) in the DEG than in the PG and/or NDEG (p < 0.05). β-diversity analysis showed significant structural differences between the DEG and both the PG and NDEG. Staphylococcus and Corynebacterium were enriched in the DEG, while commensals such as Clostridia and Bacteroidota showed higher relative abundances in the NDEG. DEG exhibited specific activation of stress pathways (NF-κB signaling, macroautophagy) and a bidirectional dysregulation of the coagulation-complement system, a pattern suggestive of a potential "thromboinflammation"-like state. Weighted gene co-expression network analysis delineated three axes: an overactive "Metabolism-Stress Axis", and impaired "Homeostatic Regulation Axis" and "Orderly Repair Axis" in the DEG.
CONCLUSIONS: In this cross-sectional analysis, the presence of DED after SMILE is associated with a distinct shift in the ocular surface microbiome towards a pro-inflammatory state and a concomitant breakdown of host proteomic homeostasis. The observed correlation between microbial dysbiosis and dysregulation of host pathways, particularly the coagulation-complement system, suggests a potential integrated mechanism for postoperative dry eye. These findings identify candidate biomarkers for risk prediction and new therapeutic targets.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Dry Eye Syndromes/microbiology/etiology/metabolism
*Proteomics
*Microbiota
Female
Tears/microbiology/chemistry
Cross-Sectional Studies
Male
RNA, Ribosomal, 16S/genetics
Prospective Studies
Adult
*Bacteria/classification/genetics/isolation & purification
Conjunctiva/microbiology
*Proteome/analysis
Middle Aged
Multiomics
*Postoperative Complications/microbiology
RevDate: 2026-07-30
CmpDate: 2026-07-30
Comprehensive Assessment of the Health and Nutritional Status of Active-Duty United States Army Soldiers: The Military Health and Nutrition Examination Study Protocol.
Current developments in nutrition, 10(8):109420.
BACKGROUND: The Military Health and Nutrition Examination Study (MHANES) is modeled after the National Health and Nutrition Examination Survey (NHANES). NHANES does not enroll active-duty Service Members, who are exposed to unique and adverse occupational challenges compared with civilians. Therefore, NHANES data are not generalizable to Service Members.
OBJECTIVES: The objective of MHANES is to fill this gap by assessing dietary intake, cardiometabolic health, body composition, biomarkers of nutritional status and health, mental well-being, injury prevalence, genetics, gut microbiome composition, and physical performance in a representative sample of Army Soldiers.
METHODS: MHANES recruited Soldiers (n = 648) from Army installations across the United States. Participants attended an in-person visit to complete a 24-h dietary recall and questionnaires regarding demographics, physical and mental health, physical activity and performance, and dietary supplement and medication use. Height, weight, blood pressure, resting heart rate variability, physical activity, sleep, resting metabolic rate, hemoglobin mass, and blood volume were measured. Body composition was assessed using bioelectrical impedance, 3-dimensional body imaging, dual-energy X-ray absorptiometry, and circumference measurements. Blood and urine samples were collected to measure biomarkers of nutritional status, health, and genetics. Stool samples were collected to assess microbial diversity and composition. A second 24-h dietary recall was administered 3 to 10 d after the in-person visit.
CONCLUSIONS: Data collected will be used to determine disease risk and prevalence and to investigate relationships between dietary intake, nutritional status, and markers of health and disease in Army Soldiers. Findings will guide evidence-based screening, education, intervention strategies, and policy decisions to improve Army health. Although the current study is focused exclusively on United States Army Soldiers, a long-term goal is to expand this research to other service branches and include additional sampling cycles similar to NHANES.This trial was registered at clinicaltrials.gov as NCT06380322.
Additional Links: PMID-42529388
PubMed:
Citation:
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@article {pmid42529388,
year = {2026},
author = {Berryman, CE and Bukhari, AS and Rood, JC and Hughes, DA and Lowe, AC and Niclou, AM and Beckner, ME and Weschenfelder, C and Riley, TM and Barney, DE and Dugan, C and Bukhari, SB and Bukhari, FH and Smith, MP and Turner, BS and Sanford, CM and Karl, JP and McClung, JP and Smith, TJ and Owens, BA and Beyl, RA and Heymsfield, SB and Greenway, FL and Hennigar, SR and Lieberman, HR},
title = {Comprehensive Assessment of the Health and Nutritional Status of Active-Duty United States Army Soldiers: The Military Health and Nutrition Examination Study Protocol.},
journal = {Current developments in nutrition},
volume = {10},
number = {8},
pages = {109420},
pmid = {42529388},
issn = {2475-2991},
abstract = {BACKGROUND: The Military Health and Nutrition Examination Study (MHANES) is modeled after the National Health and Nutrition Examination Survey (NHANES). NHANES does not enroll active-duty Service Members, who are exposed to unique and adverse occupational challenges compared with civilians. Therefore, NHANES data are not generalizable to Service Members.
OBJECTIVES: The objective of MHANES is to fill this gap by assessing dietary intake, cardiometabolic health, body composition, biomarkers of nutritional status and health, mental well-being, injury prevalence, genetics, gut microbiome composition, and physical performance in a representative sample of Army Soldiers.
METHODS: MHANES recruited Soldiers (n = 648) from Army installations across the United States. Participants attended an in-person visit to complete a 24-h dietary recall and questionnaires regarding demographics, physical and mental health, physical activity and performance, and dietary supplement and medication use. Height, weight, blood pressure, resting heart rate variability, physical activity, sleep, resting metabolic rate, hemoglobin mass, and blood volume were measured. Body composition was assessed using bioelectrical impedance, 3-dimensional body imaging, dual-energy X-ray absorptiometry, and circumference measurements. Blood and urine samples were collected to measure biomarkers of nutritional status, health, and genetics. Stool samples were collected to assess microbial diversity and composition. A second 24-h dietary recall was administered 3 to 10 d after the in-person visit.
CONCLUSIONS: Data collected will be used to determine disease risk and prevalence and to investigate relationships between dietary intake, nutritional status, and markers of health and disease in Army Soldiers. Findings will guide evidence-based screening, education, intervention strategies, and policy decisions to improve Army health. Although the current study is focused exclusively on United States Army Soldiers, a long-term goal is to expand this research to other service branches and include additional sampling cycles similar to NHANES.This trial was registered at clinicaltrials.gov as NCT06380322.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Spatial organization of cutaneous microbiomes reveals putative microbial contributions to host chemical defenses in the American toad.
Frontiers in microbiology, 17:1860796.
Chemical defenses are widely evolved throughout the tree of life. Animals can exploit mutualisms with toxin-producing symbionts as a mechanism of chemical defense. However, this has only begun to be explored in depth, and how these mutualisms may relate to how animals synthesize or acquire their toxins has been even less studied. True toads synthesize their own toxins and offer a novel system to study the interplay between the cutaneous skin microbiome and how it may contribute to toxin synthesis or biotransformation. In this study, we investigated whether the cutaneous microbiome of the American toad (Anaxyrus americanus) was spatially structured across body surfaces in relation to toxin storage and secretion and assessed whether microbial communities exhibit distinctive bacterial taxa involved in toxin-related biochemical pathways. To do this, we used 16S rRNA gene sequencing, diversity metrics, differential abundance comparisons, functional pathway predictions, and ecological interaction networks. Our results indicate that the dorsal and ventral cutaneous surfaces harbor distinct bacterial assemblages, with the dorsal surface being enriched for bacterial taxa associated with the predicted potential to degrade or transform structurally complex organic compounds. This study provides insights into how the toad skin microbiome may contribute to the chemical defenses of toads and could reveal novel aspects of host-microbiome interactions in amphibians.
Additional Links: PMID-42529424
PubMed:
Citation:
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@article {pmid42529424,
year = {2026},
author = {McCammon, SD and Chen See, JR and Wright, JR and Anderson, SLC and Russell, TJ and Lamendella, RM and Firneno, TJ},
title = {Spatial organization of cutaneous microbiomes reveals putative microbial contributions to host chemical defenses in the American toad.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1860796},
pmid = {42529424},
issn = {1664-302X},
abstract = {Chemical defenses are widely evolved throughout the tree of life. Animals can exploit mutualisms with toxin-producing symbionts as a mechanism of chemical defense. However, this has only begun to be explored in depth, and how these mutualisms may relate to how animals synthesize or acquire their toxins has been even less studied. True toads synthesize their own toxins and offer a novel system to study the interplay between the cutaneous skin microbiome and how it may contribute to toxin synthesis or biotransformation. In this study, we investigated whether the cutaneous microbiome of the American toad (Anaxyrus americanus) was spatially structured across body surfaces in relation to toxin storage and secretion and assessed whether microbial communities exhibit distinctive bacterial taxa involved in toxin-related biochemical pathways. To do this, we used 16S rRNA gene sequencing, diversity metrics, differential abundance comparisons, functional pathway predictions, and ecological interaction networks. Our results indicate that the dorsal and ventral cutaneous surfaces harbor distinct bacterial assemblages, with the dorsal surface being enriched for bacterial taxa associated with the predicted potential to degrade or transform structurally complex organic compounds. This study provides insights into how the toad skin microbiome may contribute to the chemical defenses of toads and could reveal novel aspects of host-microbiome interactions in amphibians.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Gut bacterial O-demethylation in microbiome-dependent drug response.
Gut microbes reports, 3(1):2709263.
The gut microbiota is recognized as an important contributor to drug metabolism and therapeutic variability. By directly transforming orally administered drugs, gut microbes can influence drug exposure, efficacy, and toxicity. Among these microbial reactions, O-demethylation of methoxy-containing drugs remains relatively underexplored, despite the prevalence of this structural motif in many therapeutic agents. Recent studies suggest that gut bacterial O-demethylation can alter parent-drug exposure and generate metabolites with distinct biological activities, with potential consequences for therapeutic efficacy and toxicity across clinical settings. In this mini-review, we discuss gut bacterial O-demethylation as a distinct mechanism in microbiome-dependent pharmacology, with emphasis on its chemical logic, microbial basis, pharmacokinetic and toxicologic consequences, and translational potential for microbiome-targeted interventions and biomarker development.
Additional Links: PMID-42529721
PubMed:
Citation:
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@article {pmid42529721,
year = {2026},
author = {Chiang, CK and Dibello, BS and Park, J and Rondinella, J and Wu, Q},
title = {Gut bacterial O-demethylation in microbiome-dependent drug response.},
journal = {Gut microbes reports},
volume = {3},
number = {1},
pages = {2709263},
pmid = {42529721},
issn = {2993-3935},
abstract = {The gut microbiota is recognized as an important contributor to drug metabolism and therapeutic variability. By directly transforming orally administered drugs, gut microbes can influence drug exposure, efficacy, and toxicity. Among these microbial reactions, O-demethylation of methoxy-containing drugs remains relatively underexplored, despite the prevalence of this structural motif in many therapeutic agents. Recent studies suggest that gut bacterial O-demethylation can alter parent-drug exposure and generate metabolites with distinct biological activities, with potential consequences for therapeutic efficacy and toxicity across clinical settings. In this mini-review, we discuss gut bacterial O-demethylation as a distinct mechanism in microbiome-dependent pharmacology, with emphasis on its chemical logic, microbial basis, pharmacokinetic and toxicologic consequences, and translational potential for microbiome-targeted interventions and biomarker development.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
The maternal microbiome-epigenome axis in gestational diabetes: pathogenesis, diagnosis, and emerging therapies.
Journal of developmental origins of health and disease, 17:e35 pii:S2040174426100695.
Gestational diabetes mellitus (GDM) is a common pregnancy complication with profound short- and long-term consequences for both mother and offspring. Beyond transient hyperglycemia, GDM represents a multifactorial metabolic condition shaped by the interplay of genetic predisposition, epigenetic regulation, and alterations in the maternal microbiome. Dysbiosis of the gut and reproductive tract microbiota contributes to inflammation, insulin resistance, and dyslipidemia during pregnancy, while microbial metabolites influence placental physiology and epigenetic remodeling of key metabolic and imprinted genes. These modifications, including changes in DNA methylation and non-coding RNA expression, link maternal hyperglycemia and microbial shifts to persistent alterations in gene expression that affect trophoblast activity, fetal growth trajectories, and long-term metabolic risk in offspring. Vertical transmission of maternal microbiota further imprints the neonatal microbiome, establishing an early-life foundation for reproductive and metabolic health. Although current diagnostic criteria and biomarkers remain inconsistent across populations, recent advances highlight the microbiome-epigenome axis as a promising source of predictive markers and therapeutic targets. Interventions such as probiotics, prebiotics, synbiotics, and dietary modulation show potential for improving maternal glycemic control, shaping placental function, and modulating fetal programming, although evidence for long-term efficacy is still emerging. Viewing GDM as both a metabolic stress test and a window of reproductive opportunity underscores the importance of early diagnosis and precision strategies. Integrating microbiome research and epigenetic insights into clinical practice offers new avenues to improve maternal outcomes, optimize fetal development, and reduce the intergenerational transmission of reproductive and metabolic disease risk.
Additional Links: PMID-42529871
Publisher:
PubMed:
Citation:
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@article {pmid42529871,
year = {2026},
author = {Rizvi, AA and Abbas, M and Ansari, AI and Verma, S and Sinha, A and Mahdi, F},
title = {The maternal microbiome-epigenome axis in gestational diabetes: pathogenesis, diagnosis, and emerging therapies.},
journal = {Journal of developmental origins of health and disease},
volume = {17},
number = {},
pages = {e35},
doi = {10.1017/S2040174426100695},
pmid = {42529871},
issn = {2040-1752},
mesh = {Humans ; Pregnancy ; Female ; *Diabetes, Gestational/therapy/diagnosis/microbiology/genetics ; *Microbiota/physiology ; *Epigenesis, Genetic ; *Epigenome ; Developmental Origins of Health and Disease ; Fetal Development ; *Gastrointestinal Microbiome/physiology ; Dysbiosis ; },
abstract = {Gestational diabetes mellitus (GDM) is a common pregnancy complication with profound short- and long-term consequences for both mother and offspring. Beyond transient hyperglycemia, GDM represents a multifactorial metabolic condition shaped by the interplay of genetic predisposition, epigenetic regulation, and alterations in the maternal microbiome. Dysbiosis of the gut and reproductive tract microbiota contributes to inflammation, insulin resistance, and dyslipidemia during pregnancy, while microbial metabolites influence placental physiology and epigenetic remodeling of key metabolic and imprinted genes. These modifications, including changes in DNA methylation and non-coding RNA expression, link maternal hyperglycemia and microbial shifts to persistent alterations in gene expression that affect trophoblast activity, fetal growth trajectories, and long-term metabolic risk in offspring. Vertical transmission of maternal microbiota further imprints the neonatal microbiome, establishing an early-life foundation for reproductive and metabolic health. Although current diagnostic criteria and biomarkers remain inconsistent across populations, recent advances highlight the microbiome-epigenome axis as a promising source of predictive markers and therapeutic targets. Interventions such as probiotics, prebiotics, synbiotics, and dietary modulation show potential for improving maternal glycemic control, shaping placental function, and modulating fetal programming, although evidence for long-term efficacy is still emerging. Viewing GDM as both a metabolic stress test and a window of reproductive opportunity underscores the importance of early diagnosis and precision strategies. Integrating microbiome research and epigenetic insights into clinical practice offers new avenues to improve maternal outcomes, optimize fetal development, and reduce the intergenerational transmission of reproductive and metabolic disease risk.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Pregnancy
Female
*Diabetes, Gestational/therapy/diagnosis/microbiology/genetics
*Microbiota/physiology
*Epigenesis, Genetic
*Epigenome
Developmental Origins of Health and Disease
Fetal Development
*Gastrointestinal Microbiome/physiology
Dysbiosis
RevDate: 2026-07-30
Functional roles and nutritional potential of human milk oligosaccharides in swine gut health.
The British journal of nutrition pii:S0007114526107776 [Epub ahead of print].
Human milk oligosaccharides (HMOs) are a prominent class of bioactive glycans recognized for their pivotal roles as prebiotics, anti-adhesive antimicrobials, and immunomodulators in neonatal development. While traditionally studied in the context of infant nutrition, scalable biotechnological production now allows for their evaluation in swine production to address the relatively lower structural complexity of the porcine milk glycome compared to humans. This review critically evaluates the structural diversity and biosynthesis of HMOs, detailing how specific fucosylated and sialylated structures modulate the porcine gut microbiome and reinforce intestinal barrier integrity. We synthesize current evidence regarding the metabolic fate of these glycans in the piglet and address the translational relevance of using swine as high-fidelity models for human gastrointestinal physiology. Furthermore, the review identifies critical knowledge gaps, specifically the lack of large-scale longitudinal studies and comprehensive cost-benefit analyses required to validate the economic feasibility of HMOs in commercial agriculture. By consolidating these mechanistic insights within the context of global efforts to reduce reliance on antibiotic growth promoters, this work underscores the potential of HMOs as precision nutritional tools to enhance resilience and productivity in sustainable animal production systems.
Additional Links: PMID-42529941
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PubMed:
Citation:
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@article {pmid42529941,
year = {2026},
author = {El Bouhi, R and Hu, Q and Zhong, J and Zhou, P and Zhang, Y and Liu, L and Yan, H},
title = {Functional roles and nutritional potential of human milk oligosaccharides in swine gut health.},
journal = {The British journal of nutrition},
volume = {},
number = {},
pages = {1-44},
doi = {10.1017/S0007114526107776},
pmid = {42529941},
issn = {1475-2662},
abstract = {Human milk oligosaccharides (HMOs) are a prominent class of bioactive glycans recognized for their pivotal roles as prebiotics, anti-adhesive antimicrobials, and immunomodulators in neonatal development. While traditionally studied in the context of infant nutrition, scalable biotechnological production now allows for their evaluation in swine production to address the relatively lower structural complexity of the porcine milk glycome compared to humans. This review critically evaluates the structural diversity and biosynthesis of HMOs, detailing how specific fucosylated and sialylated structures modulate the porcine gut microbiome and reinforce intestinal barrier integrity. We synthesize current evidence regarding the metabolic fate of these glycans in the piglet and address the translational relevance of using swine as high-fidelity models for human gastrointestinal physiology. Furthermore, the review identifies critical knowledge gaps, specifically the lack of large-scale longitudinal studies and comprehensive cost-benefit analyses required to validate the economic feasibility of HMOs in commercial agriculture. By consolidating these mechanistic insights within the context of global efforts to reduce reliance on antibiotic growth promoters, this work underscores the potential of HMOs as precision nutritional tools to enhance resilience and productivity in sustainable animal production systems.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Remembering stress, shaping resilience: plant adaptation across scales.
Essays in biochemistry, 70(1):1-3.
Plants face unprecedented environmental challenges arising from climate change, including increasing temperatures, altered nutrient availability, shifting seasonal patterns, and intensified biotic pressures. The present editorial introduces the special issue Plant Adaptation to Changing Environments, which brings together reviews examining plant adaptation from molecular to ecosystem levels. Collectively, these articles highlight how resilience emerges through the integration of signalling networks, metabolic regulation, developmental plasticity, ecological interactions, and environmental history. Together, they emphasise the need for interdisciplinary approaches to understand, predict, and enhance plant resilience in a rapidly changing world.
Additional Links: PMID-42530007
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PubMed:
Citation:
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@article {pmid42530007,
year = {2026},
author = {Luna, E},
title = {Remembering stress, shaping resilience: plant adaptation across scales.},
journal = {Essays in biochemistry},
volume = {70},
number = {1},
pages = {1-3},
doi = {10.1042/EBC20260069},
pmid = {42530007},
issn = {1744-1358},
support = {NE/V021346/1//UK Research and Innovation (UKRI)/ ; },
mesh = {*Stress, Physiological ; *Adaptation, Physiological ; *Plant Physiological Phenomena ; Climate Change ; *Plants/metabolism ; Ecosystem ; },
abstract = {Plants face unprecedented environmental challenges arising from climate change, including increasing temperatures, altered nutrient availability, shifting seasonal patterns, and intensified biotic pressures. The present editorial introduces the special issue Plant Adaptation to Changing Environments, which brings together reviews examining plant adaptation from molecular to ecosystem levels. Collectively, these articles highlight how resilience emerges through the integration of signalling networks, metabolic regulation, developmental plasticity, ecological interactions, and environmental history. Together, they emphasise the need for interdisciplinary approaches to understand, predict, and enhance plant resilience in a rapidly changing world.},
}
MeSH Terms:
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hide MeSH Terms
*Stress, Physiological
*Adaptation, Physiological
*Plant Physiological Phenomena
Climate Change
*Plants/metabolism
Ecosystem
RevDate: 2026-07-30
It takes a village: how plant-associated bacterial communities socialise to shape plant growth and health.
Essays in biochemistry pii:237875 [Epub ahead of print].
Plants outsource many functions to an associated microbiome, an 'outside gut' composed of socially interacting bacterial communities that support plant growth and health. These dynamic and diverse microbiomes span different plant microenvironments and form complex networks shaped by the environmental context and the plant's genetics. While some microbes cause disease, many others contribute to essential functions, influencing plant fitness, survival, and ultimately soil health. Although the host genetics and abiotic factors structure these communities, the functional diversity and ecological roles of plant-associated bacteria are ultimately shaped by microbe-microbe interactions. These interactions also play a critical role in the successful colonisation of plant tissues. Beneficial members of these communities enhance plant nutrient uptake, modulate phytohormones to shape root architecture, or prime plant systemic immunity to repel pathogens. Deciphering how plant-associated bacterial communities assemble and interact, both with their host and with one another, is essential for uncovering the mechanisms that underpin bacterial social behaviours within the plant holobiont, such as quorum sensing, metabolite exchange, and contact-dependent interactions. Here we review several recent publications that shed new light on the social lives of plant-associated bacteria, with a particular focus on their competition mechanisms and strategies for colonisation and establishment. In this context, we highlight how the rational design of plant bioinoculants based on microbial consortia represents a powerful strategy for promoting sustainable agriculture in a rapidly changing environment.
Additional Links: PMID-42530018
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PubMed:
Citation:
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@article {pmid42530018,
year = {2026},
author = {Escudero-Martínez, C and Tkacz, A and Albareda, M and Sánchez-Cañizares, C},
title = {It takes a village: how plant-associated bacterial communities socialise to shape plant growth and health.},
journal = {Essays in biochemistry},
volume = {},
number = {},
pages = {},
doi = {10.1042/EBC20250038},
pmid = {42530018},
issn = {1744-1358},
support = {PID2024-162207NA-I00//Ministerio de Ciencia, Innovación y Universidades (MCIU)/ ; OTR15203//Programa de Atraccion de Talento de la Fundacion Salamanca Ciudad de Cultura y Saberes y Ayuntamiento de Salamanca/ ; Alianzas 25CLEX-A-01//CLU-2025-2-02 "Unit of Excellence IRNASA-CSIC", from the regional Government of Junta Castilla y Leon/ ; UID/04326/2025, UID/PRR/04326/2025 and LA/P/0101/2020//MEC | Fundação para a Ciência e a Tecnologia (FCT)/ ; PID2021-1059124344OB-I00//Ministerio de Ciencia e Innovación (MCIN)/ ; },
abstract = {Plants outsource many functions to an associated microbiome, an 'outside gut' composed of socially interacting bacterial communities that support plant growth and health. These dynamic and diverse microbiomes span different plant microenvironments and form complex networks shaped by the environmental context and the plant's genetics. While some microbes cause disease, many others contribute to essential functions, influencing plant fitness, survival, and ultimately soil health. Although the host genetics and abiotic factors structure these communities, the functional diversity and ecological roles of plant-associated bacteria are ultimately shaped by microbe-microbe interactions. These interactions also play a critical role in the successful colonisation of plant tissues. Beneficial members of these communities enhance plant nutrient uptake, modulate phytohormones to shape root architecture, or prime plant systemic immunity to repel pathogens. Deciphering how plant-associated bacterial communities assemble and interact, both with their host and with one another, is essential for uncovering the mechanisms that underpin bacterial social behaviours within the plant holobiont, such as quorum sensing, metabolite exchange, and contact-dependent interactions. Here we review several recent publications that shed new light on the social lives of plant-associated bacteria, with a particular focus on their competition mechanisms and strategies for colonisation and establishment. In this context, we highlight how the rational design of plant bioinoculants based on microbial consortia represents a powerful strategy for promoting sustainable agriculture in a rapidly changing environment.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Dual Roles of Free Fatty Acids in Gout Pathogenesis: Inflammatory Drivers and Metabolic Mediators.
International journal of rheumatic diseases, 29(8):e70799.
Gout, a prototypical crystal-induced arthropathy, is characterized by a complex interaction between metabolic dysregulation and inflammatory activation. Although monosodium urate (MSU) crystal deposition remains the central pathognomonic feature, accumulating evidence suggests that free fatty acids (FFAs) play a significant role as co-modulators in the disease's pathogenesis. This review systematically examines the dual role of FFAs in gout pathophysiology: (1) their pro-inflammatory effects during gout flares through direct modulation of innate immune responses, and (2) their role as metabolic modulators contributing to disease comorbidities. We explore the molecular mechanisms by which saturated and n-6 polyunsaturated fatty acids (PUFAs) promote NLRP3 inflammasome activation, ultimately leading to cytokine storm formation and acute inflammatory responses. Paradoxically, short-chain fatty acids and n-3 polyunsaturated fatty acids exhibit anti-inflammatory properties and confer protection against gout flares via distinct immunomodulatory pathways. The review further examines FFA-mediated metabolic disturbances associated with gout, such as insulin resistance, renal fibrosis, and non-alcoholic fatty liver disease. Additionally, this review provides novel insights into targeted therapeutic strategies for the adjuvant treatment of gout, including lipid-targeted therapy, microbiome modulation, and dietary recommendations regarding polyunsaturated fatty acids.
Additional Links: PMID-42530131
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Citation:
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@article {pmid42530131,
year = {2026},
author = {Lin, N and Shao, C},
title = {Dual Roles of Free Fatty Acids in Gout Pathogenesis: Inflammatory Drivers and Metabolic Mediators.},
journal = {International journal of rheumatic diseases},
volume = {29},
number = {8},
pages = {e70799},
pmid = {42530131},
issn = {1756-185X},
mesh = {Humans ; *Gout/metabolism/immunology/drug therapy/physiopathology ; *Inflammation Mediators/metabolism/immunology ; *Fatty Acids, Nonesterified/metabolism/immunology ; Animals ; Inflammasomes/metabolism/immunology ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism/immunology ; Signal Transduction ; Immunity, Innate ; },
abstract = {Gout, a prototypical crystal-induced arthropathy, is characterized by a complex interaction between metabolic dysregulation and inflammatory activation. Although monosodium urate (MSU) crystal deposition remains the central pathognomonic feature, accumulating evidence suggests that free fatty acids (FFAs) play a significant role as co-modulators in the disease's pathogenesis. This review systematically examines the dual role of FFAs in gout pathophysiology: (1) their pro-inflammatory effects during gout flares through direct modulation of innate immune responses, and (2) their role as metabolic modulators contributing to disease comorbidities. We explore the molecular mechanisms by which saturated and n-6 polyunsaturated fatty acids (PUFAs) promote NLRP3 inflammasome activation, ultimately leading to cytokine storm formation and acute inflammatory responses. Paradoxically, short-chain fatty acids and n-3 polyunsaturated fatty acids exhibit anti-inflammatory properties and confer protection against gout flares via distinct immunomodulatory pathways. The review further examines FFA-mediated metabolic disturbances associated with gout, such as insulin resistance, renal fibrosis, and non-alcoholic fatty liver disease. Additionally, this review provides novel insights into targeted therapeutic strategies for the adjuvant treatment of gout, including lipid-targeted therapy, microbiome modulation, and dietary recommendations regarding polyunsaturated fatty acids.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gout/metabolism/immunology/drug therapy/physiopathology
*Inflammation Mediators/metabolism/immunology
*Fatty Acids, Nonesterified/metabolism/immunology
Animals
Inflammasomes/metabolism/immunology
NLR Family, Pyrin Domain-Containing 3 Protein/metabolism/immunology
Signal Transduction
Immunity, Innate
RevDate: 2026-07-30
Rome V criteria for pediatric disorders of gut - brain interaction: key updates and clinical implications.
Expert review of gastroenterology & hepatology [Epub ahead of print].
INTRODUCTION: The Rome criteria have provided the acclaimed global standard for diagnosing pediatric functional gastrointestinal disorders. With the release of Rome criteria V in 2026, the field has undergone a major transformation. The notable changes are the replacement of the term functional gastrointestinal disorders with disorders of gut - brain interaction (DGBIs) and shifting from age-based subdivisions to an anatomical and symptom cluster framework.
AREA COVERED: We reviewed pediatric Rome V documents and available evidence to cover both upper and lower gastrointestinal disorders of gut-brain interaction (DGBI). The new diagnostic entities such as reflux hypersensitivity, reflux negative esophageal pain disorder, supragastric belching, functional pediatric feeding disorders, centrally mediated abdominal pain syndrome, biliary pain syndrome, proctalgia fugax, functional diarrhea, functional bloating, and infant distress syndrome were discussed in detail.
EXPERT OPINION: Rome V provides clinicians with a more precise diagnostic framework. However, many new entities remain descriptive, highlighting the urgent need for epidemiological studies, mechanistic research, and biomarker discovery. Large multicenter trials, in DGBI should be conducted using physiological studies, microbiome analysis, and psychosocial profiles to generate robust evidence on pathophysiology, and management strategies. Ultimately, Rome V should be seen as a launchpad for discovery - transforming descriptive categories into mechanically defined, therapeutically actionable disorders that improve outcomes for children worldwide.
Additional Links: PMID-42530324
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PubMed:
Citation:
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@article {pmid42530324,
year = {2026},
author = {Rajindrajith, S and Devanarayana, N and Hathagoda, W and Benninga, M},
title = {Rome V criteria for pediatric disorders of gut - brain interaction: key updates and clinical implications.},
journal = {Expert review of gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1080/17474124.2026.2712930},
pmid = {42530324},
issn = {1747-4132},
abstract = {INTRODUCTION: The Rome criteria have provided the acclaimed global standard for diagnosing pediatric functional gastrointestinal disorders. With the release of Rome criteria V in 2026, the field has undergone a major transformation. The notable changes are the replacement of the term functional gastrointestinal disorders with disorders of gut - brain interaction (DGBIs) and shifting from age-based subdivisions to an anatomical and symptom cluster framework.
AREA COVERED: We reviewed pediatric Rome V documents and available evidence to cover both upper and lower gastrointestinal disorders of gut-brain interaction (DGBI). The new diagnostic entities such as reflux hypersensitivity, reflux negative esophageal pain disorder, supragastric belching, functional pediatric feeding disorders, centrally mediated abdominal pain syndrome, biliary pain syndrome, proctalgia fugax, functional diarrhea, functional bloating, and infant distress syndrome were discussed in detail.
EXPERT OPINION: Rome V provides clinicians with a more precise diagnostic framework. However, many new entities remain descriptive, highlighting the urgent need for epidemiological studies, mechanistic research, and biomarker discovery. Large multicenter trials, in DGBI should be conducted using physiological studies, microbiome analysis, and psychosocial profiles to generate robust evidence on pathophysiology, and management strategies. Ultimately, Rome V should be seen as a launchpad for discovery - transforming descriptive categories into mechanically defined, therapeutically actionable disorders that improve outcomes for children worldwide.},
}
RevDate: 2026-07-30
Microbial Diversity in Odontogenic Sinusitis: Next-Generation Sequencing Versus Culture.
American journal of rhinology & allergy [Epub ahead of print].
BackgroundOdontogenic sinusitis (ODS) is a common cause of unilateral infectious maxillary sinusitis but is frequently underdiagnosed due to nonspecific symptoms, subtle dental findings on imaging, and limitations of traditional bacterial cultures-particularly for anaerobic organisms. Next-generation DNA sequencing (NGS) may enhance detection of odontogenic bacteria.ObjectiveThis study compared bacterial detection between standard cultures versus NGS in patients with confirmed ODS.MethodsTwenty consecutive adults with confirmed ODS were enrolled. Maxillary sinus purulence was collected endoscopically and submitted for routine aerobic and anaerobic bacterial cultures and for NGS-based microbial profiling using 16S rRNA gene sequencing. Detected organisms were categorized by aerotolerance and ODS relationship, and likely nasal colonizers were excluded from analyses. Alpha diversity, beta diversity, and compositional differences between methods were analyzed statistically.ResultsNGS detected significantly more bacterial species per specimen than culture (mean 4.9 vs 2.7; P = .0015). Compared to cultures, NGS identified more anaerobic bacteria (4.2 vs 0.9; P = .00004) and more ODS-related species (4.4 vs 1.0; P = .0001), while detection of aerobic species was similar between methods. Cultures also often yielded nonspeciated results, whereas NGS consistently revealed polymicrobial communities dominated by oral anaerobes. Microbial composition differed significantly between detection methods.ConclusionIn confirmed ODS, NGS detected significantly more anaerobic and ODS-related species than culture from the same specimens. These findings suggest that culture alone may underestimate odontogenic contributions to purulent sinusitis. Future studies should explore he utility of NGS as an adjunctive tool to facilitate diagnosis and treatment in the setting of possible ODS.
Additional Links: PMID-42530539
Publisher:
PubMed:
Citation:
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@article {pmid42530539,
year = {2026},
author = {Abdurrob, A and Cho, DY and Eide, JG and Ray, A and Ancira, JS and Tipton, C and Hanna, Z and Craig, J},
title = {Microbial Diversity in Odontogenic Sinusitis: Next-Generation Sequencing Versus Culture.},
journal = {American journal of rhinology & allergy},
volume = {},
number = {},
pages = {19458924261474104},
doi = {10.1177/19458924261474104},
pmid = {42530539},
issn = {1945-8932},
abstract = {BackgroundOdontogenic sinusitis (ODS) is a common cause of unilateral infectious maxillary sinusitis but is frequently underdiagnosed due to nonspecific symptoms, subtle dental findings on imaging, and limitations of traditional bacterial cultures-particularly for anaerobic organisms. Next-generation DNA sequencing (NGS) may enhance detection of odontogenic bacteria.ObjectiveThis study compared bacterial detection between standard cultures versus NGS in patients with confirmed ODS.MethodsTwenty consecutive adults with confirmed ODS were enrolled. Maxillary sinus purulence was collected endoscopically and submitted for routine aerobic and anaerobic bacterial cultures and for NGS-based microbial profiling using 16S rRNA gene sequencing. Detected organisms were categorized by aerotolerance and ODS relationship, and likely nasal colonizers were excluded from analyses. Alpha diversity, beta diversity, and compositional differences between methods were analyzed statistically.ResultsNGS detected significantly more bacterial species per specimen than culture (mean 4.9 vs 2.7; P = .0015). Compared to cultures, NGS identified more anaerobic bacteria (4.2 vs 0.9; P = .00004) and more ODS-related species (4.4 vs 1.0; P = .0001), while detection of aerobic species was similar between methods. Cultures also often yielded nonspeciated results, whereas NGS consistently revealed polymicrobial communities dominated by oral anaerobes. Microbial composition differed significantly between detection methods.ConclusionIn confirmed ODS, NGS detected significantly more anaerobic and ODS-related species than culture from the same specimens. These findings suggest that culture alone may underestimate odontogenic contributions to purulent sinusitis. Future studies should explore he utility of NGS as an adjunctive tool to facilitate diagnosis and treatment in the setting of possible ODS.},
}
RevDate: 2026-07-30
Clinical applications of gut microbiome for non-invasive diagnosis of colorectal neoplasia.
Journal of gastroenterology [Epub ahead of print].
Colorectal cancer (CRC) is the third most common malignancy and the second leading cause of cancer-related death worldwide. While screening programs have reduced mortality, current stool-based tests such as the faecal immunochemical test (FIT) and tumour marker assays, remain limited in sensitivity for adenoma detection and rely on relatively later-stage biological signals in the carcinogenic process. False positives lead to unnecessary invasive procedures, whilst missed adenomas continue to progress, highlighting the need for alternative strategies. Accumulating evidence implicates the gut microbiome in CRC pathogenesis, which involves tumour-associated dysbiosis and microbial ecosystem shifts. Multinational metagenomic studies have consistently identified reproducible microbial signatures that can serve as biomarkers of disease and may predate the biological signals used in conventional screening. PCR-based microbial markers have emerged as practical tools for clinical application, enabling sensitive and specific detection of adenomas and CRC. A recent microbial panel incorporating Fusobacterium nucleatum, Hungatella hathewayi, Christensenella hongkongensis, and a novel bacterial gene marker m3 from Lachnoclostridium demonstrated improved sensitivity for adenomas whilst maintaining comparable accuracy for CRC. International guidelines have begun to recommend combining microbiome-based assays with FIT into integrated screening programs that target multiple biologic processes across the pathogenesis. Microbiome-based stool testing represents a promising non-invasive approach that improves detection of adenomas in early-stage disease, often missed by FIT alone and could enable more refined risk stratification. Further validation across diverse populations, assessment of cost-effectiveness, and integration into established screening infrastructures will be critical for broad clinical adoption.
Additional Links: PMID-42530606
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Citation:
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@article {pmid42530606,
year = {2026},
author = {Cui, C and Shi, H and Naito, Y and Otani, K and Chan, FKL},
title = {Clinical applications of gut microbiome for non-invasive diagnosis of colorectal neoplasia.},
journal = {Journal of gastroenterology},
volume = {},
number = {},
pages = {},
pmid = {42530606},
issn = {1435-5922},
abstract = {Colorectal cancer (CRC) is the third most common malignancy and the second leading cause of cancer-related death worldwide. While screening programs have reduced mortality, current stool-based tests such as the faecal immunochemical test (FIT) and tumour marker assays, remain limited in sensitivity for adenoma detection and rely on relatively later-stage biological signals in the carcinogenic process. False positives lead to unnecessary invasive procedures, whilst missed adenomas continue to progress, highlighting the need for alternative strategies. Accumulating evidence implicates the gut microbiome in CRC pathogenesis, which involves tumour-associated dysbiosis and microbial ecosystem shifts. Multinational metagenomic studies have consistently identified reproducible microbial signatures that can serve as biomarkers of disease and may predate the biological signals used in conventional screening. PCR-based microbial markers have emerged as practical tools for clinical application, enabling sensitive and specific detection of adenomas and CRC. A recent microbial panel incorporating Fusobacterium nucleatum, Hungatella hathewayi, Christensenella hongkongensis, and a novel bacterial gene marker m3 from Lachnoclostridium demonstrated improved sensitivity for adenomas whilst maintaining comparable accuracy for CRC. International guidelines have begun to recommend combining microbiome-based assays with FIT into integrated screening programs that target multiple biologic processes across the pathogenesis. Microbiome-based stool testing represents a promising non-invasive approach that improves detection of adenomas in early-stage disease, often missed by FIT alone and could enable more refined risk stratification. Further validation across diverse populations, assessment of cost-effectiveness, and integration into established screening infrastructures will be critical for broad clinical adoption.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Quorum-sensing, microbiome interactions, and emerging artificial intelligence-assisted anti-virulence strategies in Salmonella Typhi: a critical review of translational opportunities and challenges.
Archives of microbiology, 208(10):.
Typhoid fever, caused by Salmonella enterica subsp. enterica serovar Typhi (Salmonella Typhi), remains a significant global health challenge that is increasingly complicated by the emergence and spread of multidrug-resistant (MDR) and extensively drug-resistant strains. Growing limitations of antibiotic-centered treatment strategies have stimulated interest in anti-virulence approaches targeting bacterial regulatory networks rather than viability alone. Among these, quorum-sensing (QS), particularly the LuxS-mediated autoinducer-2 (AI-2) signaling system, has emerged as a potential regulator of virulence-associated phenotypes, biofilm formation, stress adaptation, microbial communication, and host-associated persistence. This review critically evaluated the current understanding of QS biology in S. Typhi while distinguishing experimentally validated findings from evidence extrapolated from non-typhoidal Salmonella and other enteric bacteria. We examine the ecological interplay between QS, gut microbiome dynamics, and host responses, highlighting how microbial communication networks influence pathogen adaptation and colonization resistance. Emerging anti-QS strategies, including microbiome-mediated quorum quenching, probiotics, postbiotics, phytochemicals, antimicrobial peptides, bacteriophage-associated approaches, signal-degrading enzymes, and nucleic acid-based interventions, are comparatively assessed with respect to their mechanisms, evidence strength, translational readiness, and limitations. The review further explores the role of artificial intelligence (AI), multi-omics integration, and systems-level analytical frameworks in target identification, microbial network reconstruction, biomarker discovery, and therapeutic prioritization. Despite promising advances, substantial barriers remain, including limited in vivo validation, insufficient mechanistic evidence in S. Typhi, lack of clinically validated QS-associated biomarkers, microbiome variability, ecological safety concerns, and challenges related to delivery, scalability, and regulatory approval. Collectively, current evidence supports QS-targeted interventions as promising but predominantly investigational strategies that may complement existing antimicrobial, vaccine-based, and public-health approaches for typhoid control.
Additional Links: PMID-42530739
PubMed:
Citation:
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@article {pmid42530739,
year = {2026},
author = {Bhuiyan, MNI and Saha, BK and Miah, MAS},
title = {Quorum-sensing, microbiome interactions, and emerging artificial intelligence-assisted anti-virulence strategies in Salmonella Typhi: a critical review of translational opportunities and challenges.},
journal = {Archives of microbiology},
volume = {208},
number = {10},
pages = {},
pmid = {42530739},
issn = {1432-072X},
mesh = {*Quorum Sensing ; *Salmonella typhi/pathogenicity/physiology/drug effects/genetics ; Virulence/drug effects ; Humans ; *Artificial Intelligence ; *Typhoid Fever/microbiology ; *Microbiota ; Animals ; Anti-Bacterial Agents/pharmacology ; Homoserine/analogs & derivatives ; Lactones ; },
abstract = {Typhoid fever, caused by Salmonella enterica subsp. enterica serovar Typhi (Salmonella Typhi), remains a significant global health challenge that is increasingly complicated by the emergence and spread of multidrug-resistant (MDR) and extensively drug-resistant strains. Growing limitations of antibiotic-centered treatment strategies have stimulated interest in anti-virulence approaches targeting bacterial regulatory networks rather than viability alone. Among these, quorum-sensing (QS), particularly the LuxS-mediated autoinducer-2 (AI-2) signaling system, has emerged as a potential regulator of virulence-associated phenotypes, biofilm formation, stress adaptation, microbial communication, and host-associated persistence. This review critically evaluated the current understanding of QS biology in S. Typhi while distinguishing experimentally validated findings from evidence extrapolated from non-typhoidal Salmonella and other enteric bacteria. We examine the ecological interplay between QS, gut microbiome dynamics, and host responses, highlighting how microbial communication networks influence pathogen adaptation and colonization resistance. Emerging anti-QS strategies, including microbiome-mediated quorum quenching, probiotics, postbiotics, phytochemicals, antimicrobial peptides, bacteriophage-associated approaches, signal-degrading enzymes, and nucleic acid-based interventions, are comparatively assessed with respect to their mechanisms, evidence strength, translational readiness, and limitations. The review further explores the role of artificial intelligence (AI), multi-omics integration, and systems-level analytical frameworks in target identification, microbial network reconstruction, biomarker discovery, and therapeutic prioritization. Despite promising advances, substantial barriers remain, including limited in vivo validation, insufficient mechanistic evidence in S. Typhi, lack of clinically validated QS-associated biomarkers, microbiome variability, ecological safety concerns, and challenges related to delivery, scalability, and regulatory approval. Collectively, current evidence supports QS-targeted interventions as promising but predominantly investigational strategies that may complement existing antimicrobial, vaccine-based, and public-health approaches for typhoid control.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Quorum Sensing
*Salmonella typhi/pathogenicity/physiology/drug effects/genetics
Virulence/drug effects
Humans
*Artificial Intelligence
*Typhoid Fever/microbiology
*Microbiota
Animals
Anti-Bacterial Agents/pharmacology
Homoserine/analogs & derivatives
Lactones
RevDate: 2026-07-30
CmpDate: 2026-07-30
Bacterial-based cancer therapy: mechanisms and therapeutic advances.
Molecular biomedicine, 7(1):.
Targeted cancer therapies increasingly require platforms that can penetrate poorly perfused tumor regions while minimizing systemic toxicity. Bacteria, owing to their intrinsic tumor tropism, genetic programmability, and immunostimulatory properties, have re-emerged as versatile anticancer agents, ranging from attenuated tumor-colonizing strains to highly engineered "living therapeutics." In this review, we synthesize the mechanistic foundations and therapeutic advances of bacterial-based cancer therapy through four major themes. First, we examine foundational mechanisms, including tumor-selective colonization, direct oncolysis and cytotoxicity, activation of innate and adaptive immunity, and remodeling of the tumor microenvironment. Second, we discuss engineering strategies that enable controllable delivery of therapeutic payloads, such as cytokines, antibodies and nanobodies, enzyme-prodrug systems, toxins, and nucleic-acid therapeutics, while also improving biosafety and biocontainment. Third, we evaluate combination strategies integrating bacteria with chemotherapy, radiotherapy, phototherapy, and immunotherapy, with emphasis on how bacteria complement conventional modalities by targeting hypoxic, necrotic, and immunologically refractory tumor niches. Fourth, we summarize translational progress, including representative early-phase clinical experiences, manufacturing challenges, and major safety constraints. We also highlight emerging microbiome-disease databases and computational resources that may support target selection, biomarker discovery, and therapy-response stratification. Current evidence supports bacteria as a promising precision modality, particularly for immunologically "cold" or hypoxic tumors; however, major challenges remain in the predictability of intratumoral distribution, host clearance, genetic stability, and long-term safety. Addressing these barriers through rigorous engineering, standardized manufacturing, and clinically meaningful endpoints will be essential for the next generation of bacterial therapeutics in oncology.
Additional Links: PMID-42530837
PubMed:
Citation:
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@article {pmid42530837,
year = {2026},
author = {Sharifi, AH and Phong, NHT and Marek, A and Kamal, MA and Al-Kodmany, S and Tran, DB and Yamada, T},
title = {Bacterial-based cancer therapy: mechanisms and therapeutic advances.},
journal = {Molecular biomedicine},
volume = {7},
number = {1},
pages = {},
pmid = {42530837},
issn = {2662-8651},
support = {R01CA272564/CA/NCI NIH HHS/United States ; R01CA289701/CA/NCI NIH HHS/United States ; R21CA280814/CA/NCI NIH HHS/United States ; },
mesh = {Humans ; *Neoplasms/therapy/immunology ; *Bacteria/genetics/metabolism ; Animals ; Tumor Microenvironment ; Immunotherapy/methods ; },
abstract = {Targeted cancer therapies increasingly require platforms that can penetrate poorly perfused tumor regions while minimizing systemic toxicity. Bacteria, owing to their intrinsic tumor tropism, genetic programmability, and immunostimulatory properties, have re-emerged as versatile anticancer agents, ranging from attenuated tumor-colonizing strains to highly engineered "living therapeutics." In this review, we synthesize the mechanistic foundations and therapeutic advances of bacterial-based cancer therapy through four major themes. First, we examine foundational mechanisms, including tumor-selective colonization, direct oncolysis and cytotoxicity, activation of innate and adaptive immunity, and remodeling of the tumor microenvironment. Second, we discuss engineering strategies that enable controllable delivery of therapeutic payloads, such as cytokines, antibodies and nanobodies, enzyme-prodrug systems, toxins, and nucleic-acid therapeutics, while also improving biosafety and biocontainment. Third, we evaluate combination strategies integrating bacteria with chemotherapy, radiotherapy, phototherapy, and immunotherapy, with emphasis on how bacteria complement conventional modalities by targeting hypoxic, necrotic, and immunologically refractory tumor niches. Fourth, we summarize translational progress, including representative early-phase clinical experiences, manufacturing challenges, and major safety constraints. We also highlight emerging microbiome-disease databases and computational resources that may support target selection, biomarker discovery, and therapy-response stratification. Current evidence supports bacteria as a promising precision modality, particularly for immunologically "cold" or hypoxic tumors; however, major challenges remain in the predictability of intratumoral distribution, host clearance, genetic stability, and long-term safety. Addressing these barriers through rigorous engineering, standardized manufacturing, and clinically meaningful endpoints will be essential for the next generation of bacterial therapeutics in oncology.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Neoplasms/therapy/immunology
*Bacteria/genetics/metabolism
Animals
Tumor Microenvironment
Immunotherapy/methods
RevDate: 2026-07-30
Phase-dependent Disruption of Microbiome-Metabolome Coordination Is Associated with Diet-Induced MASLD.
American journal of physiology. Gastrointestinal and liver physiology [Epub ahead of print].
Metabolic-dysfunction-associated steatotic liver disease (MASLD) is typically attributed to caloric overload, lipotoxicity, and static gut dysbiosis, but how chronic diet alters the temporal organization of gut-liver communication remains unclear. We combined a phase stratified multi omics framework, cecal 16S rRNA profiling, dual compartment (cecum and serum) metabolomics, and hepatic clock and lipogenic gene expression in C57BL/6J male mice fed a high fat, palmitate and cholesterol enriched (FPC) diet containing high sucrose for 22 weeks. FPC feeding was associated with severe MASLD and markedly attenuated homeostatic phase dependent differences in hepatic clock and lipogenic transcripts, consistent with a persistently lipogenic transcriptional state across the light-dark cycle. This temporal disruption coincided with reduced phase structured ecological organization in the cecal microbiome and the emergence of a constrained, dysbiotic community dominated by a few taxa. Dual-compartment metabolomics revealed that, despite retaining overall phase structure, local (cecal) and systemic (serum) metabolite pools showed misalignment: pro inflammatory and bile acid species showed exaggerated luminal variations but flattened, persistently elevated profiles in serum. High-stringency covariance network analysis identified diet-associated differences in microbiome-metabolome covariance patterns. These findings are consistent with a model in which diet-induced MASLD is associated with altered spatial and phase-dependent coordination across microbiome-host metabolic and transcriptional networks, suggesting disruption of integrated microbiome-host organization beyond static dysbiosis and lipotoxic stress.
Additional Links: PMID-42531150
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PubMed:
Citation:
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@article {pmid42531150,
year = {2026},
author = {De, AJ and Upadhyaya, B and Aich, P},
title = {Phase-dependent Disruption of Microbiome-Metabolome Coordination Is Associated with Diet-Induced MASLD.},
journal = {American journal of physiology. Gastrointestinal and liver physiology},
volume = {},
number = {},
pages = {},
doi = {10.1152/ajpgi.00163.2026},
pmid = {42531150},
issn = {1522-1547},
support = {NA//Department of Atomic Energy, Government of India (DAE)/ ; },
abstract = {Metabolic-dysfunction-associated steatotic liver disease (MASLD) is typically attributed to caloric overload, lipotoxicity, and static gut dysbiosis, but how chronic diet alters the temporal organization of gut-liver communication remains unclear. We combined a phase stratified multi omics framework, cecal 16S rRNA profiling, dual compartment (cecum and serum) metabolomics, and hepatic clock and lipogenic gene expression in C57BL/6J male mice fed a high fat, palmitate and cholesterol enriched (FPC) diet containing high sucrose for 22 weeks. FPC feeding was associated with severe MASLD and markedly attenuated homeostatic phase dependent differences in hepatic clock and lipogenic transcripts, consistent with a persistently lipogenic transcriptional state across the light-dark cycle. This temporal disruption coincided with reduced phase structured ecological organization in the cecal microbiome and the emergence of a constrained, dysbiotic community dominated by a few taxa. Dual-compartment metabolomics revealed that, despite retaining overall phase structure, local (cecal) and systemic (serum) metabolite pools showed misalignment: pro inflammatory and bile acid species showed exaggerated luminal variations but flattened, persistently elevated profiles in serum. High-stringency covariance network analysis identified diet-associated differences in microbiome-metabolome covariance patterns. These findings are consistent with a model in which diet-induced MASLD is associated with altered spatial and phase-dependent coordination across microbiome-host metabolic and transcriptional networks, suggesting disruption of integrated microbiome-host organization beyond static dysbiosis and lipotoxic stress.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Longitudinal omics study of transcriptional dynamics in Lactobacillus crispatus.
PloS one, 21(7):e0354930 pii:PONE-D-26-11487.
BACKGROUND: The vaginal microbiome is an important component of female reproductive health. Community State Type I (CST-I), which is dominated by Lactobacillus crispatus, is generally considered to be closely associated with a healthy vaginal microecological state. Although the taxonomic composition of CST-I communities remains relatively stable, the transcriptional dynamics of Lactobacillus crispatus across different phases of the menstrual cycle remain unclear.
METHODS: A healthy reproductive-age woman with a stable CST-I vaginal microbiome was enrolled in this longitudinal study. Vaginal secretion samples were collected at six non-menstrual time points throughout a menstrual cycle. Third-generation full-length 16S rRNA gene sequencing and metatranscriptomic sequencing were performed. Differential transcript expression analysis, KEGG pathway enrichment analysis, and Mfuzz time-series clustering were applied to systematically characterize the transcriptional dynamics of the vaginal microbiome across different phases.
RESULTS: Full-length 16S rRNA gene sequencing confirmed that Lactobacillus crispatus remained the dominant species at all six sampling time points, with no substantial changes in overall community composition. However, metatranscriptomic analysis revealed pronounced phase-specific transcriptional reprogramming. During the pre-ovulatory phase, pathways involved in DNA replication, biosynthesis, and central carbon metabolism were upregulated. On the first day after ovulation, pathways associated with carbohydrate utilization, quorum sensing, and redox homeostasis were selectively upregulated. During the mid-to-late luteal phase, pathways related to cell proliferation and growth were generally downregulated, whereas pathways involved in cofactor biosynthesis, the pentose phosphate pathway, and D-amino acid metabolism showed increased expression. Mfuzz clustering further revealed distinct phase-specific functional transitions in L. crispatus that were absent in non-L. crispatus lactobacilli.
CONCLUSION: The ecological dominance of Lactobacillus crispatus is maintained not solely through numerical abundance, but also through rhythmic and phase-specific transcriptional regulation. Dynamic functional remodeling and metabolic plasticity may represent important mechanisms underlying its long-term persistence and ecological dominance within healthy CST-I vaginal communities.
Additional Links: PMID-42531262
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PubMed:
Citation:
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@article {pmid42531262,
year = {2026},
author = {Ren, S and Jiang, H and Liu, X and Zhou, D and Liu, L and Wang, L and Lan, Y and Xiao, Y and Tang, L},
title = {Longitudinal omics study of transcriptional dynamics in Lactobacillus crispatus.},
journal = {PloS one},
volume = {21},
number = {7},
pages = {e0354930},
doi = {10.1371/journal.pone.0354930},
pmid = {42531262},
issn = {1932-6203},
mesh = {*Lactobacillus crispatus/genetics/metabolism ; Female ; RNA, Ribosomal, 16S/genetics ; *Vagina/microbiology ; Humans ; Longitudinal Studies ; Microbiota/genetics ; *Transcription, Genetic ; Gene Expression Profiling ; Transcriptome ; Gene Expression Regulation, Bacterial ; },
abstract = {BACKGROUND: The vaginal microbiome is an important component of female reproductive health. Community State Type I (CST-I), which is dominated by Lactobacillus crispatus, is generally considered to be closely associated with a healthy vaginal microecological state. Although the taxonomic composition of CST-I communities remains relatively stable, the transcriptional dynamics of Lactobacillus crispatus across different phases of the menstrual cycle remain unclear.
METHODS: A healthy reproductive-age woman with a stable CST-I vaginal microbiome was enrolled in this longitudinal study. Vaginal secretion samples were collected at six non-menstrual time points throughout a menstrual cycle. Third-generation full-length 16S rRNA gene sequencing and metatranscriptomic sequencing were performed. Differential transcript expression analysis, KEGG pathway enrichment analysis, and Mfuzz time-series clustering were applied to systematically characterize the transcriptional dynamics of the vaginal microbiome across different phases.
RESULTS: Full-length 16S rRNA gene sequencing confirmed that Lactobacillus crispatus remained the dominant species at all six sampling time points, with no substantial changes in overall community composition. However, metatranscriptomic analysis revealed pronounced phase-specific transcriptional reprogramming. During the pre-ovulatory phase, pathways involved in DNA replication, biosynthesis, and central carbon metabolism were upregulated. On the first day after ovulation, pathways associated with carbohydrate utilization, quorum sensing, and redox homeostasis were selectively upregulated. During the mid-to-late luteal phase, pathways related to cell proliferation and growth were generally downregulated, whereas pathways involved in cofactor biosynthesis, the pentose phosphate pathway, and D-amino acid metabolism showed increased expression. Mfuzz clustering further revealed distinct phase-specific functional transitions in L. crispatus that were absent in non-L. crispatus lactobacilli.
CONCLUSION: The ecological dominance of Lactobacillus crispatus is maintained not solely through numerical abundance, but also through rhythmic and phase-specific transcriptional regulation. Dynamic functional remodeling and metabolic plasticity may represent important mechanisms underlying its long-term persistence and ecological dominance within healthy CST-I vaginal communities.},
}
MeSH Terms:
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*Lactobacillus crispatus/genetics/metabolism
Female
RNA, Ribosomal, 16S/genetics
*Vagina/microbiology
Humans
Longitudinal Studies
Microbiota/genetics
*Transcription, Genetic
Gene Expression Profiling
Transcriptome
Gene Expression Regulation, Bacterial
RevDate: 2026-07-30
Viruses help shape microbiome response to polyphenol rewiring of methane-suppressed peat microcosms.
PLoS biology, 24(7):e3003925 pii:PBIOLOGY-D-26-00309 [Epub ahead of print].
Human activities are accelerating permafrost thaw and subsequent methane emissions from increased microbial activity, prompting microbiome engineering efforts as an emissions mitigation strategy. We recently demonstrated that catechin amendment could drastically reduce methane emissions (>80%) in peat microcosms by enriching catechin-degrading prokaryotes that outcompeted methanogens for hydrogen. However, viral contributions to such microbiome-level responses remain unexplored and we hypothesized that viral dynamics could help shape the microbiome response as nutrient amendments may alter cellular physiology in ways that could induce lytic viral activity. Here, we performed virus eco-genomics analyses of the previously-studied time-resolved multi-omics data collected from catechin-amended peat microcosms. We conservatively identified 900 putatively lytic viral operational taxonomic units (vOTUs), with 41% predicted to infect active host genomes including the most transcriptionally active vOTUs predicted to infect key catechin-degrading genera (Clostridium and undescribed Bacillota JAGFXR01). Notably, a single JAGFXR01-targeting vOTU dominating the viral response (>40% of community viral transcription; 20-156-fold more abundant than its host), which we interpreted as induction resulting in intense lytic activity that could release catechin degradation intermediates to other community members. Consistent with this, gene expression analysis revealed elevated catechin-intermediate degradation and hydrogenase signals in 34 additional polyphenol-degrading metagenome-assembled genomes. These findings support a model consistent with a viral shunt-like process that extends our previous prokaryote-centric model: viral lysis of fast-growing catechin degraders redistributes phenolic intermediates to diverse phenol-degrading taxa that sustain methane suppression via hydrogen consumption. Beyond carbon cycling importance in this system, elucidating unintended virus-mediated responses to nutrient and prebiotic interventions will enable more predictable and effective microbiome engineering strategies across soil, ocean, and human ecosystems.
Additional Links: PMID-42531353
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PubMed:
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@article {pmid42531353,
year = {2026},
author = {Riddell V, J and Shatadru, RN and Smith, GJ and McGivern, BB and Ellenbogen, JB and Jurgensen, SK and Fofana, A and Tfaily, MM and Wrighton, KC and Sullivan, MB},
title = {Viruses help shape microbiome response to polyphenol rewiring of methane-suppressed peat microcosms.},
journal = {PLoS biology},
volume = {24},
number = {7},
pages = {e3003925},
doi = {10.1371/journal.pbio.3003925},
pmid = {42531353},
issn = {1545-7885},
abstract = {Human activities are accelerating permafrost thaw and subsequent methane emissions from increased microbial activity, prompting microbiome engineering efforts as an emissions mitigation strategy. We recently demonstrated that catechin amendment could drastically reduce methane emissions (>80%) in peat microcosms by enriching catechin-degrading prokaryotes that outcompeted methanogens for hydrogen. However, viral contributions to such microbiome-level responses remain unexplored and we hypothesized that viral dynamics could help shape the microbiome response as nutrient amendments may alter cellular physiology in ways that could induce lytic viral activity. Here, we performed virus eco-genomics analyses of the previously-studied time-resolved multi-omics data collected from catechin-amended peat microcosms. We conservatively identified 900 putatively lytic viral operational taxonomic units (vOTUs), with 41% predicted to infect active host genomes including the most transcriptionally active vOTUs predicted to infect key catechin-degrading genera (Clostridium and undescribed Bacillota JAGFXR01). Notably, a single JAGFXR01-targeting vOTU dominating the viral response (>40% of community viral transcription; 20-156-fold more abundant than its host), which we interpreted as induction resulting in intense lytic activity that could release catechin degradation intermediates to other community members. Consistent with this, gene expression analysis revealed elevated catechin-intermediate degradation and hydrogenase signals in 34 additional polyphenol-degrading metagenome-assembled genomes. These findings support a model consistent with a viral shunt-like process that extends our previous prokaryote-centric model: viral lysis of fast-growing catechin degraders redistributes phenolic intermediates to diverse phenol-degrading taxa that sustain methane suppression via hydrogen consumption. Beyond carbon cycling importance in this system, elucidating unintended virus-mediated responses to nutrient and prebiotic interventions will enable more predictable and effective microbiome engineering strategies across soil, ocean, and human ecosystems.},
}
RevDate: 2026-07-30
Association Characteristics and Potential Mechanisms of Aging, Gut Microbiota, and Hearing Loss.
Integrative zoology [Epub ahead of print].
Age-related hearing loss (ARHL) is the leading sensory disability among the global elderly, yet its pathogenesis remains unclear. The "gut-ear axis" hypothesis offers a novel perspective. Using young, middle-aged, and aging C57BL/6 mice, we systematically investigated the interplay between aging, gut microbiota, and hearing loss through auditory function tests, cochlear histology, microbiome, and metabolome profiling. Results showed that aging induced a gradient hearing decline starting at high frequencies, progressing to severe pan-frequency loss in old age. Histology confirmed the degeneration of inner hair cells and synaptic connections, alongside hair cell loss in the basal cochlea. While gut microbiota α-diversity remained stable, β-diversity shifted significantly, marked by increased Bacteroidota and decreased Bacillota. Furthermore, 22 genera, 67 species, and 207 functional pathways were identified as being commonly associated with both aging and hearing loss. Metabolomic profiling further screened out 285 metabolites significantly associated with aging, 16 of which were also correlated with hearing loss. KEGG enrichment analysis suggested that chronic inflammation mediated by arachidonic acid metabolism, energy metabolic dysfunction regulated by the PPAR signaling pathway, and actin cytoskeleton homeostasis imbalance may represent a potential axis linking systemic metabolic dysregulation to cochlear‑specific damage. Moreover, these metabolites exhibited significant correlations with gut microbiota abundance. In conclusion, aging is associated with ARHL progression alongside gut microbiota remodeling and metabolic dysregulation. These findings supported a potential relationship between gut microbial-metabolic alterations and ARHL, which suggested that the gut microbiota may represent a candidate target for future mechanistic investigation.
Additional Links: PMID-42531517
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PubMed:
Citation:
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@article {pmid42531517,
year = {2026},
author = {Cheng, C and Wang, L and Li, R and Lai, W and Sun, C and Cui, J and Zhu, B and Zhang, J},
title = {Association Characteristics and Potential Mechanisms of Aging, Gut Microbiota, and Hearing Loss.},
journal = {Integrative zoology},
volume = {},
number = {},
pages = {},
doi = {10.1111/1749-4877.70156},
pmid = {42531517},
issn = {1749-4877},
support = {32370536//National Natural Science Foundation of China/ ; QNTS202304//CIB Youth Exploration Project/ ; //Tianchi Talents Fund of Xinjiang/ ; },
abstract = {Age-related hearing loss (ARHL) is the leading sensory disability among the global elderly, yet its pathogenesis remains unclear. The "gut-ear axis" hypothesis offers a novel perspective. Using young, middle-aged, and aging C57BL/6 mice, we systematically investigated the interplay between aging, gut microbiota, and hearing loss through auditory function tests, cochlear histology, microbiome, and metabolome profiling. Results showed that aging induced a gradient hearing decline starting at high frequencies, progressing to severe pan-frequency loss in old age. Histology confirmed the degeneration of inner hair cells and synaptic connections, alongside hair cell loss in the basal cochlea. While gut microbiota α-diversity remained stable, β-diversity shifted significantly, marked by increased Bacteroidota and decreased Bacillota. Furthermore, 22 genera, 67 species, and 207 functional pathways were identified as being commonly associated with both aging and hearing loss. Metabolomic profiling further screened out 285 metabolites significantly associated with aging, 16 of which were also correlated with hearing loss. KEGG enrichment analysis suggested that chronic inflammation mediated by arachidonic acid metabolism, energy metabolic dysfunction regulated by the PPAR signaling pathway, and actin cytoskeleton homeostasis imbalance may represent a potential axis linking systemic metabolic dysregulation to cochlear‑specific damage. Moreover, these metabolites exhibited significant correlations with gut microbiota abundance. In conclusion, aging is associated with ARHL progression alongside gut microbiota remodeling and metabolic dysregulation. These findings supported a potential relationship between gut microbial-metabolic alterations and ARHL, which suggested that the gut microbiota may represent a candidate target for future mechanistic investigation.},
}
RevDate: 2026-07-30
Polycystic ovary syndrome and insulin resistance: A focus on pathogenesis, risk factors, and therapeutic strategies.
Journal of reproductive immunology, 176:104943 pii:S0165-0378(26)00112-9 [Epub ahead of print].
Polycystic Ovary Syndrome (PCOS) is a common endocrine disorder characterized by significant reproductive and metabolic complications. Insulin resistance (IR) plays a central role in the pathophysiology of PCOS and contributes to several associated metabolic abnormalities. This review highlights the key mechanisms underlying PCOS, including IR, hyperandrogenism, cardiovascular disease, gut microbiota dysbiosis, and the increased risk of type 2 diabetes mellitus (T2DM), along with current and emerging therapeutic strategies for improving disease outcomes. Accumulating evidence suggests that genetic predisposition contributes to PCOS susceptibility. Polymorphisms in genes such as the androgen receptor (AR), cytochrome P450 17A1 (CYP17), and follicle-stimulating hormone receptor (FSHR) have been associated with altered steroidogenesis and ovarian dysfunction, thereby influencing disease severity. In addition to genetic factors, environmental influences, including exposure to endocrine-disrupting chemicals (EDCs) and air pollution, may exacerbate metabolic disturbances and increase the risk of developing PCOS. Conventional therapeutic approaches focus on improving insulin sensitivity and correcting hormonal imbalances. These include pharmacological treatments such as metformin, oral contraceptives, and lifestyle modifications involving diet and physical activity. Recently, novel therapeutic strategies have emerged, including glucagon-like peptide-1 receptor agonists (GLP-1RAs), microRNA-based therapies, and interleukin-22 (IL-22)-mediated interventions, which show potential in targeting IR and metabolic dysfunction in PCOS. Furthermore, modulation of gut microbiota through probiotics, prebiotics, and fecal microbiota transplantation (FMT) represents an emerging strategy for restoring metabolic homeostasis. Overall, a comprehensive and personalized therapeutic approach integrating pharmacological, lifestyle, and microbiome-targeted interventions may significantly improve PCOS management and reduce long-term metabolic and reproductive complications.
Additional Links: PMID-42531755
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PubMed:
Citation:
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@article {pmid42531755,
year = {2026},
author = {Singla, J and Yadav, S and Gayen, JR},
title = {Polycystic ovary syndrome and insulin resistance: A focus on pathogenesis, risk factors, and therapeutic strategies.},
journal = {Journal of reproductive immunology},
volume = {176},
number = {},
pages = {104943},
doi = {10.1016/j.jri.2026.104943},
pmid = {42531755},
issn = {1872-7603},
abstract = {Polycystic Ovary Syndrome (PCOS) is a common endocrine disorder characterized by significant reproductive and metabolic complications. Insulin resistance (IR) plays a central role in the pathophysiology of PCOS and contributes to several associated metabolic abnormalities. This review highlights the key mechanisms underlying PCOS, including IR, hyperandrogenism, cardiovascular disease, gut microbiota dysbiosis, and the increased risk of type 2 diabetes mellitus (T2DM), along with current and emerging therapeutic strategies for improving disease outcomes. Accumulating evidence suggests that genetic predisposition contributes to PCOS susceptibility. Polymorphisms in genes such as the androgen receptor (AR), cytochrome P450 17A1 (CYP17), and follicle-stimulating hormone receptor (FSHR) have been associated with altered steroidogenesis and ovarian dysfunction, thereby influencing disease severity. In addition to genetic factors, environmental influences, including exposure to endocrine-disrupting chemicals (EDCs) and air pollution, may exacerbate metabolic disturbances and increase the risk of developing PCOS. Conventional therapeutic approaches focus on improving insulin sensitivity and correcting hormonal imbalances. These include pharmacological treatments such as metformin, oral contraceptives, and lifestyle modifications involving diet and physical activity. Recently, novel therapeutic strategies have emerged, including glucagon-like peptide-1 receptor agonists (GLP-1RAs), microRNA-based therapies, and interleukin-22 (IL-22)-mediated interventions, which show potential in targeting IR and metabolic dysfunction in PCOS. Furthermore, modulation of gut microbiota through probiotics, prebiotics, and fecal microbiota transplantation (FMT) represents an emerging strategy for restoring metabolic homeostasis. Overall, a comprehensive and personalized therapeutic approach integrating pharmacological, lifestyle, and microbiome-targeted interventions may significantly improve PCOS management and reduce long-term metabolic and reproductive complications.},
}
RevDate: 2026-07-30
Poricoic acid a ameliorates ulcerative colitis via AMPK/PPARγ pathway-dependent cellular senescence inhibition and concomitant gut microbiota-metabolome modulation.
Phytomedicine : international journal of phytotherapy and phytopharmacology, 160:158628 pii:S0944-7113(26)00859-7 [Epub ahead of print].
BACKGROUND: Ulcerative colitis (UC) is an intractable inflammatory bowel disorder characterized by persistent intestinal inflammation and impaired gut barrier integrity. Its pathogenesis is multifactorial, involving gut microbiota dysbiosis, metabolic dysfunction, and cellular senescence. Current therapeutic regimens remain limited, underscoring an urgent need for innovative agents that target these interrelated pathological cascades.
PURPOSE: This study aimed to evaluate the pharmacological effects of poricoic acid A (PAA) on DSS-induced senescence in intestinal epithelial cells and in a murine model of ulcerative colitis (UC), as well as the underlying molecular mechanisms.
METHODS: We established a DSS-stimulated senescent intestinal epithelial cell model and a DSS-induced UC mouse model. Multi-omics and bioinformatics strategies, including network pharmacology, transcriptome profiling, gut metagenomics, and intestinal targeted metabolomics, were combined with molecular docking to predict candidate signaling axes. Subsequent pharmacological inhibition and siRNA-mediated silencing assays were performed to validate core pathways functionally.
RESULTS: PAA robustly suppressed DSS-induced senescence and inflammatory responses in intestinal epithelial cells. In vivo assays verified that PAA alleviated UC-related manifestations, including body weight loss, rectal hemorrhage, and colonic histological injury. Joint network pharmacology and transcriptomic screening identified the AMPK/PPARγ as the core pathway mediating PAA's bioactivity. Mechanistic experiments confirmed that PAA directly bound and activated PPAR, further functionally triggering downstream AMPK/SirT1/PGC1α signaling. Blockade of AMPK via pharmaceutical antagonists or siRNA largely abolished PAA's anti-senescence and anti-inflammatory capacities; PPARγ suppression, in turn, secondary deactivated the AMPK and its downstream functional effectors. In mouse models, AMPK inhibition drastically compromised PAA's protective effects against UC. Moreover, PAA treatment of UC is closely associated with remodeling of the gut microbiome-metabolome axis and restoration of intestinal homeostasis.
CONCLUSION: PAA exerts potent anti-senescence, anti-inflammatory, and colon-protective effects in UC via activating the AMPK/PPARγ signaling pathway. Such beneficial activity may be associated with the normalization of gut microbiota-metabolome homeostasis. This work identifies novel molecular targets and a promising lead compound for the intervention of ulcerative colitis.
Additional Links: PMID-42531833
Publisher:
PubMed:
Citation:
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@article {pmid42531833,
year = {2026},
author = {Wang, Y and Liu, Z and Hou, Q and Xu, Y and Chen, W and Chen, M and Liu, J and Tang, J and Wang, Y and Zhou, M and Wu, X and Wang, X},
title = {Poricoic acid a ameliorates ulcerative colitis via AMPK/PPARγ pathway-dependent cellular senescence inhibition and concomitant gut microbiota-metabolome modulation.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {160},
number = {},
pages = {158628},
doi = {10.1016/j.phymed.2026.158628},
pmid = {42531833},
issn = {1618-095X},
abstract = {BACKGROUND: Ulcerative colitis (UC) is an intractable inflammatory bowel disorder characterized by persistent intestinal inflammation and impaired gut barrier integrity. Its pathogenesis is multifactorial, involving gut microbiota dysbiosis, metabolic dysfunction, and cellular senescence. Current therapeutic regimens remain limited, underscoring an urgent need for innovative agents that target these interrelated pathological cascades.
PURPOSE: This study aimed to evaluate the pharmacological effects of poricoic acid A (PAA) on DSS-induced senescence in intestinal epithelial cells and in a murine model of ulcerative colitis (UC), as well as the underlying molecular mechanisms.
METHODS: We established a DSS-stimulated senescent intestinal epithelial cell model and a DSS-induced UC mouse model. Multi-omics and bioinformatics strategies, including network pharmacology, transcriptome profiling, gut metagenomics, and intestinal targeted metabolomics, were combined with molecular docking to predict candidate signaling axes. Subsequent pharmacological inhibition and siRNA-mediated silencing assays were performed to validate core pathways functionally.
RESULTS: PAA robustly suppressed DSS-induced senescence and inflammatory responses in intestinal epithelial cells. In vivo assays verified that PAA alleviated UC-related manifestations, including body weight loss, rectal hemorrhage, and colonic histological injury. Joint network pharmacology and transcriptomic screening identified the AMPK/PPARγ as the core pathway mediating PAA's bioactivity. Mechanistic experiments confirmed that PAA directly bound and activated PPAR, further functionally triggering downstream AMPK/SirT1/PGC1α signaling. Blockade of AMPK via pharmaceutical antagonists or siRNA largely abolished PAA's anti-senescence and anti-inflammatory capacities; PPARγ suppression, in turn, secondary deactivated the AMPK and its downstream functional effectors. In mouse models, AMPK inhibition drastically compromised PAA's protective effects against UC. Moreover, PAA treatment of UC is closely associated with remodeling of the gut microbiome-metabolome axis and restoration of intestinal homeostasis.
CONCLUSION: PAA exerts potent anti-senescence, anti-inflammatory, and colon-protective effects in UC via activating the AMPK/PPARγ signaling pathway. Such beneficial activity may be associated with the normalization of gut microbiota-metabolome homeostasis. This work identifies novel molecular targets and a promising lead compound for the intervention of ulcerative colitis.},
}
RevDate: 2026-07-30
Root exudates recruit microbial allies to override their own mobilization effects for cadmium immobilization in intercropped rice.
Journal of hazardous materials, 515:143010 pii:S0304-3894(26)01990-4 [Epub ahead of print].
Challenging the conventional view that root exudates inevitably exacerbate cadmium (Cd) bioavailability in paddy soils, this study revealed that intercropping high- and low-Cd-accumulating rice cultivars creates a distinct rhizosphere microenvironment wherein specifically enriched metabolites exert a dual function, ultimately driving net Cd immobilization. Through field experiments coupled with metabolomic and microbiome analyses, we showed that intercropping significantly reduces grain Cd concentrations by 18.45% in the high-Cd cultivar and 8.13% in the low-Cd cultivar, accompanied by substantial decreases in acid-extractable and oxidizable Cd fractions in rhizosphere soils. Mechanistic analyses revealed that intercropping reshaped the rhizosphere metabolome, enriching organic acids that exert dual functions: transient mobilization of oxidizable Cd and, more critically, recruitment of functional microorganisms, including sulfate-reducing bacteria (Candidatus Sulfobium mesophilum) and nitrifiers (Nitrospira), that promote Cd immobilization. Structural equation modeling confirmed that microbe-driven immobilization (path coefficient = -0.31) outweighs metabolite-mediated mobilization (path coefficient = 0.25), thereby reducing bioavailable Cd in the rice rhizosphere and suppressing its translocation to grains. A pot validation experiment substantiated this causal pathway: exogenous application of organic acids (citric acid) increased the abundance of the target sulfate-reducing bacterium by over 200% and induced a dose-dependent reduction in grain Cd content ranging from 32.29% to 56.25%. Collectively, our findings uncover a microbial-mediated Cd immobilization strategy triggered by intercropping-induced metabolite shifts, offering a streamlined framework that translates mechanistic insights into the efficient screening of green and cost-effective root metabolites as potential remediation agents for sustainable agriculture.
Additional Links: PMID-42531933
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PubMed:
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@article {pmid42531933,
year = {2026},
author = {Li, Y and Hou, J and Liu, M and Chen, H and Wang, X and Sun, P and Zhao, L and Yao, Y and Du, Z and An, Y},
title = {Root exudates recruit microbial allies to override their own mobilization effects for cadmium immobilization in intercropped rice.},
journal = {Journal of hazardous materials},
volume = {515},
number = {},
pages = {143010},
doi = {10.1016/j.jhazmat.2026.143010},
pmid = {42531933},
issn = {1873-3336},
abstract = {Challenging the conventional view that root exudates inevitably exacerbate cadmium (Cd) bioavailability in paddy soils, this study revealed that intercropping high- and low-Cd-accumulating rice cultivars creates a distinct rhizosphere microenvironment wherein specifically enriched metabolites exert a dual function, ultimately driving net Cd immobilization. Through field experiments coupled with metabolomic and microbiome analyses, we showed that intercropping significantly reduces grain Cd concentrations by 18.45% in the high-Cd cultivar and 8.13% in the low-Cd cultivar, accompanied by substantial decreases in acid-extractable and oxidizable Cd fractions in rhizosphere soils. Mechanistic analyses revealed that intercropping reshaped the rhizosphere metabolome, enriching organic acids that exert dual functions: transient mobilization of oxidizable Cd and, more critically, recruitment of functional microorganisms, including sulfate-reducing bacteria (Candidatus Sulfobium mesophilum) and nitrifiers (Nitrospira), that promote Cd immobilization. Structural equation modeling confirmed that microbe-driven immobilization (path coefficient = -0.31) outweighs metabolite-mediated mobilization (path coefficient = 0.25), thereby reducing bioavailable Cd in the rice rhizosphere and suppressing its translocation to grains. A pot validation experiment substantiated this causal pathway: exogenous application of organic acids (citric acid) increased the abundance of the target sulfate-reducing bacterium by over 200% and induced a dose-dependent reduction in grain Cd content ranging from 32.29% to 56.25%. Collectively, our findings uncover a microbial-mediated Cd immobilization strategy triggered by intercropping-induced metabolite shifts, offering a streamlined framework that translates mechanistic insights into the efficient screening of green and cost-effective root metabolites as potential remediation agents for sustainable agriculture.},
}
RevDate: 2026-07-30
Synergistic integration of forensic transcriptome and microbiome: A robust multi-marker strategy combined with machine learning for accurate body fluid identification.
Forensic science international. Genetics, 86:103583 pii:S1872-4973(26)00164-X [Epub ahead of print].
In recent years, the development of microbiome and transcriptome analyses has significantly improved the efficiency of forensic body fluid identification. However, challenging or limited biological samples in forensic practice demand highly efficient utilization of biological samples to minimize sample loss. In this study, we developed two independent assays based on a capillary electrophoresis (CE) approach: a 21-mRNA assay and a 10-bacteria system. The co-extracted RNA and DNA were amplified independently to identify five body fluids using mRNA profiling, and to specifically identify saliva (SA) and vaginal secretion (VS) using bacterial markers. Validation experiments of the two detection systems evaluated specificity, sensitivity, and performance on mixtures, aged, and degraded samples. In order to achieve accurate and intelligent identification of body fluid types, four machine learning (ML) models (Random Forest, K-Nearest Neighbors, Support Vector Machine, and Naive Bayes) were constructed and evaluated. Validation experiments demonstrated that both systems exhibited high overall specificity of body fluids, although certain markers showed cross-reactivity in some non-target samples. The two different assays yielded robust profiles from the samples as low as 1 ng of RNA or 0.1 ng of DNA, as well as most low-volume samples down to 1 μL or a 1/16 swab. Furthermore, the 21-mRNA and 10-bacteria systems effectively analyzed most aged or degraded samples, and mixtures. Despite suboptimal profiles from challenging samples (e.g. 1 μL semen, and aged or degraded semen samples), the SVM classifier overall outperformed other ML models, achieving a 100% classification accuracy for both single-source body fluids and pairwise mixtures on independent test sets. Overall, this study combining multi-omics biomarkers with ML models for precise body fluid identification provides strong technical support for practical forensic application.
Additional Links: PMID-42531989
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PubMed:
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@article {pmid42531989,
year = {2026},
author = {Wang, X and Liang, Q and Yuan, X and Cai, M and Zhu, B},
title = {Synergistic integration of forensic transcriptome and microbiome: A robust multi-marker strategy combined with machine learning for accurate body fluid identification.},
journal = {Forensic science international. Genetics},
volume = {86},
number = {},
pages = {103583},
doi = {10.1016/j.fsigen.2026.103583},
pmid = {42531989},
issn = {1878-0326},
abstract = {In recent years, the development of microbiome and transcriptome analyses has significantly improved the efficiency of forensic body fluid identification. However, challenging or limited biological samples in forensic practice demand highly efficient utilization of biological samples to minimize sample loss. In this study, we developed two independent assays based on a capillary electrophoresis (CE) approach: a 21-mRNA assay and a 10-bacteria system. The co-extracted RNA and DNA were amplified independently to identify five body fluids using mRNA profiling, and to specifically identify saliva (SA) and vaginal secretion (VS) using bacterial markers. Validation experiments of the two detection systems evaluated specificity, sensitivity, and performance on mixtures, aged, and degraded samples. In order to achieve accurate and intelligent identification of body fluid types, four machine learning (ML) models (Random Forest, K-Nearest Neighbors, Support Vector Machine, and Naive Bayes) were constructed and evaluated. Validation experiments demonstrated that both systems exhibited high overall specificity of body fluids, although certain markers showed cross-reactivity in some non-target samples. The two different assays yielded robust profiles from the samples as low as 1 ng of RNA or 0.1 ng of DNA, as well as most low-volume samples down to 1 μL or a 1/16 swab. Furthermore, the 21-mRNA and 10-bacteria systems effectively analyzed most aged or degraded samples, and mixtures. Despite suboptimal profiles from challenging samples (e.g. 1 μL semen, and aged or degraded semen samples), the SVM classifier overall outperformed other ML models, achieving a 100% classification accuracy for both single-source body fluids and pairwise mixtures on independent test sets. Overall, this study combining multi-omics biomarkers with ML models for precise body fluid identification provides strong technical support for practical forensic application.},
}
RevDate: 2026-07-30
The human gut microbiome: still more questions than answers.
Additional Links: PMID-42532085
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PubMed:
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@article {pmid42532085,
year = {2026},
author = {The Lancet Microbe, },
title = {The human gut microbiome: still more questions than answers.},
journal = {The Lancet. Microbe},
volume = {},
number = {},
pages = {101513},
doi = {10.1016/j.lanmic.2026.101513},
pmid = {42532085},
issn = {2666-5247},
}
RevDate: 2026-07-30
Bivalent gambogic acid-functionalized curcumin nanoparticles with insulin modulate the gut-liver-kidney network in type 2 diabetes.
Journal of controlled release : official journal of the Controlled Release Society pii:S0168-3659(26)00628-0 [Epub ahead of print].
The gut-liver-kidney (GLK) network is a critical driver of type 2 diabetes mellitus (T2DM) complications, where gut dysbiosis triggers cycle of hepatic metabolic stress and subsequent renal dysfunction through a complex, bidirectional signaling crosstalk. Despite its importance, therapeutic strategies capable of addressing this multi-organ crosstalk remain elusive. Here, we demonstrate that bivalent functionalized curcumin-encapsulating PLGA nanoparticles (nGA2-CUR) combined with subcutaneous insulin beneficially modulate the GLK network in obese T2DM mice. This combination therapy successfully stabilized systemic glucose homeostasis and restored essential endocrine signaling (insulin, GLP-1, and GIP) while significantly suppressing pro-inflammatory markers (MCP-1, haptoglobin). Microbiome profiling revealed a suppression of pathobionts alongside distinct sex-specific restorative responses, where males exhibited Muribaculaceae enrichment while females showed Bifidobacterium expansion. Integrated liver metabolomics associated these microbial shifts with unique organ-specific repair responses in each sex. Males showed elevated levels of purine salvage pathway intermediates alongside suppression of a specific pathobiont cluster (including Lautropia and Porphyromonas) correlated with oxidative stress, whereas females replenished aromatic amino acids, consistent with reduced predicted microbial proteolytic potential and lower markers of nephrotoxic uremic toxin production. Molecular analysis confirmed the downregulation of glucose-sensitive pathways (Chrebp/Srebp-1c). These systemic improvements were accompanied by an anti-inflammatory M2 macrophage profile shift, alongside suppression of renal fibrosis via the TGFβ/SMAD network and reduced injury markers (Cystatin C and Osteopontin). Our findings suggest that by reshaping the gut microbiome to alleviate upstream hepatic metabolic burden, this nanoparticle-enhanced therapy provides a sex-specific framework for attenuating irreversible diabetic renal injury.
Additional Links: PMID-42532147
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PubMed:
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@article {pmid42532147,
year = {2026},
author = {Allamreddy, SR and Ganugula, R and Gonzalez, A and Arora, M and Friend, R and Kumar, MNVR},
title = {Bivalent gambogic acid-functionalized curcumin nanoparticles with insulin modulate the gut-liver-kidney network in type 2 diabetes.},
journal = {Journal of controlled release : official journal of the Controlled Release Society},
volume = {},
number = {},
pages = {115224},
doi = {10.1016/j.jconrel.2026.115224},
pmid = {42532147},
issn = {1873-4995},
abstract = {The gut-liver-kidney (GLK) network is a critical driver of type 2 diabetes mellitus (T2DM) complications, where gut dysbiosis triggers cycle of hepatic metabolic stress and subsequent renal dysfunction through a complex, bidirectional signaling crosstalk. Despite its importance, therapeutic strategies capable of addressing this multi-organ crosstalk remain elusive. Here, we demonstrate that bivalent functionalized curcumin-encapsulating PLGA nanoparticles (nGA2-CUR) combined with subcutaneous insulin beneficially modulate the GLK network in obese T2DM mice. This combination therapy successfully stabilized systemic glucose homeostasis and restored essential endocrine signaling (insulin, GLP-1, and GIP) while significantly suppressing pro-inflammatory markers (MCP-1, haptoglobin). Microbiome profiling revealed a suppression of pathobionts alongside distinct sex-specific restorative responses, where males exhibited Muribaculaceae enrichment while females showed Bifidobacterium expansion. Integrated liver metabolomics associated these microbial shifts with unique organ-specific repair responses in each sex. Males showed elevated levels of purine salvage pathway intermediates alongside suppression of a specific pathobiont cluster (including Lautropia and Porphyromonas) correlated with oxidative stress, whereas females replenished aromatic amino acids, consistent with reduced predicted microbial proteolytic potential and lower markers of nephrotoxic uremic toxin production. Molecular analysis confirmed the downregulation of glucose-sensitive pathways (Chrebp/Srebp-1c). These systemic improvements were accompanied by an anti-inflammatory M2 macrophage profile shift, alongside suppression of renal fibrosis via the TGFβ/SMAD network and reduced injury markers (Cystatin C and Osteopontin). Our findings suggest that by reshaping the gut microbiome to alleviate upstream hepatic metabolic burden, this nanoparticle-enhanced therapy provides a sex-specific framework for attenuating irreversible diabetic renal injury.},
}
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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.
ESP Picks from Around the Web (updated 28 JUL 2024 )
Old Science
Weird Science
Treating Disease with Fecal Transplantation
Fossils of miniature humans (hobbits) discovered in Indonesia
Paleontology
Dinosaur tail, complete with feathers, found preserved in amber.
Astronomy
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.