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ESP: PubMed Auto Bibliography 05 Apr 2026 at 01:52 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: 2026-04-02
The 3M roles of the gut microbiome in pharmacotherapy for diabetes: mediator, modifier, and marker.
Trends in endocrinology and metabolism: TEM pii:S1043-2760(25)00284-X [Epub ahead of print].
The rising global prevalence of type 2 diabetes mellitus (T2DM) presents major challenges to healthcare systems; thus, more effective treatment strategies are urgently needed. In this context, the growing recognition of the gut microbiome's role in T2DM pharmacotherapy has shifted attention toward integrating microbiome-derived mechanisms to optimize drug response. This review proposes a structured '3M' framework that classifies the gut microbiome's roles in T2DM pharmacotherapy into three translational categories: mediator of drug action, modifier of therapeutic response, and marker for predicting efficacy or intolerance, based on recent clinical and mechanistic insights. Together, these insights support a translational framework that may guide the integration of microbiome-informed strategies into future T2DM pharmacotherapy.
Additional Links: PMID-41927455
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@article {pmid41927455,
year = {2026},
author = {Seo, JI and Koh, A and Lim, S and Yoo, HH},
title = {The 3M roles of the gut microbiome in pharmacotherapy for diabetes: mediator, modifier, and marker.},
journal = {Trends in endocrinology and metabolism: TEM},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tem.2025.12.006},
pmid = {41927455},
issn = {1879-3061},
abstract = {The rising global prevalence of type 2 diabetes mellitus (T2DM) presents major challenges to healthcare systems; thus, more effective treatment strategies are urgently needed. In this context, the growing recognition of the gut microbiome's role in T2DM pharmacotherapy has shifted attention toward integrating microbiome-derived mechanisms to optimize drug response. This review proposes a structured '3M' framework that classifies the gut microbiome's roles in T2DM pharmacotherapy into three translational categories: mediator of drug action, modifier of therapeutic response, and marker for predicting efficacy or intolerance, based on recent clinical and mechanistic insights. Together, these insights support a translational framework that may guide the integration of microbiome-informed strategies into future T2DM pharmacotherapy.},
}
RevDate: 2026-04-02
Multi-cohort analysis of metagenome for type 2 diabetes identified universal gut microbiota signatures across populations.
Nutrition & diabetes pii:10.1038/s41387-026-00418-w [Epub ahead of print].
BACKGROUND: Several studies have investigated the association between the gut microbiota and type 2 diabetes mellitus (T2D) in various populations. Nonetheless, noises specific to individual cohorts might distort the microbial dysbiosis characteristics and result in inconsistent findings across studies. Thus, we aimed to identify the universal features of perturbed gut microbiota across diverse populations.
METHODS: A total of 433 fecal shotgun metagenomic sequences were analyzed to profile and compare the gut microbiome shifts between patients with T2D and healthy controls from cohorts in Europe and Asia.
RESULTS: Based on cross-cohort integrative analysis, patients with T2D showed significantly higher microbial alpha diversity, and distinctive microbial structures compared to healthy individuals. By excluding bacteria exhibiting divergent directional changes, consistent characteristics with ten T2D-enriched bacteria, such as Clostridium bolteae and Clostridium citroniae and eight T2D-depleted bacteria, including Streptococcus thermophiles and Haemophilus parainfluenzae were revealed across populations. Particularly, these reliable bacterial markers, which were robust against demographic variation, distinguished patients with T2D from healthy controls with high accuracy (AUCs > 0.8) in both European and Asian cohorts. Correlation analysis demonstrated that T2D-enriched and T2D-depleted bacteria, respectively, formed their own mutualistic networks that were negatively linked to each other. Moreover, T2D-enriched bacteria were dramatically positively associated with fasting blood glucose and glycated hemoglobin. Functionally, 10 KEGG pathways with consistent directional changes across European, Asian, and combined cohorts were identified. Specifically, the Nucleotide excision repair pathway was markedly downregulated in patients with T2D, while the AGE-RAGE signaling pathway in diabetic complications was consistently enriched in patients with T2D across cohorts.
CONCLUSIONS: Our results elucidated reproducible profiles of gut commensal bacteria in patients with T2D, which are robust across populations. Identifying the universal gut microbiome signatures of T2D in heterogeneous cohorts offers valuable insights for understanding disease development and is crucial for prevention and diagnosis across diverse populations.
Additional Links: PMID-41927536
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PubMed:
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@article {pmid41927536,
year = {2026},
author = {Dong, Y and Wang, M and Zhou, X and Wang, P and Yan, K and Wang, S and Zhong, JC and Li, H and Zhao, L and Li, B and Li, J},
title = {Multi-cohort analysis of metagenome for type 2 diabetes identified universal gut microbiota signatures across populations.},
journal = {Nutrition & diabetes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41387-026-00418-w},
pmid = {41927536},
issn = {2044-4052},
abstract = {BACKGROUND: Several studies have investigated the association between the gut microbiota and type 2 diabetes mellitus (T2D) in various populations. Nonetheless, noises specific to individual cohorts might distort the microbial dysbiosis characteristics and result in inconsistent findings across studies. Thus, we aimed to identify the universal features of perturbed gut microbiota across diverse populations.
METHODS: A total of 433 fecal shotgun metagenomic sequences were analyzed to profile and compare the gut microbiome shifts between patients with T2D and healthy controls from cohorts in Europe and Asia.
RESULTS: Based on cross-cohort integrative analysis, patients with T2D showed significantly higher microbial alpha diversity, and distinctive microbial structures compared to healthy individuals. By excluding bacteria exhibiting divergent directional changes, consistent characteristics with ten T2D-enriched bacteria, such as Clostridium bolteae and Clostridium citroniae and eight T2D-depleted bacteria, including Streptococcus thermophiles and Haemophilus parainfluenzae were revealed across populations. Particularly, these reliable bacterial markers, which were robust against demographic variation, distinguished patients with T2D from healthy controls with high accuracy (AUCs > 0.8) in both European and Asian cohorts. Correlation analysis demonstrated that T2D-enriched and T2D-depleted bacteria, respectively, formed their own mutualistic networks that were negatively linked to each other. Moreover, T2D-enriched bacteria were dramatically positively associated with fasting blood glucose and glycated hemoglobin. Functionally, 10 KEGG pathways with consistent directional changes across European, Asian, and combined cohorts were identified. Specifically, the Nucleotide excision repair pathway was markedly downregulated in patients with T2D, while the AGE-RAGE signaling pathway in diabetic complications was consistently enriched in patients with T2D across cohorts.
CONCLUSIONS: Our results elucidated reproducible profiles of gut commensal bacteria in patients with T2D, which are robust across populations. Identifying the universal gut microbiome signatures of T2D in heterogeneous cohorts offers valuable insights for understanding disease development and is crucial for prevention and diagnosis across diverse populations.},
}
RevDate: 2026-04-02
The gut-heart dialogue: an epigenetic perspective on myocardial infarction.
NPJ biofilms and microbiomes pii:10.1038/s41522-026-00974-0 [Epub ahead of print].
Myocardial infarction (MI) remains a leading cause of global mortality, with adverse cardiac remodeling and heart failure presenting persistent metabolic and clinical challenges. While traditional pharmacotherapies have improved outcomes, there is an urgent need to elucidate how lifestyle and nutritional factors influence disease progression. Emerging evidence underscores the critical interplay between natural bioactive compounds (e.g., dietary fibers, polyphenols), the gut microbiota, and host metabolic regulation. This review systematically clarifies the "gut microbiota-epigenetic axis" as a pivotal mechanism linking nature-derived bioactives to cardiac repair. We delineate how the gut microbiota transforms specific bioactives into functional metabolites, such as short-chain fatty acids (SCFAs) from fibers and urolithin A from ellagitannins, which act as potent epigenetic modulators. These microbial metabolites remodel the epigenetic landscape of the host heart via histone modification and DNA methylation, thereby regulating gene networks governing inflammation, energy metabolism, and fibrosis. Synthesizing evidence from in vivo animal studies and clinical observations, we explore therapeutic strategies centered on natural bioactives, including high-fiber dietary interventions and polyphenol supplementation, alongside probiotics and postbiotics. By integrating the metabolic potential of the gut microbiome with epigenetic regulation, this review offers novel insights into how natural bioactive compounds can be leveraged for precision prevention and therapeutic strategies in myocardial infarction.
Additional Links: PMID-41927585
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@article {pmid41927585,
year = {2026},
author = {Song, J and Tang, S and Guo, Y and Hong, C and Song, T},
title = {The gut-heart dialogue: an epigenetic perspective on myocardial infarction.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-00974-0},
pmid = {41927585},
issn = {2055-5008},
support = {No. 20250602055RC//Jilin Province Science and Technology Department/ ; },
abstract = {Myocardial infarction (MI) remains a leading cause of global mortality, with adverse cardiac remodeling and heart failure presenting persistent metabolic and clinical challenges. While traditional pharmacotherapies have improved outcomes, there is an urgent need to elucidate how lifestyle and nutritional factors influence disease progression. Emerging evidence underscores the critical interplay between natural bioactive compounds (e.g., dietary fibers, polyphenols), the gut microbiota, and host metabolic regulation. This review systematically clarifies the "gut microbiota-epigenetic axis" as a pivotal mechanism linking nature-derived bioactives to cardiac repair. We delineate how the gut microbiota transforms specific bioactives into functional metabolites, such as short-chain fatty acids (SCFAs) from fibers and urolithin A from ellagitannins, which act as potent epigenetic modulators. These microbial metabolites remodel the epigenetic landscape of the host heart via histone modification and DNA methylation, thereby regulating gene networks governing inflammation, energy metabolism, and fibrosis. Synthesizing evidence from in vivo animal studies and clinical observations, we explore therapeutic strategies centered on natural bioactives, including high-fiber dietary interventions and polyphenol supplementation, alongside probiotics and postbiotics. By integrating the metabolic potential of the gut microbiome with epigenetic regulation, this review offers novel insights into how natural bioactive compounds can be leveraged for precision prevention and therapeutic strategies in myocardial infarction.},
}
RevDate: 2026-04-02
The Extreme Environment Microbiome Catalog (EEMC): a global resource for microbial diversity and antimicrobial discovery.
Nature communications pii:10.1038/s41467-026-71145-0 [Epub ahead of print].
Microorganisms in extreme environments represent a promising source of novel metabolites, yet their global diversity and biosynthetic potential remain underexplored. Here, we reconstruct 78,213 bacterial and archaeal genomes from 2293 publicly available metagenomes and 3214 microbial isolates to establish a unified database, the Extreme Environment Microbiome Catalog (EEMC). The EEMC expands known global phylogenetic diversity, encompassing 32,715 representative species and nearly 4 billion non-redundant genes, 63.00% and 19.21% of which are previously unannotated, respectively. It also comprises 163,693 biosynthetic gene clusters, grouped into 64,733 gene cluster families, 58.68% of which are classified as novel, underscoring the functional diversity of microbial communities across various extreme habitats. We further develop protein large language models to predict genome-encoded candidate antimicrobial peptides (cAMPs) from the EEMC, identifying 3032 non-toxic candidates. Of 100 synthesized peptides, 84% demonstrate antibacterial activity, and all 50 tested cAMPs exhibit low cytotoxicity. Notably, six of the most potent cAMPs show significant efficacy against multidrug-resistant, Gram-negative pathogens in vitro, indicating their biomedical potential. Together, our study establishes the EEMC as a foundational resource for uncovering novel microbial lineages and biosynthetic capabilities, highlighting its substantial potential for drug discovery and laying the foundation for future advances in biotechnology and biomedicine.
Additional Links: PMID-41927589
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@article {pmid41927589,
year = {2026},
author = {Jiang, P and Liang, Z and Kovacevic, V and Shi, J and Milicevic, N and Wang, F and Liu, L and Liu, Y and Jiang, Y and Han, M and Lin, X and Petronić, Č and Stanojevic, N and Wang, L and Wang, S and Cheng, H and Li, J and Chen, R and Zhang, Y and Li, Y and Li, J and Fang, X and Yue, Z and Xue, C and Yin, P and Chen, H},
title = {The Extreme Environment Microbiome Catalog (EEMC): a global resource for microbial diversity and antimicrobial discovery.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-71145-0},
pmid = {41927589},
issn = {2041-1723},
abstract = {Microorganisms in extreme environments represent a promising source of novel metabolites, yet their global diversity and biosynthetic potential remain underexplored. Here, we reconstruct 78,213 bacterial and archaeal genomes from 2293 publicly available metagenomes and 3214 microbial isolates to establish a unified database, the Extreme Environment Microbiome Catalog (EEMC). The EEMC expands known global phylogenetic diversity, encompassing 32,715 representative species and nearly 4 billion non-redundant genes, 63.00% and 19.21% of which are previously unannotated, respectively. It also comprises 163,693 biosynthetic gene clusters, grouped into 64,733 gene cluster families, 58.68% of which are classified as novel, underscoring the functional diversity of microbial communities across various extreme habitats. We further develop protein large language models to predict genome-encoded candidate antimicrobial peptides (cAMPs) from the EEMC, identifying 3032 non-toxic candidates. Of 100 synthesized peptides, 84% demonstrate antibacterial activity, and all 50 tested cAMPs exhibit low cytotoxicity. Notably, six of the most potent cAMPs show significant efficacy against multidrug-resistant, Gram-negative pathogens in vitro, indicating their biomedical potential. Together, our study establishes the EEMC as a foundational resource for uncovering novel microbial lineages and biosynthetic capabilities, highlighting its substantial potential for drug discovery and laying the foundation for future advances in biotechnology and biomedicine.},
}
RevDate: 2026-04-02
Oxycodone self-administration and genetic background exert community-specific effects in the gut microbiome.
Scientific reports pii:10.1038/s41598-026-41666-1 [Epub ahead of print].
Additional Links: PMID-41927609
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PubMed:
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@article {pmid41927609,
year = {2026},
author = {Duffy, EP and Sterrett, JD and Hale, LH and Ward, JO and Saba, LM and Frank, DN and Bachtell, RK and Ehringer, MA},
title = {Oxycodone self-administration and genetic background exert community-specific effects in the gut microbiome.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-41666-1},
pmid = {41927609},
issn = {2045-2322},
}
RevDate: 2026-04-02
Distinct difference of pancreatic tissue-specific microbiome in autoimmune pancreatitis and pancreatic ductal adenocarcinoma.
Scientific reports pii:10.1038/s41598-026-44821-w [Epub ahead of print].
Autoimmune pancreatitis (AIP) is a form of chronic pancreatitis that may be difficult to distinguish from pancreatic ductal adenocarcinoma (PDAC). Emerging evidence suggests the substantial involvement of gut microbiome dysbiosis in various disorders, including pancreatic diseases. This study investigates the differences in pancreatic tissue-specific microbiomes between AIP and PDAC. Pancreatic tissues were obtained from patients with type 1 AIP (n = 17) or PDAC (n = 24) via ultrasound-guided tissue acquisition and subjected to 16S rRNA sequencing. The sequences were used to determine the bacterial alpha diversity and characterize the microbiome structures related to different sample groups. The pancreatic microbiome in PDAC exhibited increased bacterial alpha diversity compared to that in AIP. The abundances of 16 bacteria were significantly different between the AIP and PDAC groups, and most of them (15/16) were increased in PDAC relative to that in AIP. The bacterial index calculated using these bacteria had a favorable discriminative ability for these different groups, with an area under the curve value of 0.91. Functional analysis demonstrated that the pentose phosphate pathway, gondoate biosynthesis, and several pathways related to adenosine biosynthesis were positively associated with the bacterial index. The findings from this preliminary study indicate that pancreatic microbiome, as a new diagnostic alternative, may potentially help with the differential diagnosis of AIP and PDAC.
Additional Links: PMID-41927721
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PubMed:
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@article {pmid41927721,
year = {2026},
author = {Nakamaru, K and Ito, T and Shimogama, T and Shijimaya, T and Tahara, T and Yamazaki, J and Orino, A and Masuda, M and Nakayama, S and Ikeura, T and Naganuma, M},
title = {Distinct difference of pancreatic tissue-specific microbiome in autoimmune pancreatitis and pancreatic ductal adenocarcinoma.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-44821-w},
pmid = {41927721},
issn = {2045-2322},
support = {22K16032//JSPS KAKENHI Grant-in-Aid for Young Scientists/ ; },
abstract = {Autoimmune pancreatitis (AIP) is a form of chronic pancreatitis that may be difficult to distinguish from pancreatic ductal adenocarcinoma (PDAC). Emerging evidence suggests the substantial involvement of gut microbiome dysbiosis in various disorders, including pancreatic diseases. This study investigates the differences in pancreatic tissue-specific microbiomes between AIP and PDAC. Pancreatic tissues were obtained from patients with type 1 AIP (n = 17) or PDAC (n = 24) via ultrasound-guided tissue acquisition and subjected to 16S rRNA sequencing. The sequences were used to determine the bacterial alpha diversity and characterize the microbiome structures related to different sample groups. The pancreatic microbiome in PDAC exhibited increased bacterial alpha diversity compared to that in AIP. The abundances of 16 bacteria were significantly different between the AIP and PDAC groups, and most of them (15/16) were increased in PDAC relative to that in AIP. The bacterial index calculated using these bacteria had a favorable discriminative ability for these different groups, with an area under the curve value of 0.91. Functional analysis demonstrated that the pentose phosphate pathway, gondoate biosynthesis, and several pathways related to adenosine biosynthesis were positively associated with the bacterial index. The findings from this preliminary study indicate that pancreatic microbiome, as a new diagnostic alternative, may potentially help with the differential diagnosis of AIP and PDAC.},
}
RevDate: 2026-04-02
Dietary plant extracts reduce methane emission and modulate rumen microbial functionality in Merino lambs.
Scientific reports pii:10.1038/s41598-026-46933-9 [Epub ahead of print].
The formation of enteric methane from ruminants represents a significant loss of dietary energy that adversely affects growth and production while also contributing to the environmental footprint of livestock production through greenhouse gas accumulation. Phytogenic feed additives rich in bioactive compounds have been proposed as sustainable alternatives to synthetic additives for improving nutrient utilisation and reducing methane. This study evaluated the effects of Moringa oleifera, Jatropha curcas, and Aloe vera extracts on growth performance, nutrient digestibility, methane production, rumen fermentation in South African Mutton Merino lambs using an in vivo feeding trial while the microbial diversity and functionality was evaluated using shotgun metagenomic sequencing. Supplementation with Moringa and Jatropha improved dry matter and crude protein digestibility (P < 0.05). Methane emission decreased in all plant extract groups, with reductions of 17% (Jatropha), 9% (Moringa), and 12% (Aloe) relative to control (P < 0.05). Ammonia nitrogen concentrations were lower in supplemented groups, particularly Moringa and Aloe (P < 0.01), while volatile fatty acids and growth performance were unaffected. Metagenomic profiling revealed Bacteroidetes as the dominant phylum and showed enrichment of genes which may be associated with protein biosynthesis and carbohydrate metabolism in Moringa and Jatropha lambs, aligning with improved digestibility and reduced methane emissions. Dietary inclusion of M. oleifera, J. curcas, and A. vera extracts reduced methane emissions and improved dry matter and crude protein digestibility without compromising growth. These results suggest that these phytogenic extracts can serve as sustainable feed additives to improve efficiency and mitigate environmental impacts in ruminant production systems.
Additional Links: PMID-41927746
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PubMed:
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@article {pmid41927746,
year = {2026},
author = {Akanmu, AM and Hassen, A and van Marle-Köster, E and Adejoro, FA},
title = {Dietary plant extracts reduce methane emission and modulate rumen microbial functionality in Merino lambs.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-46933-9},
pmid = {41927746},
issn = {2045-2322},
support = {SRUG2204254606//National Research Foundation/ ; },
abstract = {The formation of enteric methane from ruminants represents a significant loss of dietary energy that adversely affects growth and production while also contributing to the environmental footprint of livestock production through greenhouse gas accumulation. Phytogenic feed additives rich in bioactive compounds have been proposed as sustainable alternatives to synthetic additives for improving nutrient utilisation and reducing methane. This study evaluated the effects of Moringa oleifera, Jatropha curcas, and Aloe vera extracts on growth performance, nutrient digestibility, methane production, rumen fermentation in South African Mutton Merino lambs using an in vivo feeding trial while the microbial diversity and functionality was evaluated using shotgun metagenomic sequencing. Supplementation with Moringa and Jatropha improved dry matter and crude protein digestibility (P < 0.05). Methane emission decreased in all plant extract groups, with reductions of 17% (Jatropha), 9% (Moringa), and 12% (Aloe) relative to control (P < 0.05). Ammonia nitrogen concentrations were lower in supplemented groups, particularly Moringa and Aloe (P < 0.01), while volatile fatty acids and growth performance were unaffected. Metagenomic profiling revealed Bacteroidetes as the dominant phylum and showed enrichment of genes which may be associated with protein biosynthesis and carbohydrate metabolism in Moringa and Jatropha lambs, aligning with improved digestibility and reduced methane emissions. Dietary inclusion of M. oleifera, J. curcas, and A. vera extracts reduced methane emissions and improved dry matter and crude protein digestibility without compromising growth. These results suggest that these phytogenic extracts can serve as sustainable feed additives to improve efficiency and mitigate environmental impacts in ruminant production systems.},
}
RevDate: 2026-04-02
Retraction Note: Predictable regulation of gut microbiome in immunotherapeutic efficacy of gastric cancer.
Genes and immunity pii:10.1038/s41435-026-00397-z [Epub ahead of print].
Additional Links: PMID-41927935
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PubMed:
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@article {pmid41927935,
year = {2026},
author = {Gao, W and Wang, X and Shi, Y and Wu, G and Zhou, M and Lin, X},
title = {Retraction Note: Predictable regulation of gut microbiome in immunotherapeutic efficacy of gastric cancer.},
journal = {Genes and immunity},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41435-026-00397-z},
pmid = {41927935},
issn = {1476-5470},
}
RevDate: 2026-04-03
Associations of the gut microbiome and cardiometabolic risk in adolescence: the HOME study.
BMC medical genomics pii:10.1186/s12920-026-02359-w [Epub ahead of print].
Additional Links: PMID-41928235
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PubMed:
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@article {pmid41928235,
year = {2026},
author = {Arzu, JL and Fleury, ES and Cecil, KM and Chen, A and Lanphear, BP and Yolton, K and Buckley, JP and Braun, JM and Laue, HE},
title = {Associations of the gut microbiome and cardiometabolic risk in adolescence: the HOME study.},
journal = {BMC medical genomics},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12920-026-02359-w},
pmid = {41928235},
issn = {1755-8794},
}
RevDate: 2026-04-03
Longitudinal dynamics and site-specific recovery of the human respiratory microbiome following smoking cessation.
Respiratory research pii:10.1186/s12931-026-03644-z [Epub ahead of print].
Additional Links: PMID-41928236
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@article {pmid41928236,
year = {2026},
author = {Gschwendtner, S and Kovacevic, D and Gaede, KI and Herzmann, C and Overmann, J and Schloter, M and Krauss-Etschmann, S},
title = {Longitudinal dynamics and site-specific recovery of the human respiratory microbiome following smoking cessation.},
journal = {Respiratory research},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12931-026-03644-z},
pmid = {41928236},
issn = {1465-993X},
}
RevDate: 2026-04-03
Machine learning-based assessment of the healthy human gut mycobiota landscape using ITS1 DNA metabarcoding data.
BioData mining pii:10.1186/s13040-026-00532-6 [Epub ahead of print].
The human gut microbiome plays a critical role in maintaining host health and homeostasis, and current literature suggests a bidirectional relationship between microbiome ecology and host well-being. DNA metabarcoding has emerged as a powerful tool for investigating microbiome imbalances (i.e., dysbiosis). While the prokaryotic microbiome has been extensively studied, the fungal counterpart - or mycobiome - remains largely unexplored, despite its recognized role from the perinatal stage onward. Here, we present a comprehensive survey based on DNA metabarcoding analysis of approximately 1,500 publicly available ITS1 samples. This survey integrates conventional statistical approaches with Machine Learning (ML) methods coupled with explainable Artificial Intelligence (XAI). ML models successfully predicted host health status with accuracies exceeding 80%, and fungal genera such as Eurotium, Aureobasidium, Candida, and Cutaneotrichosporon emerged as key classification features. This study introduces a cutting-edge multiview analytical framework applied to publicly available mycobiome data, highlighting the potential of fungal community profiling as a non-invasive tool to support health diagnostics.
Additional Links: PMID-41928315
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PubMed:
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@article {pmid41928315,
year = {2026},
author = {Defazio, G and Lorusso, E and De Robertis, M and Mello, T and Galli, A and Pesole, G and Fosso, B},
title = {Machine learning-based assessment of the healthy human gut mycobiota landscape using ITS1 DNA metabarcoding data.},
journal = {BioData mining},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13040-026-00532-6},
pmid = {41928315},
issn = {1756-0381},
support = {H93C22000560003//Regione Puglia/ ; PNC-EJ-2022-23683266 PNC-HLS-DA//Ministero dell'Università e della Ricerca/ ; },
abstract = {The human gut microbiome plays a critical role in maintaining host health and homeostasis, and current literature suggests a bidirectional relationship between microbiome ecology and host well-being. DNA metabarcoding has emerged as a powerful tool for investigating microbiome imbalances (i.e., dysbiosis). While the prokaryotic microbiome has been extensively studied, the fungal counterpart - or mycobiome - remains largely unexplored, despite its recognized role from the perinatal stage onward. Here, we present a comprehensive survey based on DNA metabarcoding analysis of approximately 1,500 publicly available ITS1 samples. This survey integrates conventional statistical approaches with Machine Learning (ML) methods coupled with explainable Artificial Intelligence (XAI). ML models successfully predicted host health status with accuracies exceeding 80%, and fungal genera such as Eurotium, Aureobasidium, Candida, and Cutaneotrichosporon emerged as key classification features. This study introduces a cutting-edge multiview analytical framework applied to publicly available mycobiome data, highlighting the potential of fungal community profiling as a non-invasive tool to support health diagnostics.},
}
RevDate: 2026-04-03
Metagenomic insights into the global wild boar faecal microbiome reveal novel taxa and carbohydrate degraders distinguishing wild and domesticated Sus.
Microbiome pii:10.1186/s40168-026-02392-y [Epub ahead of print].
BACKGROUND: The inclusion of fibre in domestic pig diets is favourable from a digestive health, environmental, and socio-economic perspective. Unlike the highly optimized formulated diets of domestic pigs, wild boars feed opportunistically, consuming a broad range of foods that consist predominantly of plant materials. Consequently, the intestinal microbiota of wild boars is thought to be adapted to a versatile, fibre-rich diet and may represent a valuable source of probiotics for enhancing fibre degradation. However, comprehensive studies characterizing the wild boar gut microbiome, particularly its community structure and carbohydrate utilization potential, and comparison to that of domestic pigs are still lacking.
RESULTS: We collected 89 faecal samples from wild boars across four countries and analysed them primarily using metagenomic sequencing. De novo assembly yielded 3,288 high- and medium-quality metagenome-assembled genomes (MAGs) representing 968 distinct species, of which 538 were previously unknown. Incorporating these MAGs enabled robust microbiome comparisons with 125 previously published samples largely from domestic pigs, which revealed significant structural and functional differences. These differences resolved into two community types, determined not by host species but by diet and lifestyle: C1 comprising 81% of samples from free-ranging, foraging wild boars and C2 consisting of 93% of samples from captive, fed domestic pigs. The lower alpha-diversity observed in C1 likely reflected the impact of highly fluctuating dietary resources and environmental conditions, resulting in dominance of fewer resilient or adaptable taxa. Nevertheless, both community types maintained substantial carbohydrate utilization potential: while C2 exhibited a higher relative abundance of CAZyme[sub] genes associated with a broader range of carbohydrate substrate (CHO) classes, C1 was enriched in individual species that were generally richer in CAZyme[sub] genes and CHO classes. To leverage this potential, we curated a catalogue of carbohydrate degraders from both community types and identified 47 highly versatile species, with several novel species amongst them.
CONCLUSIONS: This study uncovered the previously untapped microbial diversity in the wild boar faecal microbiome and demonstrated that the faecal microbiome of Sus is primarily shaped by diet and lifestyle. The two community types identified, which differed both structurally and functionally, represent alternative states of microbiome homeostasis in wild versus domesticated Sus populations. The curated catalogue of carbohydrate degraders provides a valuable resource to guide tailored probiotic supplementation during dietary transitions to novel fibrous feedstocks. Video Abstract.
Additional Links: PMID-41928361
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@article {pmid41928361,
year = {2026},
author = {Heng, YC and Chua, JHX and Silvaraju, S and Fan, H and Low, A and Lim, ACH and Chen, B and Mane, L and Dagar, SS and Fliegerova, K and Moniello, G and Ikeda-Ohtsubo, W and Okuda, K and Seedorf, H and Lim, KJ and Kittelmann, S},
title = {Metagenomic insights into the global wild boar faecal microbiome reveal novel taxa and carbohydrate degraders distinguishing wild and domesticated Sus.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02392-y},
pmid = {41928361},
issn = {2049-2618},
support = {Project number CRG/2022/008319//Anusandhan National Research Foundation (ANRF), DST, Government of India/ ; FDS2223MONIELLO - CUP J83C22000160007//Fondazione di Sardegna, Italy/ ; University Research Fund 2020//University of Sassari/ ; WIL@NUS Corporate Laboratory, Singapore//Wilmar International/ ; },
abstract = {BACKGROUND: The inclusion of fibre in domestic pig diets is favourable from a digestive health, environmental, and socio-economic perspective. Unlike the highly optimized formulated diets of domestic pigs, wild boars feed opportunistically, consuming a broad range of foods that consist predominantly of plant materials. Consequently, the intestinal microbiota of wild boars is thought to be adapted to a versatile, fibre-rich diet and may represent a valuable source of probiotics for enhancing fibre degradation. However, comprehensive studies characterizing the wild boar gut microbiome, particularly its community structure and carbohydrate utilization potential, and comparison to that of domestic pigs are still lacking.
RESULTS: We collected 89 faecal samples from wild boars across four countries and analysed them primarily using metagenomic sequencing. De novo assembly yielded 3,288 high- and medium-quality metagenome-assembled genomes (MAGs) representing 968 distinct species, of which 538 were previously unknown. Incorporating these MAGs enabled robust microbiome comparisons with 125 previously published samples largely from domestic pigs, which revealed significant structural and functional differences. These differences resolved into two community types, determined not by host species but by diet and lifestyle: C1 comprising 81% of samples from free-ranging, foraging wild boars and C2 consisting of 93% of samples from captive, fed domestic pigs. The lower alpha-diversity observed in C1 likely reflected the impact of highly fluctuating dietary resources and environmental conditions, resulting in dominance of fewer resilient or adaptable taxa. Nevertheless, both community types maintained substantial carbohydrate utilization potential: while C2 exhibited a higher relative abundance of CAZyme[sub] genes associated with a broader range of carbohydrate substrate (CHO) classes, C1 was enriched in individual species that were generally richer in CAZyme[sub] genes and CHO classes. To leverage this potential, we curated a catalogue of carbohydrate degraders from both community types and identified 47 highly versatile species, with several novel species amongst them.
CONCLUSIONS: This study uncovered the previously untapped microbial diversity in the wild boar faecal microbiome and demonstrated that the faecal microbiome of Sus is primarily shaped by diet and lifestyle. The two community types identified, which differed both structurally and functionally, represent alternative states of microbiome homeostasis in wild versus domesticated Sus populations. The curated catalogue of carbohydrate degraders provides a valuable resource to guide tailored probiotic supplementation during dietary transitions to novel fibrous feedstocks. Video Abstract.},
}
RevDate: 2026-04-03
CmpDate: 2026-04-03
Human fecal transplantation from stunted children promotes metabolic dysfunction in mice fed with a high-fat and high-fructose corn syrup diet.
Gut microbes, 18(1):2651984.
Stunting, or impaired child growth due to poor nutrition and infections, is characterized by a low height-for-age and affects 48%-56% of school-aged children worldwide. It is associated with later weight gain and chronic diseases. The gut microbiome in undernourished children may increase obesity risk if they are exposed to high-calorie environments. To investigate this, we assessed whether the intestinal microbiome of stunted children elevates obesity risk upon exposure to an obesogenic environment. Fecal microbiota transplantation (FMT) was performed using pooled stools from healthy (n = 6) or stunted (n = 6) school-aged children from a low-income cohort in Mexico. Eight-week-old male C57BL/6 mice underwent bowel cleansing with polyethylene glycol (PEG), followed by weekly intragastric FMT for 4 weeks. The mice were subsequently fed either a control diet (CT) or a high-fat, high-fructose corn syrup diet (HFFr, including 15% HFCS-55) for 15 weeks. Metabolic outcomes were assessed through body composition, indirect calorimetry, oral glucose tolerance test, insulin tolerance test, and histological analysis of visceral adipose tissue. The microbiota composition was evaluated by 16S rRNA V3-V4 hypervariable region sequencing, and the predicted functional capacity was analyzed using PICRUSt2. FMT from stunted children increased susceptibility to diet-induced obesity, visceral adipose tissue hypertrophy, and insulin resistance. In contrast, FMT from healthy children promoted energy expenditure and visceral adipose tissue hyperplasia, conferring a protective effect against diet-induced obesity and insulin resistance in the mice. Healthy-FMT led to sustained enrichment of Akkermansia and Parabacteroides, whereas stunting-FMT increased Proteobacteria, Veillonella, Desulfovibrionaceae, and Bifidobacterium. Microbial‒phenotypic correlations showed that Akkermansia and Parabacteroides were negatively correlated with fasting glucose, body weight, and fat mass, and positively correlated with postprandial RER, VO2, and lean mass. In conclusion, stunting-FMT recipient mice showed a higher risk of obesity and metabolic issues in an obesogenic environment. Healthy-FMT confers metabolic resilience, characterized by increased abundance of taxa such as Akkermansia and Parabacteroides, which are linked to enhanced energy expenditure, improved glucose metabolism, and favorable adipose tissue structure.
Additional Links: PMID-41928384
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@article {pmid41928384,
year = {2026},
author = {Valdez-Palomares, F and Noriega, LG and Reyes-Romo, D and Canizales-Quinteros, S and Nambo-Venegas, R and Salinas-Lara, C and Tovar-Palacio, A and Menjivar, M and Peña-Espinoza, B and Ortiz, G and Palacios-González, B},
title = {Human fecal transplantation from stunted children promotes metabolic dysfunction in mice fed with a high-fat and high-fructose corn syrup diet.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2651984},
doi = {10.1080/19490976.2026.2651984},
pmid = {41928384},
issn = {1949-0984},
mesh = {Animals ; Male ; *Fecal Microbiota Transplantation/adverse effects ; Mice ; Gastrointestinal Microbiome ; Humans ; Mice, Inbred C57BL ; *Diet, High-Fat/adverse effects ; *Growth Disorders/microbiology/therapy/metabolism ; Child ; *High Fructose Corn Syrup/adverse effects/administration & dosage ; Bacteria/classification/isolation & purification/genetics ; Feces/microbiology ; Obesity/etiology/metabolism ; *Metabolic Diseases/etiology ; },
abstract = {Stunting, or impaired child growth due to poor nutrition and infections, is characterized by a low height-for-age and affects 48%-56% of school-aged children worldwide. It is associated with later weight gain and chronic diseases. The gut microbiome in undernourished children may increase obesity risk if they are exposed to high-calorie environments. To investigate this, we assessed whether the intestinal microbiome of stunted children elevates obesity risk upon exposure to an obesogenic environment. Fecal microbiota transplantation (FMT) was performed using pooled stools from healthy (n = 6) or stunted (n = 6) school-aged children from a low-income cohort in Mexico. Eight-week-old male C57BL/6 mice underwent bowel cleansing with polyethylene glycol (PEG), followed by weekly intragastric FMT for 4 weeks. The mice were subsequently fed either a control diet (CT) or a high-fat, high-fructose corn syrup diet (HFFr, including 15% HFCS-55) for 15 weeks. Metabolic outcomes were assessed through body composition, indirect calorimetry, oral glucose tolerance test, insulin tolerance test, and histological analysis of visceral adipose tissue. The microbiota composition was evaluated by 16S rRNA V3-V4 hypervariable region sequencing, and the predicted functional capacity was analyzed using PICRUSt2. FMT from stunted children increased susceptibility to diet-induced obesity, visceral adipose tissue hypertrophy, and insulin resistance. In contrast, FMT from healthy children promoted energy expenditure and visceral adipose tissue hyperplasia, conferring a protective effect against diet-induced obesity and insulin resistance in the mice. Healthy-FMT led to sustained enrichment of Akkermansia and Parabacteroides, whereas stunting-FMT increased Proteobacteria, Veillonella, Desulfovibrionaceae, and Bifidobacterium. Microbial‒phenotypic correlations showed that Akkermansia and Parabacteroides were negatively correlated with fasting glucose, body weight, and fat mass, and positively correlated with postprandial RER, VO2, and lean mass. In conclusion, stunting-FMT recipient mice showed a higher risk of obesity and metabolic issues in an obesogenic environment. Healthy-FMT confers metabolic resilience, characterized by increased abundance of taxa such as Akkermansia and Parabacteroides, which are linked to enhanced energy expenditure, improved glucose metabolism, and favorable adipose tissue structure.},
}
MeSH Terms:
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Animals
Male
*Fecal Microbiota Transplantation/adverse effects
Mice
Gastrointestinal Microbiome
Humans
Mice, Inbred C57BL
*Diet, High-Fat/adverse effects
*Growth Disorders/microbiology/therapy/metabolism
Child
*High Fructose Corn Syrup/adverse effects/administration & dosage
Bacteria/classification/isolation & purification/genetics
Feces/microbiology
Obesity/etiology/metabolism
*Metabolic Diseases/etiology
RevDate: 2026-04-03
CmpDate: 2026-04-03
Neglected kingdoms: the gut virome, mycobiome and their role in inflammatory bowel disease.
Gut microbes, 18(1):2653288.
Inflammatory bowel disease (IBD) is a chronic relapsing-remitting disorder of the gastrointestinal tract characterized by immune dysregulation, epithelial barrier dysfunction, and microbial imbalance. While bacterial dysbiosis, including depletion of short-chain fatty acid (SCFA) producers and enrichment of pathobionts, is well characterized, the gut virome and mycobiome remain comparatively neglected. Both exhibit high variability and are constrained by sequencing bias, contamination, and incomplete reference databases, leaving much of the viral and fungal diversity unresolved. Emerging evidence links fungal and viral dysbiosis to IBD pathogenesis, including Candida overgrowth, loss of Saccharomyces, expansion of Caudoviricetes phages, and detection of eukaryotic viruses such as Cytomegalovirus and Epstein-Barr virus in inflamed mucosa. These alterations disrupt barrier integrity, modulate immune signaling, and interact with bacteria and archaea in cross-kingdom networks that amplify inflammation. Translationally, the virome and mycobiome are now recognized as therapeutic targets, inspiring interventions from pre/probiotics and synbiotics to precision phage therapy and microbiota-based transplantation, including fecal virome transplantation (FVT) and fecal microbiota transplantation (FMT). This review recognizes the challenges and opportunities of studying these neglected kingdoms, reframes IBD dysbiosis and highlights new directions for biomarker discovery and multikingdom microbiota-directed therapies.
Additional Links: PMID-41928387
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@article {pmid41928387,
year = {2026},
author = {Houshyar, Y and Zhang, F and Tavakoli, P and Grimm, MC and Hold, GL},
title = {Neglected kingdoms: the gut virome, mycobiome and their role in inflammatory bowel disease.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2653288},
doi = {10.1080/19490976.2026.2653288},
pmid = {41928387},
issn = {1949-0984},
mesh = {Humans ; *Virome ; *Mycobiome ; *Inflammatory Bowel Diseases/microbiology/therapy/virology ; *Gastrointestinal Microbiome ; Dysbiosis/microbiology/virology ; *Fungi/classification/genetics/isolation & purification ; Animals ; Fecal Microbiota Transplantation ; *Viruses/classification/genetics/isolation & purification ; Bacteria/genetics ; },
abstract = {Inflammatory bowel disease (IBD) is a chronic relapsing-remitting disorder of the gastrointestinal tract characterized by immune dysregulation, epithelial barrier dysfunction, and microbial imbalance. While bacterial dysbiosis, including depletion of short-chain fatty acid (SCFA) producers and enrichment of pathobionts, is well characterized, the gut virome and mycobiome remain comparatively neglected. Both exhibit high variability and are constrained by sequencing bias, contamination, and incomplete reference databases, leaving much of the viral and fungal diversity unresolved. Emerging evidence links fungal and viral dysbiosis to IBD pathogenesis, including Candida overgrowth, loss of Saccharomyces, expansion of Caudoviricetes phages, and detection of eukaryotic viruses such as Cytomegalovirus and Epstein-Barr virus in inflamed mucosa. These alterations disrupt barrier integrity, modulate immune signaling, and interact with bacteria and archaea in cross-kingdom networks that amplify inflammation. Translationally, the virome and mycobiome are now recognized as therapeutic targets, inspiring interventions from pre/probiotics and synbiotics to precision phage therapy and microbiota-based transplantation, including fecal virome transplantation (FVT) and fecal microbiota transplantation (FMT). This review recognizes the challenges and opportunities of studying these neglected kingdoms, reframes IBD dysbiosis and highlights new directions for biomarker discovery and multikingdom microbiota-directed therapies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Virome
*Mycobiome
*Inflammatory Bowel Diseases/microbiology/therapy/virology
*Gastrointestinal Microbiome
Dysbiosis/microbiology/virology
*Fungi/classification/genetics/isolation & purification
Animals
Fecal Microbiota Transplantation
*Viruses/classification/genetics/isolation & purification
Bacteria/genetics
RevDate: 2026-04-03
Therapeutic Landscape Evolution: From Lifestyle Interventions to Precision Pharmacotherapy.
Clinical and molecular hepatology pii:cmh.2026.0125 [Epub ahead of print].
Steatotic liver disease (SLD) is a growing global epidemic, with metabolic dysfunction-associated steatotic liver disease (MASLD) now the most common chronic liver disease worldwide and closely linked to adverse cardiovascular outcomes. Lifestyle modification remains the cornerstone of management, with the Mediterranean diet as the preferred dietary intervention and emerging evidence supporting additional dietary and exercise strategies. Pharmacotherapy has advanced rapidly in recent years, with two U.S. Food and Drug Administration-approved options, resmetirom and semaglutide, for noncirrhotic metabolic dysfunction-associated steatohepatitis (MASH) with moderate-to-advanced fibrosis, alongside multiple agents in development targeting different disease mechanisms. In metabolic dysfunction- and alcohol-associated liver disease (MetALD), evidence remains limited, but management essentially focuses on alcohol cessation and optimization of cardiometabolic risk factors, with resmetirom, incretin-based therapies, and fibroblast growth factor (FGF)-21 analogues representing promising therapeutic agents that have yet to be fully evaluated in clinical trials. The field is increasingly moving toward a precision medicine paradigm integrating pharmacologic and lifestyle interventions, tailored to disease phenotype, genetic risk, and gut microbiome. Key challenges include heterogeneity in treatment response, assessment of alcohol intake, and real-world implementation barriers. This review summarizes current and emerging therapies and highlights the role of precision medicine in advancing individualized care across the SLD spectrum.
Additional Links: PMID-41928627
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@article {pmid41928627,
year = {2026},
author = {Bong, SHS and Teh, KKJ and Wong, VW},
title = {Therapeutic Landscape Evolution: From Lifestyle Interventions to Precision Pharmacotherapy.},
journal = {Clinical and molecular hepatology},
volume = {},
number = {},
pages = {},
doi = {10.3350/cmh.2026.0125},
pmid = {41928627},
issn = {2287-285X},
abstract = {Steatotic liver disease (SLD) is a growing global epidemic, with metabolic dysfunction-associated steatotic liver disease (MASLD) now the most common chronic liver disease worldwide and closely linked to adverse cardiovascular outcomes. Lifestyle modification remains the cornerstone of management, with the Mediterranean diet as the preferred dietary intervention and emerging evidence supporting additional dietary and exercise strategies. Pharmacotherapy has advanced rapidly in recent years, with two U.S. Food and Drug Administration-approved options, resmetirom and semaglutide, for noncirrhotic metabolic dysfunction-associated steatohepatitis (MASH) with moderate-to-advanced fibrosis, alongside multiple agents in development targeting different disease mechanisms. In metabolic dysfunction- and alcohol-associated liver disease (MetALD), evidence remains limited, but management essentially focuses on alcohol cessation and optimization of cardiometabolic risk factors, with resmetirom, incretin-based therapies, and fibroblast growth factor (FGF)-21 analogues representing promising therapeutic agents that have yet to be fully evaluated in clinical trials. The field is increasingly moving toward a precision medicine paradigm integrating pharmacologic and lifestyle interventions, tailored to disease phenotype, genetic risk, and gut microbiome. Key challenges include heterogeneity in treatment response, assessment of alcohol intake, and real-world implementation barriers. This review summarizes current and emerging therapies and highlights the role of precision medicine in advancing individualized care across the SLD spectrum.},
}
RevDate: 2026-04-03
CmpDate: 2026-04-03
Proximity-ligation metagenomics reveals disease-specific mobilome dynamics in disrupted gut ecosystems.
Research square pii:rs.3.rs-9142184.
Distinct ecological pressures shape accumulation of antimicrobial resistance and virulence genes in the gut microbiome. Using proximity ligation shotgun metagenomics to resolve host-mobilome relationships, we analyzed microbiomes from two patient cohorts: recurrent Clostridioides difficile infection (rCDI) and cirrhosis. While rCDI reflects antibiotic-driven disruption, cirrhosis-driven microbiome changes result from altered gut physiology. We found increased chromosomal determinants of antibiotic resistance in both, but plasmid-mediated amplification was more evident in rCDI.
Additional Links: PMID-41928791
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@article {pmid41928791,
year = {2026},
author = {Bajaj, J and Sommer, A and Auch, B and Khoruts, A},
title = {Proximity-ligation metagenomics reveals disease-specific mobilome dynamics in disrupted gut ecosystems.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-9142184/v1},
pmid = {41928791},
issn = {2693-5015},
abstract = {Distinct ecological pressures shape accumulation of antimicrobial resistance and virulence genes in the gut microbiome. Using proximity ligation shotgun metagenomics to resolve host-mobilome relationships, we analyzed microbiomes from two patient cohorts: recurrent Clostridioides difficile infection (rCDI) and cirrhosis. While rCDI reflects antibiotic-driven disruption, cirrhosis-driven microbiome changes result from altered gut physiology. We found increased chromosomal determinants of antibiotic resistance in both, but plasmid-mediated amplification was more evident in rCDI.},
}
RevDate: 2026-04-03
CmpDate: 2026-04-03
Microbiome contribution to Indy longevity in Drosophila.
bioRxiv : the preprint server for biology pii:2026.03.25.714291.
UNLABELLED: Reduction in the Indy (I'm not dead yet) gene, a plasma membrane citrate transporter, in Drosophila and its homolog in worms extends lifespan by promoting metabolic homeostasis. Indy reduction delays the onset of aging-associated pathology in the fly midgut, including preservation of intestinal barrier integrity and intestinal stem cell homeostasis. Gut microbiota has broad impacts on host metabolism, health, and aging. Age-related dysbiosis impairs intestinal barrier function and drives mortality. However, the underlying mechanisms that link increased microbial load to frailty and negative effects on health remain mostly unclear. Here we show that Indy heterozygote flies have significantly lower bacterial load and increased diversity during aging compared to controls. However, the presence of the microbiome was not required for Indy lifespan extension, though removal of microbes did enhance the effects of Indy reduction on longevity, suggesting potential interactions between the microbiome and Indy . Indy down-regulation was linked to reduced expression of the JAK/STAT signaling ligands Upd3 and Upd2 in the midgut of young flies, which likely contributes to preserved intestinal stem cell homeostasis. Altogether, our results suggest that Indy reduction impacts microbiome load and composition, which preserves gut homeostasis and extends lifespan through impacts on JAK/STAT signaling pathway.
SIGNIFICANCE STATEMENT: Indy is a fly homologue of mammalian SLC13A5 (mSLC13A5) plasma membrane citrate transporter, a central metabolic regulator involved in health, longevity, and disease. Reduction of fly Indy gene activity preserves metabolic and intestinal stem cell homeostasis and extends longevity. Gut microbiota impacts host metabolism, health, and aging. Here we show that Indy reduction prevents age-associated increases in bacterial load and expression of the JAK/STAT signaling ligands Upd3, and Upd2, while maintaining microbiome diversity. These changes likely slow activation of epithelial cell turnover in the gut and contribute to downstream lifespan effects. As the role of INDY and microbiome are conserved across organisms, our study provides a framework to study underlying mechanisms of the effects of reduced Indy and the microbiome on health and longevity.
Additional Links: PMID-41928923
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@article {pmid41928923,
year = {2026},
author = {Lesperance, DNA and Padhi, S and Macro, J and Olson, S and Stanwood, E and Kannan, K and Graveley, B and Rogina, B and Broderick, NA},
title = {Microbiome contribution to Indy longevity in Drosophila.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.25.714291},
pmid = {41928923},
issn = {2692-8205},
abstract = {UNLABELLED: Reduction in the Indy (I'm not dead yet) gene, a plasma membrane citrate transporter, in Drosophila and its homolog in worms extends lifespan by promoting metabolic homeostasis. Indy reduction delays the onset of aging-associated pathology in the fly midgut, including preservation of intestinal barrier integrity and intestinal stem cell homeostasis. Gut microbiota has broad impacts on host metabolism, health, and aging. Age-related dysbiosis impairs intestinal barrier function and drives mortality. However, the underlying mechanisms that link increased microbial load to frailty and negative effects on health remain mostly unclear. Here we show that Indy heterozygote flies have significantly lower bacterial load and increased diversity during aging compared to controls. However, the presence of the microbiome was not required for Indy lifespan extension, though removal of microbes did enhance the effects of Indy reduction on longevity, suggesting potential interactions between the microbiome and Indy . Indy down-regulation was linked to reduced expression of the JAK/STAT signaling ligands Upd3 and Upd2 in the midgut of young flies, which likely contributes to preserved intestinal stem cell homeostasis. Altogether, our results suggest that Indy reduction impacts microbiome load and composition, which preserves gut homeostasis and extends lifespan through impacts on JAK/STAT signaling pathway.
SIGNIFICANCE STATEMENT: Indy is a fly homologue of mammalian SLC13A5 (mSLC13A5) plasma membrane citrate transporter, a central metabolic regulator involved in health, longevity, and disease. Reduction of fly Indy gene activity preserves metabolic and intestinal stem cell homeostasis and extends longevity. Gut microbiota impacts host metabolism, health, and aging. Here we show that Indy reduction prevents age-associated increases in bacterial load and expression of the JAK/STAT signaling ligands Upd3, and Upd2, while maintaining microbiome diversity. These changes likely slow activation of epithelial cell turnover in the gut and contribute to downstream lifespan effects. As the role of INDY and microbiome are conserved across organisms, our study provides a framework to study underlying mechanisms of the effects of reduced Indy and the microbiome on health and longevity.},
}
RevDate: 2026-04-03
CmpDate: 2026-04-03
Female-enriched Eggerthella lenta drives neuroinflammation and IFN-γ via host receptor TLR2.
bioRxiv : the preprint server for biology pii:2026.03.16.711194.
UNLABELLED: Women are at increased risk of autoimmune diseases, including multiple sclerosis (MS); however, the degree to which sex differences in the gut microbiota impact autoimmunity remains largely unexplored. Our 27-cohort meta-analysis revealed 60 sex-associated gut bacterial species. Leveraging an independent clinical cohort, we demonstrate that female-enriched species significantly associate with MS status and clinical disability (EDSS). Top female-enriched species Eggerthella lenta drove disease in the experimental autoimmune encephalomyelitis (EAE) MS model, consistent with brain and gut lamina propria T cell infiltration and MS-associated T helper (Th) signatures. E. lenta induced intestinal Th1 and Th17 in healthy mice, independent of bacterial viability. Mechanistically, we demonstrate that TLR2 directly drives E. lenta -induced IFN-γ production in Th cells and is necessary for exacerbation of EAE. Together, we identify a causal host-microbe axis contributing to sex differences in autoimmunity and provide a framework for evaluating sex as a biological variable in human microbiome research.
HIGHLIGHTS: 27-cohort meta-analysis identifies a robust sex-signature in human gut microbiota.Female-enriched species are associated with MS risk and severity. Female-enriched Eggerthella lenta exacerbates the EAE model. E. lenta impacts neuroinflammation via toll-like receptor 2.
Additional Links: PMID-41928970
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@article {pmid41928970,
year = {2026},
author = {Rock, RR and Alexander, M and Noecker, C and Trepka, KR and Upadhyay, V and Ortega, EF and Ramirez, L and Siewert, L and Olson, CA and Halsey, T and Pröbstel, AK and Baranzini, SE and Turnbaugh, PJ},
title = {Female-enriched Eggerthella lenta drives neuroinflammation and IFN-γ via host receptor TLR2.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.16.711194},
pmid = {41928970},
issn = {2692-8205},
abstract = {UNLABELLED: Women are at increased risk of autoimmune diseases, including multiple sclerosis (MS); however, the degree to which sex differences in the gut microbiota impact autoimmunity remains largely unexplored. Our 27-cohort meta-analysis revealed 60 sex-associated gut bacterial species. Leveraging an independent clinical cohort, we demonstrate that female-enriched species significantly associate with MS status and clinical disability (EDSS). Top female-enriched species Eggerthella lenta drove disease in the experimental autoimmune encephalomyelitis (EAE) MS model, consistent with brain and gut lamina propria T cell infiltration and MS-associated T helper (Th) signatures. E. lenta induced intestinal Th1 and Th17 in healthy mice, independent of bacterial viability. Mechanistically, we demonstrate that TLR2 directly drives E. lenta -induced IFN-γ production in Th cells and is necessary for exacerbation of EAE. Together, we identify a causal host-microbe axis contributing to sex differences in autoimmunity and provide a framework for evaluating sex as a biological variable in human microbiome research.
HIGHLIGHTS: 27-cohort meta-analysis identifies a robust sex-signature in human gut microbiota.Female-enriched species are associated with MS risk and severity. Female-enriched Eggerthella lenta exacerbates the EAE model. E. lenta impacts neuroinflammation via toll-like receptor 2.},
}
RevDate: 2026-04-03
CmpDate: 2026-04-03
Environmental Gradients Shape the Hydrocarbon-Degrading Microbiome in Two Mid Atlantic Bays.
bioRxiv : the preprint server for biology pii:2026.03.25.714183.
UNLABELLED: Hydrocarbons are recalcitrant organic matter that are released into the environment via natural and anthropogenic activities. We hypothesized that abiotic and biotic factors, including salinity, temperature, seasonality, microbial interactions, and functional redundancy, influence the abundance and activity of potential hydrocarbon degraders in the Delaware and Chesapeake Bays. We identified key genes in hydrocarbon degradation pathways in metagenomes, metatranscriptomes, and metagenome assembled genomes (MAGs) from these estuaries. Aerobic aromatic and alkane degradation pathways predominated in both estuaries, with higher gene abundances observed in low-salinity spring and summer samples. Hydrocarbon degrading MAG abundance were significantly structured by salinity, temperature, nitrate, and silicate concentrations. Metatranscriptomic analyses revealed consistently higher expression of aerobic alkane and aromatic degradation genes in the Delaware compared to the Chesapeake Bay, with the highest occurring under low-salinity spring conditions in the former. Catechol degradation pathways exhibited high functional redundancy, whereas the naphthalene degradation pathway showed restricted distribution. Co-expression analysis revealed that Burkholderiales displayed condition dependent metabolic coupling while Pseudomonadales integrated hydrocarbon degradation with fermentation and central metabolism, demonstrating complementary strategies that support multi-scale ecosystem resilience. In conclusion, environmental gradients and taxon-specific metabolic strategies together govern hydrocarbon degradation potential in these estuaries, with implications for predicting ecosystem responses to hydrocarbon inputs under changing conditions.
IMPORTANCE: Coastal estuaries are among the most contaminated aquatic environments on Earth, receiving continuous hydrocarbon inputs from industrial activity, urban runoff, and natural sources. Microorganisms are the primary agents of hydrocarbon breakdown in these systems yet predicting when and where this capacity is active and how resilient it is to environmental change remains a major challenge. Using paired genomic and transcriptomic data from microbial genomes across two major mid-Atlantic estuaries, we show that hydrocarbon degradation capacity is not uniformly distributed but is instead shaped by salinity, nutrients, and seasonality in pathway-specific ways. Critically, dominant degrader taxa employ fundamentally different metabolic strategies to sustain this function across fluctuating conditions, providing a form of community-level insurance against environmental disturbance. These findings advance our ability to predict microbial hydrocarbon degradation in coastal systems and inform nature-based approaches to bioremediation under increasing climate and anthropogenic pressures.
Additional Links: PMID-41929040
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@article {pmid41929040,
year = {2026},
author = {Patabandige, DLJ and John, J and Ortiz, M and Campbell, BJ},
title = {Environmental Gradients Shape the Hydrocarbon-Degrading Microbiome in Two Mid Atlantic Bays.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.25.714183},
pmid = {41929040},
issn = {2692-8205},
abstract = {UNLABELLED: Hydrocarbons are recalcitrant organic matter that are released into the environment via natural and anthropogenic activities. We hypothesized that abiotic and biotic factors, including salinity, temperature, seasonality, microbial interactions, and functional redundancy, influence the abundance and activity of potential hydrocarbon degraders in the Delaware and Chesapeake Bays. We identified key genes in hydrocarbon degradation pathways in metagenomes, metatranscriptomes, and metagenome assembled genomes (MAGs) from these estuaries. Aerobic aromatic and alkane degradation pathways predominated in both estuaries, with higher gene abundances observed in low-salinity spring and summer samples. Hydrocarbon degrading MAG abundance were significantly structured by salinity, temperature, nitrate, and silicate concentrations. Metatranscriptomic analyses revealed consistently higher expression of aerobic alkane and aromatic degradation genes in the Delaware compared to the Chesapeake Bay, with the highest occurring under low-salinity spring conditions in the former. Catechol degradation pathways exhibited high functional redundancy, whereas the naphthalene degradation pathway showed restricted distribution. Co-expression analysis revealed that Burkholderiales displayed condition dependent metabolic coupling while Pseudomonadales integrated hydrocarbon degradation with fermentation and central metabolism, demonstrating complementary strategies that support multi-scale ecosystem resilience. In conclusion, environmental gradients and taxon-specific metabolic strategies together govern hydrocarbon degradation potential in these estuaries, with implications for predicting ecosystem responses to hydrocarbon inputs under changing conditions.
IMPORTANCE: Coastal estuaries are among the most contaminated aquatic environments on Earth, receiving continuous hydrocarbon inputs from industrial activity, urban runoff, and natural sources. Microorganisms are the primary agents of hydrocarbon breakdown in these systems yet predicting when and where this capacity is active and how resilient it is to environmental change remains a major challenge. Using paired genomic and transcriptomic data from microbial genomes across two major mid-Atlantic estuaries, we show that hydrocarbon degradation capacity is not uniformly distributed but is instead shaped by salinity, nutrients, and seasonality in pathway-specific ways. Critically, dominant degrader taxa employ fundamentally different metabolic strategies to sustain this function across fluctuating conditions, providing a form of community-level insurance against environmental disturbance. These findings advance our ability to predict microbial hydrocarbon degradation in coastal systems and inform nature-based approaches to bioremediation under increasing climate and anthropogenic pressures.},
}
RevDate: 2026-04-03
CmpDate: 2026-04-03
Metagenomic strain-resolved DNA modification patterns link extrachromosomal genetic elements to host strains.
bioRxiv : the preprint server for biology pii:2026.03.27.714056.
DNA modification is central to microbial defense against extrachromosomal genetic elements (ECEs), consequently ECEs tend to adopt their host's modification patterns. Shared ECE-host modification patterns enable linking ECEs to their hosts, but modification detection tools are designed for single genomes and are ineffective at metagenome scale. Here, we present MODIFI, software for detecting DNA modifications in metagenomes. MODIFI assumes that each k-mer in a metagenome is mostly unmodified and calculates background signal levels for that k-mer from PacBio HiFi reads, eliminating the need for matched control experiments. MODIFI ECE-host linkages were validated using >1,000 isolate and mock microbiome datasets. Illustrating the approach, we identified 315 strain-resolved, non-redundant ECE-host linkages in environmental and human metagenomes. In infant gut microbiomes, a chromosomal inversion in Enterococcus faecalis alters host and associated plasmid methylation motifs simultaneously. Overall, MODIFI solves a major bottleneck in DNA modification analysis and provides a foundational tool for understanding microbial epigenomics.
Additional Links: PMID-41929113
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@article {pmid41929113,
year = {2026},
author = {Wang, S and Guitor, AK and Valentin-Alvarado, LE and Garner, R and Zhang, P and Yan, M and Shi, LD and Schoelmerich, MC and Steininger, HM and Portik, DM and Zhang, S and Wilkinson, JE and Lynch, S and Morowitz, MJ and Hess, M and Diamond, S and Banfield, JF and Sachdeva, R},
title = {Metagenomic strain-resolved DNA modification patterns link extrachromosomal genetic elements to host strains.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.27.714056},
pmid = {41929113},
issn = {2692-8205},
abstract = {DNA modification is central to microbial defense against extrachromosomal genetic elements (ECEs), consequently ECEs tend to adopt their host's modification patterns. Shared ECE-host modification patterns enable linking ECEs to their hosts, but modification detection tools are designed for single genomes and are ineffective at metagenome scale. Here, we present MODIFI, software for detecting DNA modifications in metagenomes. MODIFI assumes that each k-mer in a metagenome is mostly unmodified and calculates background signal levels for that k-mer from PacBio HiFi reads, eliminating the need for matched control experiments. MODIFI ECE-host linkages were validated using >1,000 isolate and mock microbiome datasets. Illustrating the approach, we identified 315 strain-resolved, non-redundant ECE-host linkages in environmental and human metagenomes. In infant gut microbiomes, a chromosomal inversion in Enterococcus faecalis alters host and associated plasmid methylation motifs simultaneously. Overall, MODIFI solves a major bottleneck in DNA modification analysis and provides a foundational tool for understanding microbial epigenomics.},
}
RevDate: 2026-04-03
CmpDate: 2026-04-03
Germ-free piglets display variable neuroinflammatory-like perturbations in prefrontal cortical microglia.
bioRxiv : the preprint server for biology pii:2026.03.22.713463.
UNLABELLED: Communication between gut microbiota and immune cells within the brain is essential for neurotypical development. Specifically, microglia are known to play a key role in regulating and supporting neural progenitor stem cell production during brain development, and are sensitive to changes in the maternal gut microbial composition during perinatal development. Here, we employed a germ-free (GF) porcine paradigm to examine how the absence of the microbiome affects microglial dynamics during a key epoch of brain development. We utilized automated software to evaluate microglial density and morphology across three developmentally significant regions: the ventricular/subventricular zone (VZ/SVZ), the prefrontal subcortical white matter (PFCSWM), and layers II/III of the prefrontal cortex (PFCII-III). We found no significant differences in microglial morphology or density in the VZ/SVZ or PFCSWM. In contrast, the PFCII-III of P16 piglets exhibited an increase in microglia density paired with morphologies indicative of an activated/reactive functional state. Notably, these effects were identified with no overall changes in microglial density in any of the regions assessed. Transcriptomics on RNA isolated from the PFCII-III revealed a significant upregulation of genes related to neuroinflammation, in agreement with a region-specific microglial and immune response in the absence of microbial colonization during postnatal development. Together, these findings build on the limited knowledge available on how microbiota influence brain development in large animal model organisms with high similarities to human brain anatomy and developmental trajectories.
SIGNIFICANCE STATEMENT: The prefrontal cortex of porcine display unique, ramified microglia which are sensitive to germ-free conditions whereby they display alterations in morphology with a more transcriptionally reactive signature. These findings indicate that microglia are regionally sensitive to stimuli in the periphery, and studies in lissencephalic mammalian models may not be directly correlative to other higher-order species. The neuroanatomical heterogeneity of microglia across species is informative and understudied, but necessary, to draw conclusions on the array of perturbations spanning neurodevelopmental trajectories in health and disease.
Additional Links: PMID-41929228
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@article {pmid41929228,
year = {2026},
author = {Lester, BA and Kelly, C and Henry, SN and Elias, IP and Cevenini, SE and Hendrickson, MR and Park, T and Ashley, TD and Beltz, JM and Milner, JP and Pickrell, AM and Morton, PD},
title = {Germ-free piglets display variable neuroinflammatory-like perturbations in prefrontal cortical microglia.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.22.713463},
pmid = {41929228},
issn = {2692-8205},
abstract = {UNLABELLED: Communication between gut microbiota and immune cells within the brain is essential for neurotypical development. Specifically, microglia are known to play a key role in regulating and supporting neural progenitor stem cell production during brain development, and are sensitive to changes in the maternal gut microbial composition during perinatal development. Here, we employed a germ-free (GF) porcine paradigm to examine how the absence of the microbiome affects microglial dynamics during a key epoch of brain development. We utilized automated software to evaluate microglial density and morphology across three developmentally significant regions: the ventricular/subventricular zone (VZ/SVZ), the prefrontal subcortical white matter (PFCSWM), and layers II/III of the prefrontal cortex (PFCII-III). We found no significant differences in microglial morphology or density in the VZ/SVZ or PFCSWM. In contrast, the PFCII-III of P16 piglets exhibited an increase in microglia density paired with morphologies indicative of an activated/reactive functional state. Notably, these effects were identified with no overall changes in microglial density in any of the regions assessed. Transcriptomics on RNA isolated from the PFCII-III revealed a significant upregulation of genes related to neuroinflammation, in agreement with a region-specific microglial and immune response in the absence of microbial colonization during postnatal development. Together, these findings build on the limited knowledge available on how microbiota influence brain development in large animal model organisms with high similarities to human brain anatomy and developmental trajectories.
SIGNIFICANCE STATEMENT: The prefrontal cortex of porcine display unique, ramified microglia which are sensitive to germ-free conditions whereby they display alterations in morphology with a more transcriptionally reactive signature. These findings indicate that microglia are regionally sensitive to stimuli in the periphery, and studies in lissencephalic mammalian models may not be directly correlative to other higher-order species. The neuroanatomical heterogeneity of microglia across species is informative and understudied, but necessary, to draw conclusions on the array of perturbations spanning neurodevelopmental trajectories in health and disease.},
}
RevDate: 2026-04-03
CmpDate: 2026-04-03
Coordinated regulation of colonic fluid and mucus secretion.
Frontiers in pharmacology, 17:1757501.
The human colon, unlike the small intestine which is relatively sterile, contains a diverse microbiome which contributes to host metabolism. The luminal environment is constantly changing and responds to epithelial absorption and secretion which occurs as motility is regulated by longitudinal and circular smooth muscle. Mucous gels are crucial to lubrication and maintenance of an unstirred layer which separate the epithelium from the lumen. Gel-forming mucins are produced and released by goblet cells and become hydrated, although the source of water is not definitively understood. The purpose of this review is to summarize regulation of water movements across the colonic epithelium, goblet cell secretion of mucus and to consider how these distinct processes are functionally coupled.
Additional Links: PMID-41929259
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@article {pmid41929259,
year = {2026},
author = {Baird, AW},
title = {Coordinated regulation of colonic fluid and mucus secretion.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1757501},
pmid = {41929259},
issn = {1663-9812},
abstract = {The human colon, unlike the small intestine which is relatively sterile, contains a diverse microbiome which contributes to host metabolism. The luminal environment is constantly changing and responds to epithelial absorption and secretion which occurs as motility is regulated by longitudinal and circular smooth muscle. Mucous gels are crucial to lubrication and maintenance of an unstirred layer which separate the epithelium from the lumen. Gel-forming mucins are produced and released by goblet cells and become hydrated, although the source of water is not definitively understood. The purpose of this review is to summarize regulation of water movements across the colonic epithelium, goblet cell secretion of mucus and to consider how these distinct processes are functionally coupled.},
}
RevDate: 2026-04-03
CmpDate: 2026-04-03
Integrative Genomic, Transcriptomic, and Microbiome Profiles of Colon Cancer by Ancestry Provide Insights into Molecular Distinctions.
medRxiv : the preprint server for health sciences pii:2026.03.25.26349226.
Colorectal cancer (CRC) incidence, tumor biology, and clinical outcomes differ by patient ancestry, yet African ancestry (AFR) populations remain underrepresented in genomic and microbiome studies. Here, we comprehensively characterized genomic, transcriptomic and microbiome features of AFR and European ancestry (EUR) colon cancer patients residing in New York City and Long Island. While confirming known drivers from other large CRC studies, our AFR to EUR comparison of somatic variation also revealed a possible enrichment of functional KRAS variants in AFR tumors. Colon cancer genomes in patients in this study also exhibit distinct patterns of DNA copy number variation, correlating with consensus molecular subtypes. Fusobacterium nucleatum-positive tumors were enriched for co-occurring oral taxa, suggesting an organized oral microbial structure within the tumor microenvironment. Our findings highlight ancestry-associated differences in somatic mutation, copy number variation, and tumor microbiome composition, underscoring the urgent need to expand AFR representation in genomic studies to uncover population-specific determinants of CRC risk and to develop treatment strategies that reflect the full diversity of patients affected by this disease.
Additional Links: PMID-41929306
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@article {pmid41929306,
year = {2026},
author = {Kramer, M and Belleau, P and Tortora, SC and Deschenes, A and Founta, K and Gurjao, C and Yueh, B and Goodwin, S and Gee, D and Subhash, S and Barbi, M and Chung, C and Ozler, K and Eskiocak, O and Izar, B and Geiger, H and Chu, TR and Goldstein, Z and Winterkorn, L and Araneo, A and Whelan, RL and Rivadeneira, D and Fox, S and Kandel, A and Ozay, F and Talabong, DJA and Lanipekun, O and Talus, H and Zeng, J and Rishi, A and Chambwe, N and Robine, N and Boyd, J and Krasnitz, A and Beyaz, S and McCombie, WR and Martello, LA},
title = {Integrative Genomic, Transcriptomic, and Microbiome Profiles of Colon Cancer by Ancestry Provide Insights into Molecular Distinctions.},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.25.26349226},
pmid = {41929306},
abstract = {Colorectal cancer (CRC) incidence, tumor biology, and clinical outcomes differ by patient ancestry, yet African ancestry (AFR) populations remain underrepresented in genomic and microbiome studies. Here, we comprehensively characterized genomic, transcriptomic and microbiome features of AFR and European ancestry (EUR) colon cancer patients residing in New York City and Long Island. While confirming known drivers from other large CRC studies, our AFR to EUR comparison of somatic variation also revealed a possible enrichment of functional KRAS variants in AFR tumors. Colon cancer genomes in patients in this study also exhibit distinct patterns of DNA copy number variation, correlating with consensus molecular subtypes. Fusobacterium nucleatum-positive tumors were enriched for co-occurring oral taxa, suggesting an organized oral microbial structure within the tumor microenvironment. Our findings highlight ancestry-associated differences in somatic mutation, copy number variation, and tumor microbiome composition, underscoring the urgent need to expand AFR representation in genomic studies to uncover population-specific determinants of CRC risk and to develop treatment strategies that reflect the full diversity of patients affected by this disease.},
}
RevDate: 2026-04-03
CmpDate: 2026-04-03
Competence network inflammatory bowel diseases in Germany: 25 years of interdisciplinary and cross-sectoral research and knowledge transfer across all levels of IBD care.
Therapeutic advances in gastroenterology, 19:17562848261431187.
The Competence Network Inflammatory Bowel Diseases (Kompetenznetz Darmerkrankungen) was established in Germany in 1999 through a 10-year funding programme by the German Ministry of Education and Research. It was created to address the growing gap between the rising prevalence and therapeutic complexity of inflammatory bowel disease (IBD) and the fragmented care structures and isolated academic initiatives of the time. The network's continuing mission is to improve care for patients with Crohn's disease and ulcerative colitis by more closely integrating clinical practice, translational science and patient involvement. This review summarises the history, governance, registries, biobanking, clinical trials, educational programmes and collaborations of the Competence Network IBD. Over the past 25 years, the Competence Network IBD has established prospective national registries (e.g. RUN-CD, RUN-UC, VEDO-IBD and FilgoColitis), developed pragmatic real-world cohorts (TARGET and GeCer) and contributed to the UMBRELLA-IBD data warehouse of the Competence Network IBD in Germany. The network played a central role in creating the German IBD DNA collection and supported the Kiel University biobank, both of which link biospecimens with longitudinal clinical data to support genetic and microbiome research. It also conducts and coordinates multicentre clinical trials and has supported the development of the German evidence- and consensus-based IBD guidelines. With more than 800 members from university centres, community practices, nursing and patient organisations, it now provides a robust platform for research and knowledge transfer across all levels of IBD care. The Competence Network IBD demonstrates how long-term interdisciplinary and cross-sectoral collaboration can improve the management of chronic inflammatory diseases. By integrating research infrastructures with education and patient involvement, the network serves as a scalable and sustainable model for national and international collaboration in IBD.
Additional Links: PMID-41929401
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@article {pmid41929401,
year = {2026},
author = {Bokemeyer, B and Plachta-Danielzik, S and Helwig, U and Beuchert, P and Schreiber, S},
title = {Competence network inflammatory bowel diseases in Germany: 25 years of interdisciplinary and cross-sectoral research and knowledge transfer across all levels of IBD care.},
journal = {Therapeutic advances in gastroenterology},
volume = {19},
number = {},
pages = {17562848261431187},
pmid = {41929401},
issn = {1756-283X},
abstract = {The Competence Network Inflammatory Bowel Diseases (Kompetenznetz Darmerkrankungen) was established in Germany in 1999 through a 10-year funding programme by the German Ministry of Education and Research. It was created to address the growing gap between the rising prevalence and therapeutic complexity of inflammatory bowel disease (IBD) and the fragmented care structures and isolated academic initiatives of the time. The network's continuing mission is to improve care for patients with Crohn's disease and ulcerative colitis by more closely integrating clinical practice, translational science and patient involvement. This review summarises the history, governance, registries, biobanking, clinical trials, educational programmes and collaborations of the Competence Network IBD. Over the past 25 years, the Competence Network IBD has established prospective national registries (e.g. RUN-CD, RUN-UC, VEDO-IBD and FilgoColitis), developed pragmatic real-world cohorts (TARGET and GeCer) and contributed to the UMBRELLA-IBD data warehouse of the Competence Network IBD in Germany. The network played a central role in creating the German IBD DNA collection and supported the Kiel University biobank, both of which link biospecimens with longitudinal clinical data to support genetic and microbiome research. It also conducts and coordinates multicentre clinical trials and has supported the development of the German evidence- and consensus-based IBD guidelines. With more than 800 members from university centres, community practices, nursing and patient organisations, it now provides a robust platform for research and knowledge transfer across all levels of IBD care. The Competence Network IBD demonstrates how long-term interdisciplinary and cross-sectoral collaboration can improve the management of chronic inflammatory diseases. By integrating research infrastructures with education and patient involvement, the network serves as a scalable and sustainable model for national and international collaboration in IBD.},
}
RevDate: 2026-04-03
CmpDate: 2026-04-03
Effect of periodontal therapy on the oral microbiome and lung function: an intervention study.
Frontiers in cellular and infection microbiology, 16:1725666.
INTRODUCTION: The oral cavity harbors over 700 bacterial species, and disruption of this balance can lead to periodontitis, which has been linked to systemic conditions including respiratory disease.
METHODS: In this longitudinal clinical trial, 57 never-smoking adults with stage I-II periodontitis underwent full-mouth periodontal disinfection. Airway resistance and subgingival plaque sampling (analyzed by shotgun metagenomics) was measured at baseline and six weeks after therapy.
RESULTS: Periodontal treatment significantly improved clinical periodontal parameters, and was associated with reductions in airway resistance. Microbiome analysis showed a shift from periodontitis-associated taxa, including Prevotella, Porphyromonas, and Tannerella, toward health-associated species such as Actinomyces oris, and Rothia dentocariosa. Higher airway resistance was associated with a greater relative abundance of periodontitis-associated bacteria.
DISCUSSION: Together, findings suggest that periodontal therapy promotes a healthier oral microbiome and is associated with improved lung function in non-smokers with no prior lung disease.
Additional Links: PMID-41929449
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@article {pmid41929449,
year = {2026},
author = {Røsland, A and Amin, H and Lie, SA and Malinovschi, A and Bunæs, DF and Bertelsen, RJ},
title = {Effect of periodontal therapy on the oral microbiome and lung function: an intervention study.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1725666},
pmid = {41929449},
issn = {2235-2988},
mesh = {Humans ; *Microbiota ; Male ; *Periodontitis/therapy/microbiology ; Female ; Middle Aged ; *Mouth/microbiology ; Longitudinal Studies ; Adult ; Bacteria/classification/genetics/isolation & purification ; *Lung/physiology ; Metagenomics ; Aged ; },
abstract = {INTRODUCTION: The oral cavity harbors over 700 bacterial species, and disruption of this balance can lead to periodontitis, which has been linked to systemic conditions including respiratory disease.
METHODS: In this longitudinal clinical trial, 57 never-smoking adults with stage I-II periodontitis underwent full-mouth periodontal disinfection. Airway resistance and subgingival plaque sampling (analyzed by shotgun metagenomics) was measured at baseline and six weeks after therapy.
RESULTS: Periodontal treatment significantly improved clinical periodontal parameters, and was associated with reductions in airway resistance. Microbiome analysis showed a shift from periodontitis-associated taxa, including Prevotella, Porphyromonas, and Tannerella, toward health-associated species such as Actinomyces oris, and Rothia dentocariosa. Higher airway resistance was associated with a greater relative abundance of periodontitis-associated bacteria.
DISCUSSION: Together, findings suggest that periodontal therapy promotes a healthier oral microbiome and is associated with improved lung function in non-smokers with no prior lung disease.},
}
MeSH Terms:
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Humans
*Microbiota
Male
*Periodontitis/therapy/microbiology
Female
Middle Aged
*Mouth/microbiology
Longitudinal Studies
Adult
Bacteria/classification/genetics/isolation & purification
*Lung/physiology
Metagenomics
Aged
RevDate: 2026-04-03
CmpDate: 2026-04-03
Gut dysbiosis induces the development of asthenozoospermia through butanoate metabolism.
Frontiers in immunology, 17:1760881.
BACKGROUND: Asthenozoospermia is a leading cause of male infertility with a rising incidence. While gut dysbiosis is implicated in metabolic disease, its role in asthenozoospermia pathogenesis remains unclear.
MATERIALS AND METHODS: We conducted a case-control study comparing the fecal microbiomes of men with isolated asthenozoospermia (n=60) and healthy controls (n=60) using shotgun metagenomic sequencing. Causality was assessed by fecal microbiota transplantation (FMT) from patients or controls into germ-free male mice. Metabolic perturbations were profiled by untargeted serum metabolomics and targeted short-chain fatty acid (SCFA) quantification in humans, alongside untargeted testicular metabolomics and serum SCFAs in recipient mice.
RESULTS: Metagenomic analysis (LEfSe) identified species-level differences, with marked depletion of butyrate-producing taxa in asthenozoospermia, most notably the prototypical butyrate producer Faecalibacterium prausnitzii. The relative abundance of F. prausnitzii was significantly positively correlated with sperm motility and progressive motility, linking gut composition to sperm quality in asthenozoospermia. Untargeted serum metabolomics identified 39 differential metabolites; KEGG enrichment prioritized butanoate metabolism. Targeted SCFA profiling confirmed significantly lower serum butyrate in asthenozoospermia versus controls. In germ-free males, FMT with patient-derived microbiota reduced sperm motility and progressive motility and induced histopathological abnormalities, including decreased interstitial Leydig cells, loss and atrophy of select intratubular cells, and an increased proportion of abnormal seminiferous tubules. Following patient FMT, recipient mice exhibited significantly reduced serum butyrate; testicular metabolomics revealed distinct profiles with 140 key differential metabolites, again implicating butanoate metabolism. Mechanistically, reduced F. prausnitzii-derived butyrate might impair Leydig cell steroidogenesis via disrupted PPAR signaling.
CONCLUSIONS: Asthenozoospermia is associated with gut dysbiosis characterized by loss of butyrate-producing bacteria, systemic and testicular disturbances in butyrate metabolism, and microbiota-mediated transmission of impaired sperm quality. These findings implicate the gut-testis axis in asthenozoospermia pathogenesis and nominate butyrate metabolism as a potential therapeutic target.
Additional Links: PMID-41929479
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@article {pmid41929479,
year = {2026},
author = {Pan, Y and Li, B and Liu, L and Wang, Z and Liu, X},
title = {Gut dysbiosis induces the development of asthenozoospermia through butanoate metabolism.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1760881},
pmid = {41929479},
issn = {1664-3224},
mesh = {Male ; *Dysbiosis/complications/microbiology/metabolism ; Animals ; *Gastrointestinal Microbiome ; *Asthenozoospermia/metabolism/etiology/microbiology ; Humans ; Mice ; Case-Control Studies ; Fecal Microbiota Transplantation ; Adult ; Fatty Acids, Volatile/metabolism ; Butyrates/metabolism ; Sperm Motility ; Metabolomics ; Testis/metabolism ; },
abstract = {BACKGROUND: Asthenozoospermia is a leading cause of male infertility with a rising incidence. While gut dysbiosis is implicated in metabolic disease, its role in asthenozoospermia pathogenesis remains unclear.
MATERIALS AND METHODS: We conducted a case-control study comparing the fecal microbiomes of men with isolated asthenozoospermia (n=60) and healthy controls (n=60) using shotgun metagenomic sequencing. Causality was assessed by fecal microbiota transplantation (FMT) from patients or controls into germ-free male mice. Metabolic perturbations were profiled by untargeted serum metabolomics and targeted short-chain fatty acid (SCFA) quantification in humans, alongside untargeted testicular metabolomics and serum SCFAs in recipient mice.
RESULTS: Metagenomic analysis (LEfSe) identified species-level differences, with marked depletion of butyrate-producing taxa in asthenozoospermia, most notably the prototypical butyrate producer Faecalibacterium prausnitzii. The relative abundance of F. prausnitzii was significantly positively correlated with sperm motility and progressive motility, linking gut composition to sperm quality in asthenozoospermia. Untargeted serum metabolomics identified 39 differential metabolites; KEGG enrichment prioritized butanoate metabolism. Targeted SCFA profiling confirmed significantly lower serum butyrate in asthenozoospermia versus controls. In germ-free males, FMT with patient-derived microbiota reduced sperm motility and progressive motility and induced histopathological abnormalities, including decreased interstitial Leydig cells, loss and atrophy of select intratubular cells, and an increased proportion of abnormal seminiferous tubules. Following patient FMT, recipient mice exhibited significantly reduced serum butyrate; testicular metabolomics revealed distinct profiles with 140 key differential metabolites, again implicating butanoate metabolism. Mechanistically, reduced F. prausnitzii-derived butyrate might impair Leydig cell steroidogenesis via disrupted PPAR signaling.
CONCLUSIONS: Asthenozoospermia is associated with gut dysbiosis characterized by loss of butyrate-producing bacteria, systemic and testicular disturbances in butyrate metabolism, and microbiota-mediated transmission of impaired sperm quality. These findings implicate the gut-testis axis in asthenozoospermia pathogenesis and nominate butyrate metabolism as a potential therapeutic target.},
}
MeSH Terms:
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hide MeSH Terms
Male
*Dysbiosis/complications/microbiology/metabolism
Animals
*Gastrointestinal Microbiome
*Asthenozoospermia/metabolism/etiology/microbiology
Humans
Mice
Case-Control Studies
Fecal Microbiota Transplantation
Adult
Fatty Acids, Volatile/metabolism
Butyrates/metabolism
Sperm Motility
Metabolomics
Testis/metabolism
RevDate: 2026-04-03
CmpDate: 2026-04-03
Gut microbiota alliance to shape sceneries of familial Mediterranean fever: a scoping review detailing difference between children and adults.
Frontiers in immunology, 17:1814103.
Familial Mediterranean fever (FMF) is the most common monogenic autoinflammatory disease worldwide and a key-model to illustrate dysregulation of innate immunity, etiologically determined by pathogenic variants in the MEFV gene, encoding pyrin, leading to uncontrolled interleukin-1β and interleukin-18 release. Despite its genetic basis, FMF shows marked clinical heterogeneity in all-aged patients, mostly in children, suggesting a role of potential environmental modifiers which are far to be exactly unraveled. Recent medical literature has increasingly illuminated the importance of gut microbiota in maintaining overall health and immune functions, and its contribution has been claimed also to explain both FMF inflammatory activity and heterogeneous disease expression. This narrative review summarizes current evidence on the interaction between gut microbiota and FMF, with a specific focus on differences between children and adults. Pediatric studies dedicated to FMF have reported intestinal dysbiosis in terms of reduced microbial diversity and depletion of short-chain fatty acid-producing bacteria, with subsequent enrichment of pro-inflammatory taxa: such alteration could modulate pyrin-inflammasome activation and contribute to systemic inflammation, disease phenotype, and response to colchicine or to other drugs specifically used in colchicine-resistant FMF. Geographic and lifestyle factors may shape intestinal microbiota composition early in life, reinforcing the relevance of gut flora and confirming its activity as a crucial tessera to determine FMF sceneries, mostly in children, and a potential target for future add-on therapeutic strategies. In addition, colchicine therapy appears to partially remodel the gut microbiome, empowering a local beneficial anti-inflammatory microbial profile.
Additional Links: PMID-41929503
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@article {pmid41929503,
year = {2026},
author = {Pisa, CM and Verrone, A and Mazuy, M and Ientile, L and Rigante, D and Esposito, S},
title = {Gut microbiota alliance to shape sceneries of familial Mediterranean fever: a scoping review detailing difference between children and adults.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1814103},
pmid = {41929503},
issn = {1664-3224},
mesh = {Humans ; *Familial Mediterranean Fever/microbiology/immunology/drug therapy ; *Gastrointestinal Microbiome/immunology ; Child ; Adult ; Dysbiosis/immunology ; Colchicine/therapeutic use ; Age Factors ; Pyrin/genetics ; },
abstract = {Familial Mediterranean fever (FMF) is the most common monogenic autoinflammatory disease worldwide and a key-model to illustrate dysregulation of innate immunity, etiologically determined by pathogenic variants in the MEFV gene, encoding pyrin, leading to uncontrolled interleukin-1β and interleukin-18 release. Despite its genetic basis, FMF shows marked clinical heterogeneity in all-aged patients, mostly in children, suggesting a role of potential environmental modifiers which are far to be exactly unraveled. Recent medical literature has increasingly illuminated the importance of gut microbiota in maintaining overall health and immune functions, and its contribution has been claimed also to explain both FMF inflammatory activity and heterogeneous disease expression. This narrative review summarizes current evidence on the interaction between gut microbiota and FMF, with a specific focus on differences between children and adults. Pediatric studies dedicated to FMF have reported intestinal dysbiosis in terms of reduced microbial diversity and depletion of short-chain fatty acid-producing bacteria, with subsequent enrichment of pro-inflammatory taxa: such alteration could modulate pyrin-inflammasome activation and contribute to systemic inflammation, disease phenotype, and response to colchicine or to other drugs specifically used in colchicine-resistant FMF. Geographic and lifestyle factors may shape intestinal microbiota composition early in life, reinforcing the relevance of gut flora and confirming its activity as a crucial tessera to determine FMF sceneries, mostly in children, and a potential target for future add-on therapeutic strategies. In addition, colchicine therapy appears to partially remodel the gut microbiome, empowering a local beneficial anti-inflammatory microbial profile.},
}
MeSH Terms:
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Humans
*Familial Mediterranean Fever/microbiology/immunology/drug therapy
*Gastrointestinal Microbiome/immunology
Child
Adult
Dysbiosis/immunology
Colchicine/therapeutic use
Age Factors
Pyrin/genetics
RevDate: 2026-04-03
CmpDate: 2026-04-03
Multidimensional regulatory mechanisms and translational potential of epigenetic networks in the rheumatoid arthritis disease course.
Frontiers in immunology, 17:1792863.
Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic synovitis that may progress to irreversible joint destruction and disability, thereby substantially impairing quality of life. RA results from complex interactions among genetic predisposition, environmental exposures, and immune dysregulation; however, current therapies are not curative, and many patients continue to experience pain, morning stiffness, and recurrent inflammation. In recent years, epigenetic mechanisms have emerged as key modulators of RA heterogeneity and disease persistence. Reversible regulatory layers-including non-coding RNAs, RNA modifications, DNA methylation, histone modifications, and microbiota-host interactions-provide a conceptual framework linking environmental cues to cell-type-specific inflammatory programs. This review summarizes recent advances in the epigenetic regulation of RA and outlines six interconnected dimensions. (1) miRNA-mediated post-transcriptional regulation: dysregulated miRNAs reshape inflammatory circuits and promote synovial activation through regulatory hubs. (2) RNA m[6]A modification: aberrant m[6]A remodeling alters immune metabolism and inflammatory gene expression, thereby reinforcing pathogenic responses. (3) DNA methylation: genome-wide profiling of synovium reveals differentially methylated loci that may activate disease-relevant pathways. (4) Histone modification and chromatin remodeling: altered activity of histone-modifying enzymes (e.g., HDACs) modulates inflammatory transcriptional programs and may contribute to epigenetic memory. (5) Hypoxia-driven metabolic-epigenetic crosstalk: hypoxia-inducible factors (HIFs) coordinate metabolic adaptation and inflammatory amplification; for example, HIF-1α supports the FLSs under hypoxic conditions. (6) Microbiome-epigenome interactions: gut microbial metabolites (e.g., butyrate) regulate immune homeostasis, partly by promoting follicular regulatory T cell (TFR) differentiation and restraining inflammation. Collectively, these findings indicate that epigenetic networks exert multilevel control over RA pathogenesis and highlight translational opportunities for targeted epigenetic interventions, including RNA methylation modulators, DNA methyltransferase inhibitors, and histone deacetylase-directed strategies.
Additional Links: PMID-41929505
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@article {pmid41929505,
year = {2026},
author = {Zhang, Y and Xiao, X and Guo, J and Lei, X and Xiong, W and Wang, S and He, Y and Lei, C and Hu, X},
title = {Multidimensional regulatory mechanisms and translational potential of epigenetic networks in the rheumatoid arthritis disease course.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1792863},
pmid = {41929505},
issn = {1664-3224},
mesh = {Humans ; *Arthritis, Rheumatoid/genetics/immunology/metabolism ; *Epigenesis, Genetic ; MicroRNAs/genetics ; DNA Methylation ; Animals ; *Gene Regulatory Networks ; },
abstract = {Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic synovitis that may progress to irreversible joint destruction and disability, thereby substantially impairing quality of life. RA results from complex interactions among genetic predisposition, environmental exposures, and immune dysregulation; however, current therapies are not curative, and many patients continue to experience pain, morning stiffness, and recurrent inflammation. In recent years, epigenetic mechanisms have emerged as key modulators of RA heterogeneity and disease persistence. Reversible regulatory layers-including non-coding RNAs, RNA modifications, DNA methylation, histone modifications, and microbiota-host interactions-provide a conceptual framework linking environmental cues to cell-type-specific inflammatory programs. This review summarizes recent advances in the epigenetic regulation of RA and outlines six interconnected dimensions. (1) miRNA-mediated post-transcriptional regulation: dysregulated miRNAs reshape inflammatory circuits and promote synovial activation through regulatory hubs. (2) RNA m[6]A modification: aberrant m[6]A remodeling alters immune metabolism and inflammatory gene expression, thereby reinforcing pathogenic responses. (3) DNA methylation: genome-wide profiling of synovium reveals differentially methylated loci that may activate disease-relevant pathways. (4) Histone modification and chromatin remodeling: altered activity of histone-modifying enzymes (e.g., HDACs) modulates inflammatory transcriptional programs and may contribute to epigenetic memory. (5) Hypoxia-driven metabolic-epigenetic crosstalk: hypoxia-inducible factors (HIFs) coordinate metabolic adaptation and inflammatory amplification; for example, HIF-1α supports the FLSs under hypoxic conditions. (6) Microbiome-epigenome interactions: gut microbial metabolites (e.g., butyrate) regulate immune homeostasis, partly by promoting follicular regulatory T cell (TFR) differentiation and restraining inflammation. Collectively, these findings indicate that epigenetic networks exert multilevel control over RA pathogenesis and highlight translational opportunities for targeted epigenetic interventions, including RNA methylation modulators, DNA methyltransferase inhibitors, and histone deacetylase-directed strategies.},
}
MeSH Terms:
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Humans
*Arthritis, Rheumatoid/genetics/immunology/metabolism
*Epigenesis, Genetic
MicroRNAs/genetics
DNA Methylation
Animals
*Gene Regulatory Networks
RevDate: 2026-04-01
The phylum Fusobacteriota is associated with CRC-specific mortality: Results from the Translational Research Program in Cancer Differences across Populations.
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology pii:780784 [Epub ahead of print].
BACKGROUND: The microbiome is an important component of the tumor microenvironment implicated in colorectal cancer (CRC). However, its relationship with CRC-specific mortality remains unclear.
METHODS: We included 581 participants with CRC (167 African American, 176 Alaska Native, 118 Hispanic, 120 non-Hispanic White) from the Translational Research Program in Cancer Differences across Populations (TRPCDP). We sequenced the V4 region of the 16S rRNA bacterial gene using DNA extracted from formalin-fixed paraffin embedded tumors. 204 participants died of CRC and 377 did not die of CRC. Participants who died of CRC were matched to participants who did not die of CRC during follow-up by age, sex, tumor site, tumor stage, year of diagnosis, and population group. Logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CIs) for associations between bacterial presence with CRC-specific mortality, adjusting for matching factors and tissue macrodissection status.
RESULTS: Individuals who died from CRC were 1.71 times as likely to have bacteria from the Fusobacteriota phylum present in their tumors (OR=1.71, 95% CI: 1.19-2.47). Associations with Fusobacteriota were strongest among African American participants (OR=2.36, 95% CI: 1.14-4.99) compared to other populations, however this different was not statistically significant (OR range = 1.05-1.38, Pinteraction = 0.697). Candidate pathways of pyruvate fermentation to acetate and lactate II and peptidoglycan biosynthesis I were associated with higher odds of CRC death.
CONCLUSIONS: Fusobacteriota was significantly associated with CRC-specific mortality with noted differences across populations.
IMPACT: This finding highlights the tumor microbiome as a candidate for further investigation into CRC outcome disparities.
Additional Links: PMID-41920180
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PubMed:
Citation:
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@article {pmid41920180,
year = {2026},
author = {Thomas, CE and Loroña, NC and LaBrie, SD and Curtis, KR and Yin, H and Ma, N and Randolph, TW and Qu, C and Huyghe, JR and Thomas, S and Hsu, L and Koehne, AL and Nayemi, S and Ammar, H and Kahsai, OJ and Redwood, D and Li, CI and Li, L and Peters, U and Figueiredo, JC and Thomas, TK and Phipps, AI and Hullar, MAJ},
title = {The phylum Fusobacteriota is associated with CRC-specific mortality: Results from the Translational Research Program in Cancer Differences across Populations.},
journal = {Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology},
volume = {},
number = {},
pages = {},
doi = {10.1158/1055-9965.EPI-25-1580},
pmid = {41920180},
issn = {1538-7755},
abstract = {BACKGROUND: The microbiome is an important component of the tumor microenvironment implicated in colorectal cancer (CRC). However, its relationship with CRC-specific mortality remains unclear.
METHODS: We included 581 participants with CRC (167 African American, 176 Alaska Native, 118 Hispanic, 120 non-Hispanic White) from the Translational Research Program in Cancer Differences across Populations (TRPCDP). We sequenced the V4 region of the 16S rRNA bacterial gene using DNA extracted from formalin-fixed paraffin embedded tumors. 204 participants died of CRC and 377 did not die of CRC. Participants who died of CRC were matched to participants who did not die of CRC during follow-up by age, sex, tumor site, tumor stage, year of diagnosis, and population group. Logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CIs) for associations between bacterial presence with CRC-specific mortality, adjusting for matching factors and tissue macrodissection status.
RESULTS: Individuals who died from CRC were 1.71 times as likely to have bacteria from the Fusobacteriota phylum present in their tumors (OR=1.71, 95% CI: 1.19-2.47). Associations with Fusobacteriota were strongest among African American participants (OR=2.36, 95% CI: 1.14-4.99) compared to other populations, however this different was not statistically significant (OR range = 1.05-1.38, Pinteraction = 0.697). Candidate pathways of pyruvate fermentation to acetate and lactate II and peptidoglycan biosynthesis I were associated with higher odds of CRC death.
CONCLUSIONS: Fusobacteriota was significantly associated with CRC-specific mortality with noted differences across populations.
IMPACT: This finding highlights the tumor microbiome as a candidate for further investigation into CRC outcome disparities.},
}
RevDate: 2026-04-01
Intake of Fiber From Different Food Sources and Type 2 Diabetes Risk: An Integrated Analysis of Epidemiological and Multiomic Data.
Diabetes care pii:164656 [Epub ahead of print].
OBJECTIVE: To examine the association between fiber from various food sources and type 2 diabetes (T2D) risk, as well as the molecular profiles involved.
RESEARCH DESIGN AND METHODS: Using data from three large prospective U.S. cohorts comprising 195,222 participants observed for up to 34 years, we evaluated the association between fiber from various food sources and T2D risk. We also assessed the association between fiber intake, plasma metabolic biomarkers, and a metabolomic profile indicative of T2D risk. Additionally, we examined gut microbial features related to fiber intake and the T2D metabolomic profile.
RESULTS: During follow-up, we documented 18,369 incident T2D cases. Higher intakes of total fiber (hazard ratio [HR] comparing extreme quintiles 0.88; 95% CI 0.82, 0.94), cereal fiber (HR 0.77; 95% CI 0.73, 0.82), and fruit fiber (HR 0.82; 95% CI 0.78, 0.87) were each associated with a lower T2D risk. Greater intakes of total fiber, cereal fiber, and fruit fiber, but not vegetable fiber, were linked to more favorable plasma profiles of insulinemic, lipid, and inflammatory biomarkers and a metabolomic profile indicative of a lower T2D risk. We also identified multiple gut microbial species, such as Faecalibacterium prausnitzii, Ruminococcus lactaris, and Gemmiger formicilis, along with relevant butyric acid-producing enzymes, all of which were associated with higher fruit fiber intake and a metabolomic profile indicating a lower likelihood of T2D development.
CONCLUSIONS: Higher intakes of total, cereal, and fruit fiber are associated with a lower risk of T2D and a more favorable metabolic profile, with the gut microbiome potentially contributing to the beneficial association of fruit fiber.
Additional Links: PMID-41920710
Publisher:
PubMed:
Citation:
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@article {pmid41920710,
year = {2026},
author = {Wan, Y and Alessa, HB and Guasch-Ferré, M and Tobias, DK and Lee, KH and Manson, JE and Willett, WC and Sun, Q and Hu, FB},
title = {Intake of Fiber From Different Food Sources and Type 2 Diabetes Risk: An Integrated Analysis of Epidemiological and Multiomic Data.},
journal = {Diabetes care},
volume = {},
number = {},
pages = {},
doi = {10.2337/dc25-2957},
pmid = {41920710},
issn = {1935-5548},
support = {/NH/NIH HHS/United States ; //Novo Nordisk Foundation/ ; },
abstract = {OBJECTIVE: To examine the association between fiber from various food sources and type 2 diabetes (T2D) risk, as well as the molecular profiles involved.
RESEARCH DESIGN AND METHODS: Using data from three large prospective U.S. cohorts comprising 195,222 participants observed for up to 34 years, we evaluated the association between fiber from various food sources and T2D risk. We also assessed the association between fiber intake, plasma metabolic biomarkers, and a metabolomic profile indicative of T2D risk. Additionally, we examined gut microbial features related to fiber intake and the T2D metabolomic profile.
RESULTS: During follow-up, we documented 18,369 incident T2D cases. Higher intakes of total fiber (hazard ratio [HR] comparing extreme quintiles 0.88; 95% CI 0.82, 0.94), cereal fiber (HR 0.77; 95% CI 0.73, 0.82), and fruit fiber (HR 0.82; 95% CI 0.78, 0.87) were each associated with a lower T2D risk. Greater intakes of total fiber, cereal fiber, and fruit fiber, but not vegetable fiber, were linked to more favorable plasma profiles of insulinemic, lipid, and inflammatory biomarkers and a metabolomic profile indicative of a lower T2D risk. We also identified multiple gut microbial species, such as Faecalibacterium prausnitzii, Ruminococcus lactaris, and Gemmiger formicilis, along with relevant butyric acid-producing enzymes, all of which were associated with higher fruit fiber intake and a metabolomic profile indicating a lower likelihood of T2D development.
CONCLUSIONS: Higher intakes of total, cereal, and fruit fiber are associated with a lower risk of T2D and a more favorable metabolic profile, with the gut microbiome potentially contributing to the beneficial association of fruit fiber.},
}
RevDate: 2026-04-01
Metabolism by ex vivo cultures of human stool increases the activity of coumarin, a widespread antioxidant from herbal supplements.
Cell reports, 45(4):117199 pii:S2211-1247(26)00277-9 [Epub ahead of print].
Host and microbiome metabolism of bioactive compounds can alter their efficacy. Herbal supplements contain many bioactive compounds, but their metabolism by gut microbes and the effects on efficacy remain poorly understood. To gain clarity, we investigate coumarin, an antioxidant in food, cosmetics, and supplements and a scaffold for diverse bioactive compounds. In this study, we characterize coumarin metabolism by the human gut microbiome, which produces 3,4-dihydrocoumarin and melilotic acid. We characterize this pathway in the culturable microbiota from 9 stool donors with liquid chromatography-tandem mass spectrometry (LC-MS/MS) metabolomics and microbiome profiling. We discover that 17 microbiome species metabolize coumarin and that the E. coli gene nemA is necessary for coumarin reduction. In antioxidant assays, melilotic acid is more potent than coumarin, suggesting that this pathway may impact bioactivity, with possible contributions to supplement efficacy. Further characterization may provide insights on the metabolic fate of coumarins and contributions of the microbiome to their efficacy.
Additional Links: PMID-41920740
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PubMed:
Citation:
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@article {pmid41920740,
year = {2026},
author = {Mingolelli, G and Subedi, P and Bonitatibus, S and Johnson, JJ and Henke, M},
title = {Metabolism by ex vivo cultures of human stool increases the activity of coumarin, a widespread antioxidant from herbal supplements.},
journal = {Cell reports},
volume = {45},
number = {4},
pages = {117199},
doi = {10.1016/j.celrep.2026.117199},
pmid = {41920740},
issn = {2211-1247},
abstract = {Host and microbiome metabolism of bioactive compounds can alter their efficacy. Herbal supplements contain many bioactive compounds, but their metabolism by gut microbes and the effects on efficacy remain poorly understood. To gain clarity, we investigate coumarin, an antioxidant in food, cosmetics, and supplements and a scaffold for diverse bioactive compounds. In this study, we characterize coumarin metabolism by the human gut microbiome, which produces 3,4-dihydrocoumarin and melilotic acid. We characterize this pathway in the culturable microbiota from 9 stool donors with liquid chromatography-tandem mass spectrometry (LC-MS/MS) metabolomics and microbiome profiling. We discover that 17 microbiome species metabolize coumarin and that the E. coli gene nemA is necessary for coumarin reduction. In antioxidant assays, melilotic acid is more potent than coumarin, suggesting that this pathway may impact bioactivity, with possible contributions to supplement efficacy. Further characterization may provide insights on the metabolic fate of coumarins and contributions of the microbiome to their efficacy.},
}
RevDate: 2026-04-01
Human Milk Oligosaccharides Support Coordinated Microbiome and Immune Development and Function in Infancy.
Annals of nutrition & metabolism pii:000549867 [Epub ahead of print].
BACKGROUND: Human milk contains functional ingredients that shape the microbiome and immune development of infants. Human milk oligosaccharides (HMOs) are among the largest and most diverse components of human milk. Their heterogeneity enables unique structure-function relationships that contribute to their physiological effects. This narrative review will focus on how HMOs directly and indirectly protect the infant from pathogens and educate the immune system.
SUMMARY: Preclinical research, observational studies, and intervention trials demonstrate that HMOs provide multilayer modulation of host defense and immune development. HMOs are soluble glycans that are acetylated, sialylated, or fucosylated, which mediate their interactions with viruses and bacteria to reduce infectivity. Additionally, HMOs enhance pathogen exclusion by promoting intestinal cell maturation, mucin production, and barrier function. Moreover, HMOs directly interact with immune cells through binding to carbohydrate recognition domains. HMOs promote the growth of beneficial bacteria, particularly Bifidobacterium longum subspecies infantis, which is also immunomodulatory. Lastly, HMOs are fermented to short-chain fatty acids, which lower the pH of the intestinal lumen, providing further antimicrobial defense.
KEY MESSAGES: Breastfed infants have a reduced risk of infectious disease compared to non-breastfed infants, attributable in part to the high concentration and structural diversity of HMOs. Clinical trials using formulas supplemented with synthetic human-identical milk oligosaccharides (HiMOs) have demonstrated benefits to adaptive and innate immunity, reduced infections, increased bifidobacteria, and reduced pathogenic bacteria. These benefits are amplified in formulas containing higher concentrations and greater varieties of HiMOs. However, the clinical benefit of routinely supplementing term infant formulae with HiMOs remains unsettled due to variability across existing clinical trials. Further research in healthy infants focused on short- and long-term immune outcomes is needed.
Additional Links: PMID-41920780
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PubMed:
Citation:
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@article {pmid41920780,
year = {2026},
author = {Donovan, SM},
title = {Human Milk Oligosaccharides Support Coordinated Microbiome and Immune Development and Function in Infancy.},
journal = {Annals of nutrition & metabolism},
volume = {},
number = {},
pages = {1-15},
doi = {10.1159/000549867},
pmid = {41920780},
issn = {1421-9697},
abstract = {BACKGROUND: Human milk contains functional ingredients that shape the microbiome and immune development of infants. Human milk oligosaccharides (HMOs) are among the largest and most diverse components of human milk. Their heterogeneity enables unique structure-function relationships that contribute to their physiological effects. This narrative review will focus on how HMOs directly and indirectly protect the infant from pathogens and educate the immune system.
SUMMARY: Preclinical research, observational studies, and intervention trials demonstrate that HMOs provide multilayer modulation of host defense and immune development. HMOs are soluble glycans that are acetylated, sialylated, or fucosylated, which mediate their interactions with viruses and bacteria to reduce infectivity. Additionally, HMOs enhance pathogen exclusion by promoting intestinal cell maturation, mucin production, and barrier function. Moreover, HMOs directly interact with immune cells through binding to carbohydrate recognition domains. HMOs promote the growth of beneficial bacteria, particularly Bifidobacterium longum subspecies infantis, which is also immunomodulatory. Lastly, HMOs are fermented to short-chain fatty acids, which lower the pH of the intestinal lumen, providing further antimicrobial defense.
KEY MESSAGES: Breastfed infants have a reduced risk of infectious disease compared to non-breastfed infants, attributable in part to the high concentration and structural diversity of HMOs. Clinical trials using formulas supplemented with synthetic human-identical milk oligosaccharides (HiMOs) have demonstrated benefits to adaptive and innate immunity, reduced infections, increased bifidobacteria, and reduced pathogenic bacteria. These benefits are amplified in formulas containing higher concentrations and greater varieties of HiMOs. However, the clinical benefit of routinely supplementing term infant formulae with HiMOs remains unsettled due to variability across existing clinical trials. Further research in healthy infants focused on short- and long-term immune outcomes is needed.},
}
RevDate: 2026-04-01
Multidimensional scaling informed by F-statistic: Visualizing grouped microbiome data with inference.
PLoS computational biology, 22(4):e1014102 pii:PCOMPBIOL-D-25-00623 [Epub ahead of print].
Multidimensional scaling (MDS) is a widely used dimensionality reduction technique in microbial ecology data analysis that captures the multivariate structure of the data while preserving pairwise distances between samples. While improvements in MDS have enhanced the ability to reveal group-specific data patterns, these MDS-based methods require prior assumptions for inference, limiting their application in general microbiome analysis. In this study, we introduce a new MDS-based ordination method, "F-informed MDS," which configures the data distribution based on the F-statistic, the ratio of dispersion between groups sharing common and different characteristics. Using semisynthetic datasets, we demonstrate that the proposed method is robust to hyperparameter selection while maintaining statistical significance throughout the ordination process. Various quality metrics for evaluating dimensionality reduction confirm that F-informed MDS is comparable to state-of-the-art methods in preserving both local and global data structures. Its application to a diatom-associated bacterial community suggests the role of this new method in interpreting the community's response to the host. Our approach offers a well-founded refinement of MDS that aligns with statistical test results, which can be beneficial for broader multidimensional data analyses in microbiology and ecology. This new visualization tool can be incorporated into standard microbiome data analyses.
Additional Links: PMID-41920852
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PubMed:
Citation:
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@article {pmid41920852,
year = {2026},
author = {Kim, H and Kim, S and Kimbrel, JA and Morris, MM and Mayali, X and Buie, CR},
title = {Multidimensional scaling informed by F-statistic: Visualizing grouped microbiome data with inference.},
journal = {PLoS computational biology},
volume = {22},
number = {4},
pages = {e1014102},
doi = {10.1371/journal.pcbi.1014102},
pmid = {41920852},
issn = {1553-7358},
abstract = {Multidimensional scaling (MDS) is a widely used dimensionality reduction technique in microbial ecology data analysis that captures the multivariate structure of the data while preserving pairwise distances between samples. While improvements in MDS have enhanced the ability to reveal group-specific data patterns, these MDS-based methods require prior assumptions for inference, limiting their application in general microbiome analysis. In this study, we introduce a new MDS-based ordination method, "F-informed MDS," which configures the data distribution based on the F-statistic, the ratio of dispersion between groups sharing common and different characteristics. Using semisynthetic datasets, we demonstrate that the proposed method is robust to hyperparameter selection while maintaining statistical significance throughout the ordination process. Various quality metrics for evaluating dimensionality reduction confirm that F-informed MDS is comparable to state-of-the-art methods in preserving both local and global data structures. Its application to a diatom-associated bacterial community suggests the role of this new method in interpreting the community's response to the host. Our approach offers a well-founded refinement of MDS that aligns with statistical test results, which can be beneficial for broader multidimensional data analyses in microbiology and ecology. This new visualization tool can be incorporated into standard microbiome data analyses.},
}
RevDate: 2026-04-01
Investigating the Link between the Intestinal Microbiome and Th17/Treg Dysregulation in Hashimoto's Thyroiditis, and the Therapeutic Potential of Vitamin D.
Journal of the American Nutrition Association [Epub ahead of print].
Objective:Autoimmune disease (AD) has become a leading cause of illness in the twenty-first century, with autoimmune thyroid disease at the forefront of these conditions. Hashimoto's thyroiditis (HT) shares many features with other ADs, including associations with gastrointestinal symptoms linked to intestinal dysbiosis (ID). However, the pathogenesis of HT remains incompletely understood, particularly the role of specific T cell lymphocyte activity. The primary objective of this review was to investigate links between ID and HT pathogenesis, focusing on the relationship between a specific cluster of differentiation 4 (CD4) T cell subsets including T helper 17 (Th17) and regulatory T cells (Treg). A secondary aim was to explore whether vitamin D supplementation may serve as a viable intervention in managing HT, given existing research demonstrating links between Vitamin D status, HT pathogenesis and ID. Methods:A systematic literature search was conducted in PubMed using predefined inclusion/exclusion criteria across three tranches. A search of the review literature pertaining to thyroid autoimmunity, HT and the intestinal microbiome identified 21 papers for inclusion. A mechanistic literature search covering animal, in vitro and human studies on HT, autoimmunity, ID, intestinal microbiota, intestinal permeability (IP) and Th17 yielded 43 papers. A final search of human studies examining vitamin D status or supplementation in relation to ID, IP, Th17 and interleukin (IL)-17 identified 45 relevant papers. Accepted studies were critically appraised and synthesized in a narrative analysis.Results:Evidence across the included studies suggests an association between ID and pathogenesis of HT. Increased IP and alterations in Th17/Treg balance emerged as key contributing mechanisms. Vitamin D status was also associated with immune modulation, particularly involving Th17 activity, and was strongly linked to both ID and HT pathogenesis.Conclusions:ID may play a contributory role in HT pathogenesis through immune modulation involving CD4+ T cell subsets. Vitamin D supplementation demonstrates potential as an adjunctive strategy; however, further targeted human studies are required to clarify causality and therapeutic efficacy.
Additional Links: PMID-41920977
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@article {pmid41920977,
year = {2026},
author = {Flower, S and Gruvstad Melén, A and Seidler, K},
title = {Investigating the Link between the Intestinal Microbiome and Th17/Treg Dysregulation in Hashimoto's Thyroiditis, and the Therapeutic Potential of Vitamin D.},
journal = {Journal of the American Nutrition Association},
volume = {},
number = {},
pages = {1-19},
doi = {10.1080/27697061.2026.2644894},
pmid = {41920977},
issn = {2769-707X},
abstract = {Objective:Autoimmune disease (AD) has become a leading cause of illness in the twenty-first century, with autoimmune thyroid disease at the forefront of these conditions. Hashimoto's thyroiditis (HT) shares many features with other ADs, including associations with gastrointestinal symptoms linked to intestinal dysbiosis (ID). However, the pathogenesis of HT remains incompletely understood, particularly the role of specific T cell lymphocyte activity. The primary objective of this review was to investigate links between ID and HT pathogenesis, focusing on the relationship between a specific cluster of differentiation 4 (CD4) T cell subsets including T helper 17 (Th17) and regulatory T cells (Treg). A secondary aim was to explore whether vitamin D supplementation may serve as a viable intervention in managing HT, given existing research demonstrating links between Vitamin D status, HT pathogenesis and ID. Methods:A systematic literature search was conducted in PubMed using predefined inclusion/exclusion criteria across three tranches. A search of the review literature pertaining to thyroid autoimmunity, HT and the intestinal microbiome identified 21 papers for inclusion. A mechanistic literature search covering animal, in vitro and human studies on HT, autoimmunity, ID, intestinal microbiota, intestinal permeability (IP) and Th17 yielded 43 papers. A final search of human studies examining vitamin D status or supplementation in relation to ID, IP, Th17 and interleukin (IL)-17 identified 45 relevant papers. Accepted studies were critically appraised and synthesized in a narrative analysis.Results:Evidence across the included studies suggests an association between ID and pathogenesis of HT. Increased IP and alterations in Th17/Treg balance emerged as key contributing mechanisms. Vitamin D status was also associated with immune modulation, particularly involving Th17 activity, and was strongly linked to both ID and HT pathogenesis.Conclusions:ID may play a contributory role in HT pathogenesis through immune modulation involving CD4+ T cell subsets. Vitamin D supplementation demonstrates potential as an adjunctive strategy; however, further targeted human studies are required to clarify causality and therapeutic efficacy.},
}
RevDate: 2026-04-01
Biomarker-guided immunotherapy in gastric cancer: current insights and future perspectives.
Cancer treatment reviews, 145:103124 pii:S0305-7372(26)00038-1 [Epub ahead of print].
Gastric and gastroesophageal junction adenocarcinoma (GC) is a biologically challenging malignancy associated with suboptimal clinical outcomes due to limited effective treatment options. The recent incorporation of immune checkpoint inhibitors (ICIs) into therapeutic algorithms has improved the clinical prospects of subsets of GC patients. However, responses to anti-PD-1/PD-L1 agents remain highly heterogeneous, with only some patients deriving long-term benefits. This variability highlights the importance of identifying optimal biomarkers to enhance patient selection, thereby enabling tailored immunotherapy strategies. Whereas microsatellite instability has demonstrated a potent capacity for predicting immunotherapy benefits in GC, other predictive biomarkers, such as PD-L1 expression, remain suboptimal. Advances in gene expression and epigenetic profiling, liquid biopsy approaches, gut microbiome characterization, and artificial intelligence-driven multimodal algorithms applied to multi-omics or digital pathology are key drivers for the comprehensive characterization of the GC tumour microenvironment (TME), which could be used for better treatment selection. Similarly, elucidating the complex tumour-immune interplay with these technologies will be crucial for the success of novel immunotherapeutic approaches under clinical development, by evaluating alternative immune pathways alone or in combination with current actionable targets of GC. The current review aims to give an overview of the current immunotherapeutic landscape in GC, evaluate standard-of-care and emerging biomarkers of immunotherapy response, and discuss the translational potential of incorporating multi-omic and AI-derived biomarkers into biomarker-enriched clinical decision-making frameworks.
Additional Links: PMID-41921305
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PubMed:
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@article {pmid41921305,
year = {2026},
author = {Teixidó Mulet, M and Veas Rodriguez, J and Terán, E and Piñol, M and Vilardell, F and Iglesias, M and Hierro, C and Calvo, M and Matias-Guiu, X and Salud, A and Tabernero, J and Montal, R},
title = {Biomarker-guided immunotherapy in gastric cancer: current insights and future perspectives.},
journal = {Cancer treatment reviews},
volume = {145},
number = {},
pages = {103124},
doi = {10.1016/j.ctrv.2026.103124},
pmid = {41921305},
issn = {1532-1967},
abstract = {Gastric and gastroesophageal junction adenocarcinoma (GC) is a biologically challenging malignancy associated with suboptimal clinical outcomes due to limited effective treatment options. The recent incorporation of immune checkpoint inhibitors (ICIs) into therapeutic algorithms has improved the clinical prospects of subsets of GC patients. However, responses to anti-PD-1/PD-L1 agents remain highly heterogeneous, with only some patients deriving long-term benefits. This variability highlights the importance of identifying optimal biomarkers to enhance patient selection, thereby enabling tailored immunotherapy strategies. Whereas microsatellite instability has demonstrated a potent capacity for predicting immunotherapy benefits in GC, other predictive biomarkers, such as PD-L1 expression, remain suboptimal. Advances in gene expression and epigenetic profiling, liquid biopsy approaches, gut microbiome characterization, and artificial intelligence-driven multimodal algorithms applied to multi-omics or digital pathology are key drivers for the comprehensive characterization of the GC tumour microenvironment (TME), which could be used for better treatment selection. Similarly, elucidating the complex tumour-immune interplay with these technologies will be crucial for the success of novel immunotherapeutic approaches under clinical development, by evaluating alternative immune pathways alone or in combination with current actionable targets of GC. The current review aims to give an overview of the current immunotherapeutic landscape in GC, evaluate standard-of-care and emerging biomarkers of immunotherapy response, and discuss the translational potential of incorporating multi-omic and AI-derived biomarkers into biomarker-enriched clinical decision-making frameworks.},
}
RevDate: 2026-04-01
Deciphering pharmaceutical resistance in sulfur-driven autotrophic denitrification: an integrated multi-omics artificial intelligence-driven structural biology approach.
Water research, 298:125834 pii:S0043-1354(26)00516-6 [Epub ahead of print].
Sulfur-driven autotrophic denitrification (SdAD) is a promising low-carbon technology for nitrogen removal; however, its stability and adaptive mechanisms under pharmaceutical stress remain poorly understood. In this study, ibuprofen (IBU) was used as a representative pharmaceutical to investigate the response of an SdAD system. Throughout the 210-day operational period, the system demonstrated exceptional functional robustness, maintaining high sulfide (97.46 ± 3.18%) and inorganic nitrogen (99.17 ± 4.34%) removal efficiencies across IBU concentrations ranging from environmentally relevant levels to elevated shock loads (100-2000 μg/L). Underpinning this macroscopic stability, community-level analyses revealed that instead of succumbing to inhibition, the SdAD microbiome actively reorganized its composition and topological structure to accommodate the selective pressure. This adaptation was characterized by enhanced microbial diversity and stress-induced network modularity (particularly at 100-500 μg/L), alongside strengthened cooperative interactions between sulfur-oxidizing bacteria and denitrifiers. To unravel the specific molecular drivers of this resilience, we integrated AlphaFold-based structural modeling with machine learning-coupled molecular docking. This enabled us to resolve the three-dimensional structure of sulfide: quinone oxidoreductase (SQR) and perform the first structure-function analysis of SQR within an SdAD context under pharmaceutical stress, revealing that arginine residues serve as key interaction hotspots for IBU binding. Consistent with this binding mechanism, multi-omics data further corroborated a systemic adjustment involving the coordinated regulation of sulfur oxidation genes and the transcriptional upregulation of arginine biosynthesis pathways. Overall, these findings shed light on how the SdAD community mitigates pharmaceutical toxicity through a multi-tiered strategy involving ecological network reorganization and metabolic compensation. Methodologically, this work highlights the value of integrating artificial intelligence-driven structural biology with multi-omics analyses to decode the mechanisms of contaminant resistance in biological wastewater treatment systems.
Additional Links: PMID-41921320
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@article {pmid41921320,
year = {2026},
author = {Huang, DQ and Zhou, S and Jia, Y and Yan, Y and Lu, H},
title = {Deciphering pharmaceutical resistance in sulfur-driven autotrophic denitrification: an integrated multi-omics artificial intelligence-driven structural biology approach.},
journal = {Water research},
volume = {298},
number = {},
pages = {125834},
doi = {10.1016/j.watres.2026.125834},
pmid = {41921320},
issn = {1879-2448},
abstract = {Sulfur-driven autotrophic denitrification (SdAD) is a promising low-carbon technology for nitrogen removal; however, its stability and adaptive mechanisms under pharmaceutical stress remain poorly understood. In this study, ibuprofen (IBU) was used as a representative pharmaceutical to investigate the response of an SdAD system. Throughout the 210-day operational period, the system demonstrated exceptional functional robustness, maintaining high sulfide (97.46 ± 3.18%) and inorganic nitrogen (99.17 ± 4.34%) removal efficiencies across IBU concentrations ranging from environmentally relevant levels to elevated shock loads (100-2000 μg/L). Underpinning this macroscopic stability, community-level analyses revealed that instead of succumbing to inhibition, the SdAD microbiome actively reorganized its composition and topological structure to accommodate the selective pressure. This adaptation was characterized by enhanced microbial diversity and stress-induced network modularity (particularly at 100-500 μg/L), alongside strengthened cooperative interactions between sulfur-oxidizing bacteria and denitrifiers. To unravel the specific molecular drivers of this resilience, we integrated AlphaFold-based structural modeling with machine learning-coupled molecular docking. This enabled us to resolve the three-dimensional structure of sulfide: quinone oxidoreductase (SQR) and perform the first structure-function analysis of SQR within an SdAD context under pharmaceutical stress, revealing that arginine residues serve as key interaction hotspots for IBU binding. Consistent with this binding mechanism, multi-omics data further corroborated a systemic adjustment involving the coordinated regulation of sulfur oxidation genes and the transcriptional upregulation of arginine biosynthesis pathways. Overall, these findings shed light on how the SdAD community mitigates pharmaceutical toxicity through a multi-tiered strategy involving ecological network reorganization and metabolic compensation. Methodologically, this work highlights the value of integrating artificial intelligence-driven structural biology with multi-omics analyses to decode the mechanisms of contaminant resistance in biological wastewater treatment systems.},
}
RevDate: 2026-04-01
Gene-centric analysis of Raskinella chloraquaticus reveals a functionally conserved taxonomic group in global drinking water distribution systems.
Water research, 298:125784 pii:S0043-1354(26)00466-5 [Epub ahead of print].
A recent metagenomic survey of drinking water systems revealed that a highly prevalent and dominant uncultured bacterial genus (Raskinella) was represented globally by a single species (Raskinella chloraquaticus). R. chloraquaticus comprises of two sub-species groups, Lineages 1 and 2, the former representing a globally prevalent genomovar. The objective of this study was to perform comparative analysis of the gene content of R. chloraquaticus to characterize the gene-level diversity and determine factors shaping the diversity of this species. Pangenome analysis revealed that R. chloraquaticus possesses a core set of genes that constitute a major portion (87.74%) of the known gene content of the genome. Furthermore, most of the gene diversity of R. chloraquaticus is associated with Lineage 2 organisms, which consists of at least four distinct genomovars. Lineage 1 organisms consist of a higher proportion of identical genes than would have been expected if changes primarily occurred through random mutations and thus is potentially indicative of recombination. In contrast, Lineage 2 organisms appear to have emerged through random mutations and display stronger geographic preference. These results indicate that homologous recombination and geographic isolation likely shape the genetic repertoire of R. chloraquaticus. Further, the high level of gene conservation in R. chloraquaticus may be reflective of highly selective environment in drinking water systems. Thus, R. chloraquaticus may represent a model organism to probe selective pressures shaping the drinking water microbiome.
Additional Links: PMID-41921321
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@article {pmid41921321,
year = {2026},
author = {Sudarshan, AS and Konstantinidis, KT and Pinto, AJ},
title = {Gene-centric analysis of Raskinella chloraquaticus reveals a functionally conserved taxonomic group in global drinking water distribution systems.},
journal = {Water research},
volume = {298},
number = {},
pages = {125784},
doi = {10.1016/j.watres.2026.125784},
pmid = {41921321},
issn = {1879-2448},
abstract = {A recent metagenomic survey of drinking water systems revealed that a highly prevalent and dominant uncultured bacterial genus (Raskinella) was represented globally by a single species (Raskinella chloraquaticus). R. chloraquaticus comprises of two sub-species groups, Lineages 1 and 2, the former representing a globally prevalent genomovar. The objective of this study was to perform comparative analysis of the gene content of R. chloraquaticus to characterize the gene-level diversity and determine factors shaping the diversity of this species. Pangenome analysis revealed that R. chloraquaticus possesses a core set of genes that constitute a major portion (87.74%) of the known gene content of the genome. Furthermore, most of the gene diversity of R. chloraquaticus is associated with Lineage 2 organisms, which consists of at least four distinct genomovars. Lineage 1 organisms consist of a higher proportion of identical genes than would have been expected if changes primarily occurred through random mutations and thus is potentially indicative of recombination. In contrast, Lineage 2 organisms appear to have emerged through random mutations and display stronger geographic preference. These results indicate that homologous recombination and geographic isolation likely shape the genetic repertoire of R. chloraquaticus. Further, the high level of gene conservation in R. chloraquaticus may be reflective of highly selective environment in drinking water systems. Thus, R. chloraquaticus may represent a model organism to probe selective pressures shaping the drinking water microbiome.},
}
RevDate: 2026-04-01
Feasibility of Low-Biomass Exhaled Breath Microbiome Sequencing Using a PDC-Sampler in Febrile and Healthy Individuals.
Journal of breath research [Epub ahead of print].
Exhaled breath is a noninvasive and repeatable biological matrix offering new opportunities for respiratory microbiome analysis, yet its extremely low microbial biomass limits current high-throughput applications. Building on our previously developed phase-change drywall cyclone sampler (PDC-sampler), which integrates condensational growth with dry-wall cyclone separation, we established a validated workflow for efficient aerosol collection and multi-omics sequencing of exhaled breath. Using this platform, exhaled breath from 15 febrile patients and 6 healthy volunteers was analyzed via shotgun metagenomic and 16S rRNA sequencing to assess microbial composition, diversity, and functional features. The PDC-sampler significantly increased microbial DNA yield, enabling stable detection of bacterial taxa dominated by Pseudomonadota, Bacillota, Bacteroidota, and Actinomycetota. Functional annotations and diversity metrics revealed distinct microbial and metabolic patterns between individuals, confirming the platform's analytical sensitivity and biological representativeness. This work experimentally validates the feasibility of exhaled breath microbiome sequencing using the PDC-sampler, providing a practical and generalizable framework for noninvasive respiratory microecology studies and future diagnostic applications.
Additional Links: PMID-41921531
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@article {pmid41921531,
year = {2026},
author = {Li, W and Lv, M and Cheng, M and Han, Y and Yu, H and Huang, Y and Meng, D and Xu, X and Sun, L and Lu, Z and Liu, QL},
title = {Feasibility of Low-Biomass Exhaled Breath Microbiome Sequencing Using a PDC-Sampler in Febrile and Healthy Individuals.},
journal = {Journal of breath research},
volume = {},
number = {},
pages = {},
doi = {10.1088/1752-7163/ae5a51},
pmid = {41921531},
issn = {1752-7163},
abstract = {Exhaled breath is a noninvasive and repeatable biological matrix offering new opportunities for respiratory microbiome analysis, yet its extremely low microbial biomass limits current high-throughput applications. Building on our previously developed phase-change drywall cyclone sampler (PDC-sampler), which integrates condensational growth with dry-wall cyclone separation, we established a validated workflow for efficient aerosol collection and multi-omics sequencing of exhaled breath. Using this platform, exhaled breath from 15 febrile patients and 6 healthy volunteers was analyzed via shotgun metagenomic and 16S rRNA sequencing to assess microbial composition, diversity, and functional features. The PDC-sampler significantly increased microbial DNA yield, enabling stable detection of bacterial taxa dominated by Pseudomonadota, Bacillota, Bacteroidota, and Actinomycetota. Functional annotations and diversity metrics revealed distinct microbial and metabolic patterns between individuals, confirming the platform's analytical sensitivity and biological representativeness. This work experimentally validates the feasibility of exhaled breath microbiome sequencing using the PDC-sampler, providing a practical and generalizable framework for noninvasive respiratory microecology studies and future diagnostic applications.},
}
RevDate: 2026-04-01
Colonization of Salmonella Newport and Microbiome Analyses of Bulb Onions Grown in Artificially Contaminated Soil at Lab-Scale Under a Controlled Environment.
Journal of food protection pii:S0362-028X(26)00074-8 [Epub ahead of print].
INTRODUCTION: Several multistate Salmonella outbreaks in the United States have been linked to bulb onions. In this study we investigated the extent of Salmonella colonization on bulb onions grown in contaminated soil.
PURPOSE: The study evaluated the colonization potential and microbial community dynamics of Salmonella Newport on bulb onions grown in artificially spiked soil.
METHODS: Red bulb onions were grown from seed, and resultant seedlings were transplanted into pots containing soil. Soil surface was spiked with S. Newport at transplant and again two weeks before harvest. Three inoculum levels [10[2] (low), 10[4](medium), 10[6] (high) CFU per 200 g soil] of Salmonella Newport were investigated in triplicate, with three unspiked controls. Three independent trials were conducted using two different soil types. Microbiome analyses were performed on the bulb onions and soil from the high inoculum group in Trial 1 (field topsoil) at 0 h, 1 h, and 24 h pre-enrichment. Results Salmonella was detected in one high-inoculum bulb onion in Trial 1 (field topsoil) and in all high-inoculum onions in Trials 2 and 3 (Miracle-Gro soil). Among the medium inoculum groups, all onions in Trial 2, one in Trial 3, and none in Trial 1 were positive for Salmonella. No onions in the low inoculum group were Salmonella-positive. Microbiome analysis of control and Salmonella-spiked high inoculum field topsoil samples and associated bulb onions revealed that bacterial community composition remained stable at 0 h and 1 h pre-enrichment but underwent notable shifts after 24 h. Bacterial diversity decreased following 24 h of pre-enrichment, with increased dominance of Proteobacteria and Firmicutes. However, Salmonella spiking had minimal or no effect on microbiome dynamics. Significance These findings provide insights into the colonization capability of Salmonella Newport on bulb onions in different soil types and associated microbial community shifts after 24h pre-enrichment.
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@article {pmid41921618,
year = {2026},
author = {Khajanchi, BK and Grocholl, J and Alam, M and Hasan, NA and Wang, H and Hughes, S},
title = {Colonization of Salmonella Newport and Microbiome Analyses of Bulb Onions Grown in Artificially Contaminated Soil at Lab-Scale Under a Controlled Environment.},
journal = {Journal of food protection},
volume = {},
number = {},
pages = {100769},
doi = {10.1016/j.jfp.2026.100769},
pmid = {41921618},
issn = {1944-9097},
abstract = {INTRODUCTION: Several multistate Salmonella outbreaks in the United States have been linked to bulb onions. In this study we investigated the extent of Salmonella colonization on bulb onions grown in contaminated soil.
PURPOSE: The study evaluated the colonization potential and microbial community dynamics of Salmonella Newport on bulb onions grown in artificially spiked soil.
METHODS: Red bulb onions were grown from seed, and resultant seedlings were transplanted into pots containing soil. Soil surface was spiked with S. Newport at transplant and again two weeks before harvest. Three inoculum levels [10[2] (low), 10[4](medium), 10[6] (high) CFU per 200 g soil] of Salmonella Newport were investigated in triplicate, with three unspiked controls. Three independent trials were conducted using two different soil types. Microbiome analyses were performed on the bulb onions and soil from the high inoculum group in Trial 1 (field topsoil) at 0 h, 1 h, and 24 h pre-enrichment. Results Salmonella was detected in one high-inoculum bulb onion in Trial 1 (field topsoil) and in all high-inoculum onions in Trials 2 and 3 (Miracle-Gro soil). Among the medium inoculum groups, all onions in Trial 2, one in Trial 3, and none in Trial 1 were positive for Salmonella. No onions in the low inoculum group were Salmonella-positive. Microbiome analysis of control and Salmonella-spiked high inoculum field topsoil samples and associated bulb onions revealed that bacterial community composition remained stable at 0 h and 1 h pre-enrichment but underwent notable shifts after 24 h. Bacterial diversity decreased following 24 h of pre-enrichment, with increased dominance of Proteobacteria and Firmicutes. However, Salmonella spiking had minimal or no effect on microbiome dynamics. Significance These findings provide insights into the colonization capability of Salmonella Newport on bulb onions in different soil types and associated microbial community shifts after 24h pre-enrichment.},
}
RevDate: 2026-04-03
The oral-gut microbiome axis in diabetes mellitus: a systematic review and emerging clinical perspectives.
Diabetes research and clinical practice, 235:113232 pii:S0168-8227(26)00151-8 [Epub ahead of print].
Emerging evidence suggests that diabetes mellitus (DM) is not only a metabolic disorder but also a mucosal disease shaped by microbial interactions across body niches. This review synthesizes current evidence on the oral-gut microbiome axis in DM, focusing on microbial transmission, functional overlap, and clinical relevance. A systematic search of six databases identified studies profiling paired oral and gut microbiomes in individuals with diabetes. Across included studies, consistent findings demonstrate concurrent dysbiosis in both niches. Notably, oral-associated taxa such as Streptococcus, Prevotella, Fusobacterium, and Porphyromonas were detected in the gut, suggesting ectopic colonization and inter-niche microbial transmission. Functional analyses revealed shared disruptions in key metabolic pathways, including short-chain fatty acid production and glycine betaine metabolism, with downstream effects on inflammation and insulin resistance. These microbial alterations correlated with established clinical markers such as HbA1c, fasting glucose, and inflammatory indices. Emerging machine-learning models integrating oral and gut microbiota demonstrated promising diagnostic performance (AUC > 0.83). Collectively, these findings support a potential bidirectional oral-gut axis associated with metabolic dysregulation in DM. Despite limitations including cross-sectional design and heterogeneity, this axis represents a novel target for biomarker development and therapeutic intervention. Future longitudinal and interventional studies are required to determine causal relationships and clinical utility.
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@article {pmid41921761,
year = {2026},
author = {Nee, GW and Agrawal, K and Dalan, R and Kasahara, K and Xiang Darren, LY and Ali, Y and Wong, S},
title = {The oral-gut microbiome axis in diabetes mellitus: a systematic review and emerging clinical perspectives.},
journal = {Diabetes research and clinical practice},
volume = {235},
number = {},
pages = {113232},
doi = {10.1016/j.diabres.2026.113232},
pmid = {41921761},
issn = {1872-8227},
abstract = {Emerging evidence suggests that diabetes mellitus (DM) is not only a metabolic disorder but also a mucosal disease shaped by microbial interactions across body niches. This review synthesizes current evidence on the oral-gut microbiome axis in DM, focusing on microbial transmission, functional overlap, and clinical relevance. A systematic search of six databases identified studies profiling paired oral and gut microbiomes in individuals with diabetes. Across included studies, consistent findings demonstrate concurrent dysbiosis in both niches. Notably, oral-associated taxa such as Streptococcus, Prevotella, Fusobacterium, and Porphyromonas were detected in the gut, suggesting ectopic colonization and inter-niche microbial transmission. Functional analyses revealed shared disruptions in key metabolic pathways, including short-chain fatty acid production and glycine betaine metabolism, with downstream effects on inflammation and insulin resistance. These microbial alterations correlated with established clinical markers such as HbA1c, fasting glucose, and inflammatory indices. Emerging machine-learning models integrating oral and gut microbiota demonstrated promising diagnostic performance (AUC > 0.83). Collectively, these findings support a potential bidirectional oral-gut axis associated with metabolic dysregulation in DM. Despite limitations including cross-sectional design and heterogeneity, this axis represents a novel target for biomarker development and therapeutic intervention. Future longitudinal and interventional studies are required to determine causal relationships and clinical utility.},
}
RevDate: 2026-04-01
The microbiome and eating disorders: a new framework at the interface of interoception and reward.
Neuroscience pii:S0306-4522(26)00242-3 [Epub ahead of print].
Accumulating evidence suggests that the gut microbiome can modulate brain and behaviour including those relevant to eating behaviours and reward signalling through the dynamic communication pathways of the microbiota-gut-brain-axis. Emerging evidence links altered gut microbial composition to disordered eating patterns, implicating the gut microbiome as a possible mechanism underlying eating disorders, as well as a potential therapeutic target for these conditions. In this review, we synthesise evidence across preclinical and clinical research to propose an integrated framework wherein the gut microbiome, interoception and reward circuits may interact to shape disordered eating behaviours. We firstly explore how microbial signals modulate homeostatic and reward feeding systems via vagal afferents, neurotransmitter modulation and immune-neural pathways, and how these signals converge in brain regions implicated in reward systems and interoception. Particular attention is given to how these interactions may occur in under- and over-eating phenotypes of disordered eating. The therapeutic potential of microbiota-targeted interventions to modulate eating disorder-induced dysregulations in interoception and reward signalling is discussed. Combined evidence suggests a paradigm shift in the etiological considerations of eating disorders is warranted taking into account dysregulations of gut microbiota and its effects on reward processing and interoceptive signalling. Specifically, we propose that EDs are underpinned by dysregulations of gut microbiota, reward processing and interoceptive signalling, rather than neurobehaviour alone. The novel, integrated, and transdiagnostic framework posited in this review could represent a conceptual shift in the aetiological understanding of eating disorders with the potential to derive new neurobiological targets for intervention.
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@article {pmid41921818,
year = {2026},
author = {Ziade, I and McDermott, MM and O'Riordan, KJ and Cryan, JF and Schneider, E},
title = {The microbiome and eating disorders: a new framework at the interface of interoception and reward.},
journal = {Neuroscience},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.neuroscience.2026.03.050},
pmid = {41921818},
issn = {1873-7544},
abstract = {Accumulating evidence suggests that the gut microbiome can modulate brain and behaviour including those relevant to eating behaviours and reward signalling through the dynamic communication pathways of the microbiota-gut-brain-axis. Emerging evidence links altered gut microbial composition to disordered eating patterns, implicating the gut microbiome as a possible mechanism underlying eating disorders, as well as a potential therapeutic target for these conditions. In this review, we synthesise evidence across preclinical and clinical research to propose an integrated framework wherein the gut microbiome, interoception and reward circuits may interact to shape disordered eating behaviours. We firstly explore how microbial signals modulate homeostatic and reward feeding systems via vagal afferents, neurotransmitter modulation and immune-neural pathways, and how these signals converge in brain regions implicated in reward systems and interoception. Particular attention is given to how these interactions may occur in under- and over-eating phenotypes of disordered eating. The therapeutic potential of microbiota-targeted interventions to modulate eating disorder-induced dysregulations in interoception and reward signalling is discussed. Combined evidence suggests a paradigm shift in the etiological considerations of eating disorders is warranted taking into account dysregulations of gut microbiota and its effects on reward processing and interoceptive signalling. Specifically, we propose that EDs are underpinned by dysregulations of gut microbiota, reward processing and interoceptive signalling, rather than neurobehaviour alone. The novel, integrated, and transdiagnostic framework posited in this review could represent a conceptual shift in the aetiological understanding of eating disorders with the potential to derive new neurobiological targets for intervention.},
}
RevDate: 2026-04-03
Virulence and antimicrobial resistance profiling of Klebsiella pneumoniae isolated from foxes in northern China.
Microbial pathogenesis, 215:108476 pii:S0882-4010(26)00202-0 [Epub ahead of print].
Klebsiella pneumoniae is a significant opportunistic pathogen in animal farming. To investigate the occurrence of K. pneumoniae and associated antimicrobial resistance risk in foxes, this study collected 350 fecal samples from foxes across five northern Chinese provinces. A total of 163 K. pneumoniae isolates were recovered (isolation rate: 46.57%), and all isolates were classified as multidrug-resistant (MDR). All isolates were resistant to azithromycin and sulfisoxazole, with high resistance to enrofloxacin (98.16%), ciprofloxacin (87.12%), and tetracycline (70.55%). Resistance to tigecycline and polymyxin B was lower. Notably, all isolates were susceptible to meropenem. Antimicrobial resistance gene (ARG) analysis revealed high carriage rates of tet(E), aac(3)-IIa, and qnrS, alongside the colistin resistance genes mcr-1 and mcr-8. Whole-genome sequencing of 66 isolates revealed substantial genetic diversity: 45 sequence types (STs) were identified among 64 typeable isolates, with ST35 and ST603 being the most common (5/64, 7.81% each), and lineages previously reported in human clinical settings (e.g., ST307 and ST15) were also detected; however, no direct cross-host transmission was evaluated in this study. Capsular types KL22 (10/64, 15.63%) was the most common. Metagenomic analysis further showed that the fox gut microbiome harbored diverse ARGs, with 29 ARGs detected in both K. pneumoniae isolates and fox gut resistome datasets (descriptive overlap). Among these, 20 genes (e.g., blaCTX-M-55 and aac(3)-IIa) were located on predicted plasmids or transposons, suggesting potential mobility rather than confirmed transfer. Conjugation assays provided limited proof-of-concept evidence for plasmid-mediated transfer of tet(A) and tet(E). Collectively, these findings suggest that farmed foxes may serve as potential reservoirs of MDR K. pneumoniae and transferable resistance determinants, supporting the need for continued surveillance and prudent antibiotic use within a One Health framework.
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@article {pmid41921920,
year = {2026},
author = {Yang, MT and Qin, Y and Xu, C and Leng, X and Li, XM and Hou, QY and Sun, YZ and Zhao, Q and Liu, S and Tang, LY and Ma, H and Chen, BN and Zhang, XX and Li, ZY and Ni, HB},
title = {Virulence and antimicrobial resistance profiling of Klebsiella pneumoniae isolated from foxes in northern China.},
journal = {Microbial pathogenesis},
volume = {215},
number = {},
pages = {108476},
doi = {10.1016/j.micpath.2026.108476},
pmid = {41921920},
issn = {1096-1208},
abstract = {Klebsiella pneumoniae is a significant opportunistic pathogen in animal farming. To investigate the occurrence of K. pneumoniae and associated antimicrobial resistance risk in foxes, this study collected 350 fecal samples from foxes across five northern Chinese provinces. A total of 163 K. pneumoniae isolates were recovered (isolation rate: 46.57%), and all isolates were classified as multidrug-resistant (MDR). All isolates were resistant to azithromycin and sulfisoxazole, with high resistance to enrofloxacin (98.16%), ciprofloxacin (87.12%), and tetracycline (70.55%). Resistance to tigecycline and polymyxin B was lower. Notably, all isolates were susceptible to meropenem. Antimicrobial resistance gene (ARG) analysis revealed high carriage rates of tet(E), aac(3)-IIa, and qnrS, alongside the colistin resistance genes mcr-1 and mcr-8. Whole-genome sequencing of 66 isolates revealed substantial genetic diversity: 45 sequence types (STs) were identified among 64 typeable isolates, with ST35 and ST603 being the most common (5/64, 7.81% each), and lineages previously reported in human clinical settings (e.g., ST307 and ST15) were also detected; however, no direct cross-host transmission was evaluated in this study. Capsular types KL22 (10/64, 15.63%) was the most common. Metagenomic analysis further showed that the fox gut microbiome harbored diverse ARGs, with 29 ARGs detected in both K. pneumoniae isolates and fox gut resistome datasets (descriptive overlap). Among these, 20 genes (e.g., blaCTX-M-55 and aac(3)-IIa) were located on predicted plasmids or transposons, suggesting potential mobility rather than confirmed transfer. Conjugation assays provided limited proof-of-concept evidence for plasmid-mediated transfer of tet(A) and tet(E). Collectively, these findings suggest that farmed foxes may serve as potential reservoirs of MDR K. pneumoniae and transferable resistance determinants, supporting the need for continued surveillance and prudent antibiotic use within a One Health framework.},
}
RevDate: 2026-04-01
Aspirin reprograms platelet signaling and the intrahepatic microbiome to suppress RyR2-driven inflammation and fibrosis in preclinical chronic liver disease.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 198:119296 pii:S0753-3322(26)00329-X [Epub ahead of print].
Platelet deactivation by aspirin possibly helps in regression of liver fibrosis, though the mechanisms are unclear. We administered aspirin in a murine model of liver fibrosis and studied molecular signatures associated with fibrosis regression; both in vivo (murine model/ patients) and in vitro. Increase in intrahepatic PF4, p-selectin, PDGFR-β levels (platelet activation) correlated with increase in liver fibrosis (p < 0.05, r[2]>0.3). Aspirin reduced the number and activation of intrahepatic platelets, inflammation and fibrosis (p < 0.05). Platelet deactivation using aspirin in murine model increased autophagy, glutathione, energy metabolism and decreased arachidonic acid and butanoate metabolism (p < 0.05). Aspirin modulated liver microenvironment and showed decrease in intrahepatic immune cell activation (blood transcription module) which correlated with histidine and tryptophan metabolism (r2 > 0.5, p < 0.05). The intrahepatic microbiome post-aspirin showed increased abundance of Firmicutes (Ruminococcaceae, Lachnospiraceae, and Clostridiaceae) and improved functionality (p < 0.05). Aspirin caused decreased expression of Ryanodine-receptor-2 (RyR2), Arginase-1 and Kynurenine-3-monooxygenase, which correlate with reduction in α-SMA and degree of hepatic fibrosis (r2 > 0.75; p < 0.05). In addition, pan specific blocking of RyR2 by carvedilol/flecainide markedly inhibited HSC activation and proliferation in-vitro by reducing Ca[2+] overload, ER/mitochondrial stress (p < 0.05). Further, RyR2 blockade in HSCs reduced its activation by activated platelet secretome or TGFβ1 (p < 0.05). CONCLUSIONS: Platelet deactivation using aspirin regresses hepatic fibrosis by decreasing intrahepatic platelet accumulation/activation, inflammation and modulation of intrahepatic microbiome. Induction of RyR2 is critical for fibrosis development and pharmacological inhibition of RyR2 could ameliorate liver fibrosis.
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@article {pmid41922110,
year = {2026},
author = {Bhat, A and Chaudhary, S and Kumari, A and Sharma, S and Sarin, SK and Maras, JS},
title = {Aspirin reprograms platelet signaling and the intrahepatic microbiome to suppress RyR2-driven inflammation and fibrosis in preclinical chronic liver disease.},
journal = {Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie},
volume = {198},
number = {},
pages = {119296},
doi = {10.1016/j.biopha.2026.119296},
pmid = {41922110},
issn = {1950-6007},
abstract = {Platelet deactivation by aspirin possibly helps in regression of liver fibrosis, though the mechanisms are unclear. We administered aspirin in a murine model of liver fibrosis and studied molecular signatures associated with fibrosis regression; both in vivo (murine model/ patients) and in vitro. Increase in intrahepatic PF4, p-selectin, PDGFR-β levels (platelet activation) correlated with increase in liver fibrosis (p < 0.05, r[2]>0.3). Aspirin reduced the number and activation of intrahepatic platelets, inflammation and fibrosis (p < 0.05). Platelet deactivation using aspirin in murine model increased autophagy, glutathione, energy metabolism and decreased arachidonic acid and butanoate metabolism (p < 0.05). Aspirin modulated liver microenvironment and showed decrease in intrahepatic immune cell activation (blood transcription module) which correlated with histidine and tryptophan metabolism (r2 > 0.5, p < 0.05). The intrahepatic microbiome post-aspirin showed increased abundance of Firmicutes (Ruminococcaceae, Lachnospiraceae, and Clostridiaceae) and improved functionality (p < 0.05). Aspirin caused decreased expression of Ryanodine-receptor-2 (RyR2), Arginase-1 and Kynurenine-3-monooxygenase, which correlate with reduction in α-SMA and degree of hepatic fibrosis (r2 > 0.75; p < 0.05). In addition, pan specific blocking of RyR2 by carvedilol/flecainide markedly inhibited HSC activation and proliferation in-vitro by reducing Ca[2+] overload, ER/mitochondrial stress (p < 0.05). Further, RyR2 blockade in HSCs reduced its activation by activated platelet secretome or TGFβ1 (p < 0.05). CONCLUSIONS: Platelet deactivation using aspirin regresses hepatic fibrosis by decreasing intrahepatic platelet accumulation/activation, inflammation and modulation of intrahepatic microbiome. Induction of RyR2 is critical for fibrosis development and pharmacological inhibition of RyR2 could ameliorate liver fibrosis.},
}
RevDate: 2026-04-01
CmpDate: 2026-04-01
Rhizosphere Microbiome as an Underexplored Resource for Agroecosystem Sustainability: Insights From the Carrot Root Zone.
Environmental microbiology reports, 18(2):e70325.
Rhizosphere microbiome is critical for nutrient turnover, pathogen suppression, and stress modulation, forming the basis of microbial products relevant to agriculture. However, microbial communities associated with carrot root zone remain relatively underexplored, with limited studies focused beyond descriptive surveys. Here, we synthesise existing information on the structural, functional, and ecological dynamics of the carrot rhizomicrobiome, highlighting its emerging yet underdeveloped mechanistic profiling. Existing literature indicates that carrot-associated microbes may play a role in nutrient mobilisation, growth promotion, and antagonism. The early proof-of-concept works demonstrate that the microbes may gain potential applications in biofertilizers, biostimulants, and biocontrol agents. While these functions are strongly influenced by soil properties, genotype, and management, only a few carrot-specific isolates/consortia have been multi-environmentally validated. The limited progress partly reflects the overall underrepresentation of vegetables in microbiome-based studies, compared to other major crops. We explored the key characteristics, economic, and agricultural significance of the carrot rhizosphere, highlighting its richness with beneficial microorganisms. Among the gaps identified are inadequate functional-level and field trial, and insufficient multi-omics integration, which currently limit biotechnological translation. Addressing these gaps through targeted isolation, mechanistic functional and field validation could position carrot rhizosphere microbiome as a valuable yet underexplored resource for enhancing agroecosystem sustainability.
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@article {pmid41922261,
year = {2026},
author = {Adebayo, AA and Babalola, OO},
title = {Rhizosphere Microbiome as an Underexplored Resource for Agroecosystem Sustainability: Insights From the Carrot Root Zone.},
journal = {Environmental microbiology reports},
volume = {18},
number = {2},
pages = {e70325},
pmid = {41922261},
issn = {1758-2229},
support = {CRP/ZAF22-93//International Centre for Genetic Engineering and Biotechnology/ ; },
mesh = {*Daucus carota/microbiology/growth & development ; *Rhizosphere ; *Plant Roots/microbiology ; *Microbiota ; *Soil Microbiology ; Agriculture ; Bacteria/classification/genetics/isolation & purification/metabolism ; },
abstract = {Rhizosphere microbiome is critical for nutrient turnover, pathogen suppression, and stress modulation, forming the basis of microbial products relevant to agriculture. However, microbial communities associated with carrot root zone remain relatively underexplored, with limited studies focused beyond descriptive surveys. Here, we synthesise existing information on the structural, functional, and ecological dynamics of the carrot rhizomicrobiome, highlighting its emerging yet underdeveloped mechanistic profiling. Existing literature indicates that carrot-associated microbes may play a role in nutrient mobilisation, growth promotion, and antagonism. The early proof-of-concept works demonstrate that the microbes may gain potential applications in biofertilizers, biostimulants, and biocontrol agents. While these functions are strongly influenced by soil properties, genotype, and management, only a few carrot-specific isolates/consortia have been multi-environmentally validated. The limited progress partly reflects the overall underrepresentation of vegetables in microbiome-based studies, compared to other major crops. We explored the key characteristics, economic, and agricultural significance of the carrot rhizosphere, highlighting its richness with beneficial microorganisms. Among the gaps identified are inadequate functional-level and field trial, and insufficient multi-omics integration, which currently limit biotechnological translation. Addressing these gaps through targeted isolation, mechanistic functional and field validation could position carrot rhizosphere microbiome as a valuable yet underexplored resource for enhancing agroecosystem sustainability.},
}
MeSH Terms:
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*Daucus carota/microbiology/growth & development
*Rhizosphere
*Plant Roots/microbiology
*Microbiota
*Soil Microbiology
Agriculture
Bacteria/classification/genetics/isolation & purification/metabolism
RevDate: 2026-04-01
Hypoalbuminemia and reduced sputum microbiome diversity associated with antibiotic treatment failure in nursing and healthcare-associated pneumonia.
Drug discoveries & therapeutics [Epub ahead of print].
Nursing and healthcare-associated pneumonia (NHCAP) pose significant challenges in older populations, yet factors predicting antibiotic treatment failure remain elusive. This exploratory secondary analysis of a multicenter phase IV trial aimed to identify the clinical and microbiome predictors of treatment failure in patients with NHCAP treated with lascufloxacin. Among the 56 evaluable patients (median age 86 years; cured n = 44, not cured n = 12), paired sputum and tongue samples were analyzed using 16S ribosomal RNA gene clone library sequencing. Alpha diversity was assessed using the Shannon index, Simpson index, observed richness, and Pielou's evenness, whereas beta diversity was calculated using Bray-Curtis dissimilarity and visualized by principal coordinate analysis. Serum albumin was significantly lower in not cured patients (3.0 vs. 3.5 g/dL, p = 0.0497) and emerged as the strongest predictor of treatment failure in univariate logistic regression (odds ratio 0.18, 95% confidence interval 0.05-0.73, p = 0.016). Sputum Pielou's evenness showed a comparable predictive ability (odds ratio 0.010, p = 0.047). The overall microbiome community composition did not differ according to the outcome. Notably, patients with hypoalbuminemia (< 2.85 g/dL) exhibited significantly reduced sputum alpha diversity (Shannon p = 0.034, Simpson p = 0.025, Pielou's evenness p = 0.010). A simple risk stratification combining hypoalbuminemia and denture use identified a high-risk subgroup with markedly elevated treatment failure rates (75.0% vs. 12.5%, p = 0.001). These findings suggest an interconnected pathophysiology linking nutritional status and respiratory microbiome stability in patients with NHCAP. Nutritional status and oral health may be modifiable targets for improving treatment outcomes in high-risk patients.
Additional Links: PMID-41922263
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PubMed:
Citation:
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@article {pmid41922263,
year = {2026},
author = {Hosogaya, N and Fukui, S and Takazono, T and Fukushima, K and Morio, R and Irifune, S and Morimoto, S and Nakada, N and Yoshida, M and Takeda, K and Ide, S and Iwanaga, N and Nemoto, K and Izumikawa, K and Yatera, K and Yanagihara, K and Mukae, H},
title = {Hypoalbuminemia and reduced sputum microbiome diversity associated with antibiotic treatment failure in nursing and healthcare-associated pneumonia.},
journal = {Drug discoveries & therapeutics},
volume = {},
number = {},
pages = {},
doi = {10.5582/ddt.2026.01005},
pmid = {41922263},
issn = {1881-784X},
abstract = {Nursing and healthcare-associated pneumonia (NHCAP) pose significant challenges in older populations, yet factors predicting antibiotic treatment failure remain elusive. This exploratory secondary analysis of a multicenter phase IV trial aimed to identify the clinical and microbiome predictors of treatment failure in patients with NHCAP treated with lascufloxacin. Among the 56 evaluable patients (median age 86 years; cured n = 44, not cured n = 12), paired sputum and tongue samples were analyzed using 16S ribosomal RNA gene clone library sequencing. Alpha diversity was assessed using the Shannon index, Simpson index, observed richness, and Pielou's evenness, whereas beta diversity was calculated using Bray-Curtis dissimilarity and visualized by principal coordinate analysis. Serum albumin was significantly lower in not cured patients (3.0 vs. 3.5 g/dL, p = 0.0497) and emerged as the strongest predictor of treatment failure in univariate logistic regression (odds ratio 0.18, 95% confidence interval 0.05-0.73, p = 0.016). Sputum Pielou's evenness showed a comparable predictive ability (odds ratio 0.010, p = 0.047). The overall microbiome community composition did not differ according to the outcome. Notably, patients with hypoalbuminemia (< 2.85 g/dL) exhibited significantly reduced sputum alpha diversity (Shannon p = 0.034, Simpson p = 0.025, Pielou's evenness p = 0.010). A simple risk stratification combining hypoalbuminemia and denture use identified a high-risk subgroup with markedly elevated treatment failure rates (75.0% vs. 12.5%, p = 0.001). These findings suggest an interconnected pathophysiology linking nutritional status and respiratory microbiome stability in patients with NHCAP. Nutritional status and oral health may be modifiable targets for improving treatment outcomes in high-risk patients.},
}
RevDate: 2026-04-01
Characterizing the Microbiome and Prevalence of Wolbachia in Culex pipiens Complex and Culex restuans Mosquitoes in the Midwest United States.
Microbial ecology pii:10.1007/s00248-026-02750-1 [Epub ahead of print].
Additional Links: PMID-41922553
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PubMed:
Citation:
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@article {pmid41922553,
year = {2026},
author = {Cloud, RE and Irwin, P and Muturi, EJ and Cáceres, CE},
title = {Characterizing the Microbiome and Prevalence of Wolbachia in Culex pipiens Complex and Culex restuans Mosquitoes in the Midwest United States.},
journal = {Microbial ecology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00248-026-02750-1},
pmid = {41922553},
issn = {1432-184X},
support = {DEB - 1754115//National Science Foundation/ ; DEB - 1754115//National Science Foundation/ ; DBI - 2022049//Genomics and Eco-evolution of Multi-scale Symbioses Institute/ ; },
}
RevDate: 2026-04-01
Patient-derived intestinal organoids as a model for site-specific mucosal bacterial interactions in paediatric inflammatory bowel disease.
Scientific reports pii:10.1038/s41598-026-46184-8 [Epub ahead of print].
Inflammatory bowel disease (IBD) is secondary to an abnormal immune response to the microbiota. To study this, models of host-microbe interactions that represent mucosal bacterial communities and inter-patient diversity are required. Human intestinal organoids (HIOs) are an established model to investigate epithelial responses. Here, we describe a technique of culturing bacteria directly from the sites of inflammation in IBD, while simultaneously sampling host tissue. We generated HIOs from a cohort of newly diagnosed paediatric IBD patients, without confounding treatments or comorbidities, and explored their response to site-specific bacteria. A unique biobank of matched HIOs and cultured mucosa-attached bacteria was established from 27 paediatric patients. Transcriptional profiling revealed differential gene expression between control and IBD-derived organoids. We used microinjection to introduce bacteria to the apical surface of the epithelium, to determine the effect of bacteria on host epithelial cells. We measured survival and growth of bacteria within the HIOs and tested several related bacterial isolates for their impact on the epithelium. An isolate from a control patient stimulated inflammatory signalling pathways but this was not observed in response to a closely related isolate originating from an IBD patient. This study demonstrates the feasibility of isolating bacteria and generating organoids from the same biopsy tissue, to explore personalised host-microbe interactions. The microinjections, while labour-intensive, demonstrate that closely related bacteria can induce very different epithelial responses, with downstream implications for immune response. This highlights the importance of understanding host-microbe interactions in a strain- and site-specific manner and developing techniques for personalised microbiome-based therapeutics.
Additional Links: PMID-41922622
Publisher:
PubMed:
Citation:
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@article {pmid41922622,
year = {2026},
author = {Chan, E and Chan, WH and Kerr, G and Archer, SK and Jardé, T and Engel, RM and Gould, JA and Amarasinghe, SL and Rutten, EL and D'Adamo, GL and Gulliver, EL and Gearing, LJ and Forster, SC and Giles, EM and Abud, HE},
title = {Patient-derived intestinal organoids as a model for site-specific mucosal bacterial interactions in paediatric inflammatory bowel disease.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-46184-8},
pmid = {41922622},
issn = {2045-2322},
support = {1188689//National Health and Medical Research Council of Australia/ ; 1188689//National Health and Medical Research Council of Australia/ ; },
abstract = {Inflammatory bowel disease (IBD) is secondary to an abnormal immune response to the microbiota. To study this, models of host-microbe interactions that represent mucosal bacterial communities and inter-patient diversity are required. Human intestinal organoids (HIOs) are an established model to investigate epithelial responses. Here, we describe a technique of culturing bacteria directly from the sites of inflammation in IBD, while simultaneously sampling host tissue. We generated HIOs from a cohort of newly diagnosed paediatric IBD patients, without confounding treatments or comorbidities, and explored their response to site-specific bacteria. A unique biobank of matched HIOs and cultured mucosa-attached bacteria was established from 27 paediatric patients. Transcriptional profiling revealed differential gene expression between control and IBD-derived organoids. We used microinjection to introduce bacteria to the apical surface of the epithelium, to determine the effect of bacteria on host epithelial cells. We measured survival and growth of bacteria within the HIOs and tested several related bacterial isolates for their impact on the epithelium. An isolate from a control patient stimulated inflammatory signalling pathways but this was not observed in response to a closely related isolate originating from an IBD patient. This study demonstrates the feasibility of isolating bacteria and generating organoids from the same biopsy tissue, to explore personalised host-microbe interactions. The microinjections, while labour-intensive, demonstrate that closely related bacteria can induce very different epithelial responses, with downstream implications for immune response. This highlights the importance of understanding host-microbe interactions in a strain- and site-specific manner and developing techniques for personalised microbiome-based therapeutics.},
}
RevDate: 2026-04-01
CmpDate: 2026-04-01
Toward microbiome-assisted remediation: Vanadium-titanium magnetite mining reshapes cropland soil chemistry and rhizosphere microbiomes.
Crop health, 4(1):.
Vanadium-titanium magnetite (VTM) mining can modify cropland soils and root-associated microbiomes with implications for crop health. However, how crop rhizosphere microbiomes reorganize under VTM-derived stress-particularly when bacteria and fungi are considered together-remains poorly understood. In the Hongge district (Panzhihua, China), we sampled bulk soils and rhizospheres of lettuce, rapeseed, and pea from croplands within the VTM mining influence zone (mining-impacted fields) and paired croplands outside the zone (reference fields). We measured soil chemistry and profiled bacterial and fungal communities using 16S rRNA and ITS amplicon sequencing, respectively. Mining-impacted soils generally showed a VTM geochemical imprint, neutral-alkaline pH, and reduced plant-available P and K. Bray-Curtis-based ordinations indicated a clear separation between mining-impacted and reference rhizospheres, and taxonomic profiles suggested host-dependent reassembly of both bacterial and fungal communities. Putative functional profiling suggested a shift toward stress-accommodation processes, and fungal guild assignments tended to tilt toward saprotrophic/endophytic categories. Mantel analyses identified pH as one of the strongest correlates of community turnover, whereas structural equation modeling was consistent with nutrient availability (available N/P/K composite) explaining a substantial portion of the VTM effect; the composite total-metal-load axis (Fe/V/Ti/Zn) showed limited explanatory power, especially for fungi. Together, these field-based, two-kingdom signals link VTM-altered soil chemistry to rhizosphere restructuring in edible crops and provide actionable indicators for crop health management.
Additional Links: PMID-41922662
PubMed:
Citation:
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@article {pmid41922662,
year = {2026},
author = {Liu, B and Huang, X and Chang, C and Wan, X and Liu, M and Li, R and Li, J and Li, Q and Tao, Y},
title = {Toward microbiome-assisted remediation: Vanadium-titanium magnetite mining reshapes cropland soil chemistry and rhizosphere microbiomes.},
journal = {Crop health},
volume = {4},
number = {1},
pages = {},
pmid = {41922662},
issn = {2948-1945},
support = {2024NSFSC1202//Natural Science Foundation of Sichuan Province/ ; 25FTZLCL0012//Open Projects of the Sichuan Provincial Key Laboratory for Critical Strategic Materials of Vanadium and Titanium/ ; TYNSYS-2023-Z-03//Open Projects of the Sichuan Provincial University Key Laboratory for Solar Energy Technology Integration and Application Promotion/ ; Z3785//the start-up funds provided by Chengdu University/ ; },
abstract = {Vanadium-titanium magnetite (VTM) mining can modify cropland soils and root-associated microbiomes with implications for crop health. However, how crop rhizosphere microbiomes reorganize under VTM-derived stress-particularly when bacteria and fungi are considered together-remains poorly understood. In the Hongge district (Panzhihua, China), we sampled bulk soils and rhizospheres of lettuce, rapeseed, and pea from croplands within the VTM mining influence zone (mining-impacted fields) and paired croplands outside the zone (reference fields). We measured soil chemistry and profiled bacterial and fungal communities using 16S rRNA and ITS amplicon sequencing, respectively. Mining-impacted soils generally showed a VTM geochemical imprint, neutral-alkaline pH, and reduced plant-available P and K. Bray-Curtis-based ordinations indicated a clear separation between mining-impacted and reference rhizospheres, and taxonomic profiles suggested host-dependent reassembly of both bacterial and fungal communities. Putative functional profiling suggested a shift toward stress-accommodation processes, and fungal guild assignments tended to tilt toward saprotrophic/endophytic categories. Mantel analyses identified pH as one of the strongest correlates of community turnover, whereas structural equation modeling was consistent with nutrient availability (available N/P/K composite) explaining a substantial portion of the VTM effect; the composite total-metal-load axis (Fe/V/Ti/Zn) showed limited explanatory power, especially for fungi. Together, these field-based, two-kingdom signals link VTM-altered soil chemistry to rhizosphere restructuring in edible crops and provide actionable indicators for crop health management.},
}
RevDate: 2026-04-01
Pathophysiology of colitis-associated colorectal cancer.
Nature reviews. Gastroenterology & hepatology [Epub ahead of print].
Colitis-associated colorectal cancer (caCRC) is a subset of lower gastrointestinal tract malignancies that occurs in patients with inflammatory bowel disease (IBD), such as ulcerative colitis and Crohn's disease. The global prevalence of IBD is increasing, putting more individuals at risk of developing caCRC. The pathophysiological mechanisms that underlie the initiation and growth of caCRC remain to be fully elucidated. Nevertheless, studies have provided novel insights into the pathophysiology of caCRC, underscoring the distinguishing characteristics of caCRC compared with sporadic forms of CRC. In this Review, we describe the key mechanisms that drive caCRC. Starting from a clinical perspective and highlighting key features of the tumour epithelium, we discuss typical caCRC-related characteristics among subtypes of CRC, with a particular focus on the role of stromal cells in the tumour microenvironment. In addition, we review the contributions of immune cells to tumour control versus tumour promotion, and how signals from the gut microbiome might influence tumour development in caCRC. We also discuss various aspects of the pathophysiological heterogeneity of caCRC. Finally, we outline potential implications for therapy, and how these findings could be translated into future strategies of personalized medicine targeting caCRC.
Additional Links: PMID-41922722
PubMed:
Citation:
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@article {pmid41922722,
year = {2026},
author = {Neufert, C and Neurath, MF},
title = {Pathophysiology of colitis-associated colorectal cancer.},
journal = {Nature reviews. Gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
pmid = {41922722},
issn = {1759-5053},
abstract = {Colitis-associated colorectal cancer (caCRC) is a subset of lower gastrointestinal tract malignancies that occurs in patients with inflammatory bowel disease (IBD), such as ulcerative colitis and Crohn's disease. The global prevalence of IBD is increasing, putting more individuals at risk of developing caCRC. The pathophysiological mechanisms that underlie the initiation and growth of caCRC remain to be fully elucidated. Nevertheless, studies have provided novel insights into the pathophysiology of caCRC, underscoring the distinguishing characteristics of caCRC compared with sporadic forms of CRC. In this Review, we describe the key mechanisms that drive caCRC. Starting from a clinical perspective and highlighting key features of the tumour epithelium, we discuss typical caCRC-related characteristics among subtypes of CRC, with a particular focus on the role of stromal cells in the tumour microenvironment. In addition, we review the contributions of immune cells to tumour control versus tumour promotion, and how signals from the gut microbiome might influence tumour development in caCRC. We also discuss various aspects of the pathophysiological heterogeneity of caCRC. Finally, we outline potential implications for therapy, and how these findings could be translated into future strategies of personalized medicine targeting caCRC.},
}
RevDate: 2026-04-01
Development of gut microbiota composition in captive Asian elephants: a year-long analysis.
Scientific reports pii:10.1038/s41598-026-46586-8 [Epub ahead of print].
The establishment of gut microbiota is vital for the health and development of elephant calves, especially during their first year of life. This study investigates the transformation of the gut microbiome in captive Asian elephant calves, focusing the influence of maternal milk and subsequent dietary transitions on microbial colonization. A single meconium was collected at birth, followed by monthly fresh fecal samples during the first year. Mothers' fecal samples were also collected when calves reached three months of age. Gut microbiota profiling was conducted using 16 S rRNA gene sequencing. Meconium exhibited a diverse microbiota with moderate richness at birth. Richness subsequently declined in the monthly fecal samples, reaching its lowest point by three months of age. Firmicutes, Actinobacteriota, and Bacteroidota were the dominant bacterial phyla throughout the first year. A major shift was observed around 7 to 8 months of age with emergence of the archaeal genus Methanobrevibacter from phylum Euryarchaeota, which subsequently declined by 11 to 12 months. By this age, the calf microbial community had become more similar to that of adult elephants; however, species richness and diversity remained lower, indicating that microbial maturation was still ongoing. These findings advance our understanding of gut microbiota development in elephant calves and underscore the critical role of dietary management in promoting gut health and survival, providing essential data for captive conservation and management strategies.
Additional Links: PMID-41922727
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PubMed:
Citation:
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@article {pmid41922727,
year = {2026},
author = {Klinhom, S and Kunasol, C and Sriwichaiin, S and Kerdphoo, S and Chattipakorn, N and Chattipakorn, SC and Thitaram, C},
title = {Development of gut microbiota composition in captive Asian elephants: a year-long analysis.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-46586-8},
pmid = {41922727},
issn = {2045-2322},
support = {59/2565//The CMU Presidential Scholarship and Chiang Mai University/ ; N42A660301//The Distinguished Research Professor Grant from the National Research Council of Thailand/ ; RSA6280095//Thailand Research Fund/ ; },
abstract = {The establishment of gut microbiota is vital for the health and development of elephant calves, especially during their first year of life. This study investigates the transformation of the gut microbiome in captive Asian elephant calves, focusing the influence of maternal milk and subsequent dietary transitions on microbial colonization. A single meconium was collected at birth, followed by monthly fresh fecal samples during the first year. Mothers' fecal samples were also collected when calves reached three months of age. Gut microbiota profiling was conducted using 16 S rRNA gene sequencing. Meconium exhibited a diverse microbiota with moderate richness at birth. Richness subsequently declined in the monthly fecal samples, reaching its lowest point by three months of age. Firmicutes, Actinobacteriota, and Bacteroidota were the dominant bacterial phyla throughout the first year. A major shift was observed around 7 to 8 months of age with emergence of the archaeal genus Methanobrevibacter from phylum Euryarchaeota, which subsequently declined by 11 to 12 months. By this age, the calf microbial community had become more similar to that of adult elephants; however, species richness and diversity remained lower, indicating that microbial maturation was still ongoing. These findings advance our understanding of gut microbiota development in elephant calves and underscore the critical role of dietary management in promoting gut health and survival, providing essential data for captive conservation and management strategies.},
}
RevDate: 2026-04-01
Forensic analysis of environmental and skin microbiome differences in college dormitories based on 16 S rRNA.
International journal of legal medicine [Epub ahead of print].
Additional Links: PMID-41922879
PubMed:
Citation:
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@article {pmid41922879,
year = {2026},
author = {Dou, S and Shen, J and Wang, C and Ma, G and Fu, G and Fu, L and Cong, B and Li, S},
title = {Forensic analysis of environmental and skin microbiome differences in college dormitories based on 16 S rRNA.},
journal = {International journal of legal medicine},
volume = {},
number = {},
pages = {},
pmid = {41922879},
issn = {1437-1596},
support = {82572154//National Natural Science Foundation of China/ ; 30705010060//HeBei Medical University Postdoctoral Fund/ ; },
}
RevDate: 2026-04-02
Porphyromonas gingivalis induces intestinal inflammation through gingipain-dependent gut microbiome dysbiosis.
Microbiome pii:10.1186/s40168-026-02389-7 [Epub ahead of print].
BACKGROUND: Porphyromonas gingivalis (Pg), a key pathogen in periodontitis, is implicated in various systemic diseases such as pancreatic cancer and Alzheimer's disease. However, as a periodontal pathogen that can directly enter the lower gastrointestinal tract via saliva, its potential impact on the gut microbiome, intestinal inflammation, and its underlying mechanisms remains largely elusive.
RESULTS: Here, we observed that oral administration of Pg exacerbates intestinal inflammation in mice by inducing gut microbiome dysbiosis, increasing Th17 cells and the release of pro-inflammatory cytokines. Inhibition of Th17 activity with GSK805 or an anti-IL-17A blocking antibody mitigated this inflammatory response, highlighting the mediating role of Th17 cells. Gingipains, the virulence factors of Pg, played a crucial role in this process. Sequential knockout of gingipain genes revealed a gradual reduction in inflammatory phenotypes, with statistically significant alleviation observed when all three gingipain genes were deleted. Co-housing experiments showed that gut microbiota remodeling effectively protected against Th17-driven inflammatory response. Furthermore, immunization with inactivated Pg effectively prevented gut microbiome dysbiosis and Th17 cell-mediated inflammation.
CONCLUSION: Our findings suggest that Pg may exacerbate intestinal inflammation, potentially via its gingipain virulence proteases, which are linked to gut microbiota dysbiosis and enhanced Th17-mediated immune responses. These results suggest that gingipains could be promising targets for further investigation in Pg-associated intestinal disorders. Video Abstract.
Additional Links: PMID-41923122
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PubMed:
Citation:
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@article {pmid41923122,
year = {2026},
author = {Li, M and Cui, J and Qu, R and Liu, R and Sun, Y and Li, P and Liu, J and Low, A and Huang, X and Gan, F and Xu, ZZ},
title = {Porphyromonas gingivalis induces intestinal inflammation through gingipain-dependent gut microbiome dysbiosis.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02389-7},
pmid = {41923122},
issn = {2049-2618},
support = {2025AHGXZK40069//Natural Science Foundation of Education Department of Anhui Province/ ; },
abstract = {BACKGROUND: Porphyromonas gingivalis (Pg), a key pathogen in periodontitis, is implicated in various systemic diseases such as pancreatic cancer and Alzheimer's disease. However, as a periodontal pathogen that can directly enter the lower gastrointestinal tract via saliva, its potential impact on the gut microbiome, intestinal inflammation, and its underlying mechanisms remains largely elusive.
RESULTS: Here, we observed that oral administration of Pg exacerbates intestinal inflammation in mice by inducing gut microbiome dysbiosis, increasing Th17 cells and the release of pro-inflammatory cytokines. Inhibition of Th17 activity with GSK805 or an anti-IL-17A blocking antibody mitigated this inflammatory response, highlighting the mediating role of Th17 cells. Gingipains, the virulence factors of Pg, played a crucial role in this process. Sequential knockout of gingipain genes revealed a gradual reduction in inflammatory phenotypes, with statistically significant alleviation observed when all three gingipain genes were deleted. Co-housing experiments showed that gut microbiota remodeling effectively protected against Th17-driven inflammatory response. Furthermore, immunization with inactivated Pg effectively prevented gut microbiome dysbiosis and Th17 cell-mediated inflammation.
CONCLUSION: Our findings suggest that Pg may exacerbate intestinal inflammation, potentially via its gingipain virulence proteases, which are linked to gut microbiota dysbiosis and enhanced Th17-mediated immune responses. These results suggest that gingipains could be promising targets for further investigation in Pg-associated intestinal disorders. Video Abstract.},
}
RevDate: 2026-04-02
Associations between phloem microbiota and metabolomes in three North American ash species (Fraxinus spp.) susceptible to emerald ash borer (Agrilus planipennis).
Environmental microbiome pii:10.1186/s40793-026-00884-w [Epub ahead of print].
BACKGROUND: Microorganisms play crucial roles in the survival and fitness of their plant and insects hosts, including invasive species. The emerald ash borer (Agrilus planipennis, Fairmaire; EAB) is an invasive insect from Asia. It represents a significant threat to North American forest ecosystems, causing widespread mortality in susceptible native ash (Fraxinus) species. While previous studies have shown differences in specific plant defense metabolites between susceptible North American ash species and their more resistant Asian counterparts, widely targeted metabolite profiles and their interactions with phloem microbiota in response to EAB infestation has thus far received little attention. This study aimed to profile microbial communities associated with ash phloem and EAB larval guts and their relationship to ash phloem metabolites in three native susceptible North American ash species: F. pennsylvanica (green ash), F. nigra (black ash) and F. americana (white ash).
RESULTS: Using metabarcoding to characterize the microbial communities associated with the larval gut and host tree phloem and widely targeted metabolomics to establish the first global metabolomic profile of phloem in these ash species, we examined interspecies differences in profiles and associations of ash phloem microbiota and metabolites in relation to EAB infestation. Multivariate analysis revealed that fungal communities were distinct in all ash species, while F. pennsylvanica (green ash) harbored bacterial communities distinct from black ash. Only black ash showed a phloem profile significantly associated with EAB attack symptoms and had the largest number of differentially abundant bacterial taxa. In contrast, larval gut bacterial communities from green ash were distinct from those in other ash species. Green ash displayed a distinct global metabolite profile from the other two species and had the highest number of differentially regulated metabolites, while black ash had the least. Green and white ash shared a strong upregulation of terpenoid compounds, several of which were among compounds significantly associated with microbial communities in green ash phloem or the EAB larval gut.
CONCLUSIONS: Our results provide the first comparative analysis of phloem-associated microbial communities and metabolomes across three susceptible North American ash species and their response to EAB. We found that microbiota and metabolites in green ash showed a distinct response to EAB infestation from the other ash species and we identified specific metabolites exhibiting significant correlations with microbial communities in ash phloem or the EAB larval gut. These findings contribute novel insights into interspecies variability in host-associated microbial communities and metabolomes and their response to an invasive insect.
Additional Links: PMID-41923148
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PubMed:
Citation:
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@article {pmid41923148,
year = {2026},
author = {Mogouong Tambue, J and Yager, C and Bushley, KE},
title = {Associations between phloem microbiota and metabolomes in three North American ash species (Fraxinus spp.) susceptible to emerald ash borer (Agrilus planipennis).},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-026-00884-w},
pmid = {41923148},
issn = {2524-6372},
support = {DEB 2030036//National Science Foundation/ ; },
abstract = {BACKGROUND: Microorganisms play crucial roles in the survival and fitness of their plant and insects hosts, including invasive species. The emerald ash borer (Agrilus planipennis, Fairmaire; EAB) is an invasive insect from Asia. It represents a significant threat to North American forest ecosystems, causing widespread mortality in susceptible native ash (Fraxinus) species. While previous studies have shown differences in specific plant defense metabolites between susceptible North American ash species and their more resistant Asian counterparts, widely targeted metabolite profiles and their interactions with phloem microbiota in response to EAB infestation has thus far received little attention. This study aimed to profile microbial communities associated with ash phloem and EAB larval guts and their relationship to ash phloem metabolites in three native susceptible North American ash species: F. pennsylvanica (green ash), F. nigra (black ash) and F. americana (white ash).
RESULTS: Using metabarcoding to characterize the microbial communities associated with the larval gut and host tree phloem and widely targeted metabolomics to establish the first global metabolomic profile of phloem in these ash species, we examined interspecies differences in profiles and associations of ash phloem microbiota and metabolites in relation to EAB infestation. Multivariate analysis revealed that fungal communities were distinct in all ash species, while F. pennsylvanica (green ash) harbored bacterial communities distinct from black ash. Only black ash showed a phloem profile significantly associated with EAB attack symptoms and had the largest number of differentially abundant bacterial taxa. In contrast, larval gut bacterial communities from green ash were distinct from those in other ash species. Green ash displayed a distinct global metabolite profile from the other two species and had the highest number of differentially regulated metabolites, while black ash had the least. Green and white ash shared a strong upregulation of terpenoid compounds, several of which were among compounds significantly associated with microbial communities in green ash phloem or the EAB larval gut.
CONCLUSIONS: Our results provide the first comparative analysis of phloem-associated microbial communities and metabolomes across three susceptible North American ash species and their response to EAB. We found that microbiota and metabolites in green ash showed a distinct response to EAB infestation from the other ash species and we identified specific metabolites exhibiting significant correlations with microbial communities in ash phloem or the EAB larval gut. These findings contribute novel insights into interspecies variability in host-associated microbial communities and metabolomes and their response to an invasive insect.},
}
RevDate: 2026-04-02
Phenotypic resistance profiles and resistome variations between endophytic and epiphytic bacteria in apple fruits.
Environmental microbiome pii:10.1186/s40793-026-00880-0 [Epub ahead of print].
BACKGROUND: In recent years, there has been increasing concerns about antibiotic resistance. Although studies have investigated resistance in food-associated bacteria, fresh produce microbes remain underexplored as potential hub of resistance genes capable for horizontal transfer to human via consumption. To this end, we tested the antibiotic resistance profiles of bacterial isolates recovered from Golden Reinders and Mandy apple cultivars. We aimed to investigate the effects of orchard-cultivar combinations and microbial lifestyle on the antibiotic resistance profiles. The apples (Golden Reinders and Mandy) were sampled from four separate orchards (EEL-Lleida, Esterri, Fruits-de-Ponent and Gotarta) in Spain. We used combination of culture-dependent and whole genome sequencing approaches to analyse the antibiotic resistance profiles.
RESULTS: A total of 516 bacterial isolates were screened for susceptibility against seven different classes of antibiotics. Results showed that 272 isolates were resistant to at least one antibiotic. From those, 203 were epiphytes and 95 classified as endophytes (isolated from surface-sterilized apple peels), whereas 26 isolates were shared between the groups. The resistance profiles varied across the antibiotics, with over 50% of the isolates exhibiting resistance to tetracycline, quinolones and cephalosporins. In contrast, none of the isolates showed resistance to imipenem. Whole genome sequencing (WGS) was performed on 18 isolates, however, only 10 genomes passed quality-control thresholds and were included in subsequent resistome analyses. We found ARGs encoding resistance to 14 main antibiotic classes, with the majority of the confirmed resistances attributed to multidrug resistance (MDR). Only few target-specific ARGs were annotated, including (Rif)iri (rifampicin), lnu(A) (lincomycin) and FosD (Fosfomycin). Pantoea agglomerans possessed higher number of ARGs, while Staphylococcus arlettae exhibited notable prevalence of plasmid-encoded ARGs.
CONCLUSION: Overall, the study highlights the prevalence of antibiotic resistance in apple microbiomes. The presence of multidrug-resistance (MDR) genes further underscores the persistent threat of 'antibiotic resistance', underlining the necessity for deeper insight into antibiotic resistance within food chain.
Additional Links: PMID-41923164
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PubMed:
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@article {pmid41923164,
year = {2026},
author = {Kiplimo, D and Sánchez, AM and Ramakrishnan, DK and Wicaksono, WA and Mwirichia, R and Teixidó, N and Berg, G and Abdelfattah, A},
title = {Phenotypic resistance profiles and resistome variations between endophytic and epiphytic bacteria in apple fruits.},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-026-00880-0},
pmid = {41923164},
issn = {2524-6372},
support = {PID2020-117607RR-I00 (ENVIRONAPPLE)//University of Lleida and IRTA predoctoral UdL-IRTA Sponsored Fellowship 2021, Spanish 'Agencia Estatal de Investigación' (AEI), European Regional Development Fund (ERDF), 2021 SGR 01477 grant and the CERCA Programme from the 'Generalitat de Catalunya'/ ; },
abstract = {BACKGROUND: In recent years, there has been increasing concerns about antibiotic resistance. Although studies have investigated resistance in food-associated bacteria, fresh produce microbes remain underexplored as potential hub of resistance genes capable for horizontal transfer to human via consumption. To this end, we tested the antibiotic resistance profiles of bacterial isolates recovered from Golden Reinders and Mandy apple cultivars. We aimed to investigate the effects of orchard-cultivar combinations and microbial lifestyle on the antibiotic resistance profiles. The apples (Golden Reinders and Mandy) were sampled from four separate orchards (EEL-Lleida, Esterri, Fruits-de-Ponent and Gotarta) in Spain. We used combination of culture-dependent and whole genome sequencing approaches to analyse the antibiotic resistance profiles.
RESULTS: A total of 516 bacterial isolates were screened for susceptibility against seven different classes of antibiotics. Results showed that 272 isolates were resistant to at least one antibiotic. From those, 203 were epiphytes and 95 classified as endophytes (isolated from surface-sterilized apple peels), whereas 26 isolates were shared between the groups. The resistance profiles varied across the antibiotics, with over 50% of the isolates exhibiting resistance to tetracycline, quinolones and cephalosporins. In contrast, none of the isolates showed resistance to imipenem. Whole genome sequencing (WGS) was performed on 18 isolates, however, only 10 genomes passed quality-control thresholds and were included in subsequent resistome analyses. We found ARGs encoding resistance to 14 main antibiotic classes, with the majority of the confirmed resistances attributed to multidrug resistance (MDR). Only few target-specific ARGs were annotated, including (Rif)iri (rifampicin), lnu(A) (lincomycin) and FosD (Fosfomycin). Pantoea agglomerans possessed higher number of ARGs, while Staphylococcus arlettae exhibited notable prevalence of plasmid-encoded ARGs.
CONCLUSION: Overall, the study highlights the prevalence of antibiotic resistance in apple microbiomes. The presence of multidrug-resistance (MDR) genes further underscores the persistent threat of 'antibiotic resistance', underlining the necessity for deeper insight into antibiotic resistance within food chain.},
}
RevDate: 2026-04-02
Coral color morphs exhibit distinct microbial and proteomic profiles linked to stress and immune mechanisms in a changing ocean.
Microbiome pii:10.1186/s40168-026-02391-z [Epub ahead of print].
BACKGROUND: Coral phenotypic plasticity facilitates acclimation and adaptation to environmental variability. Coral species often display a variety of color morphs, yet key biological and ecological implications of such phenotypic variation remain underexplored. Here, we present the first proteomic and untargeted lipidomic and metabolomic survey to explore the biological characteristics and potential ecological significance of different color morphs (pink and brown) of healthy Pocillopora verrucosa sampled along a latitudinal gradient.
RESULTS: Our multi-omic approach elucidated distinct mechanisms associated with these dominant color morphs. We discovered bacterial indicators specific to each morph: putative pathogens such as Salmonella, Escherichia-Shigella, and carotenoid-producing Gemmatimonas were notably associated with the pink morph, whereas the brown morph was associated with potentially beneficial bacteria, such as Lysobacter, Acinetobacter, and Endozoicomonas. Despite these microbiome differences, the lipidome and metabolome of P. verrucosa were surprisingly homogeneous across colors and locations, suggesting similar metabolic performances during summer conditions. Key polar and apolar lipid classes, such as fatty acids, glycerophosphocholines, and retinoids, were prevalent. Notably, our proteomic analysis revealed morph-specific expressions, with pink morphs exhibiting enhanced levels of GFP-like proteins, Ankyrin, and the enzyme pullulanase, suggesting novel putative protective roles. In contrast, the brown morphs showed a higher abundance of heat shock proteins, indicating putative differential stress response capabilities.
CONCLUSION: This comprehensive study provides the first proteomic survey of P. verrucosa and identifies key physiological pathways and trade-offs linked to color morphs, which can further contribute to enhancing our understanding of coral resilience in the face of climate change.
SIGNIFICANCE STATEMENT: Understanding the phenotypic plasticity of corals is crucial for uncovering mechanisms of resilience in warming oceans, yet the biological significance of coral color morphs still needs to be explored. Using an innovative multi-omic approach (proteomics, lipidomics, and metabolomics), we provide the first comprehensive analysis of differences between pink and brown morphs of Pocillopora verrucosa. Our data reveal key taxa, potentially pathogenic or beneficial, associated with each morph, and suggest different strategies for each color morph to cope with heat stress, either expressing proteins involved in UV protection and heterotrophic activity or enhanced levels of heat stress resilience and DNA repair. These findings offer insights into the phenotypic plasticity of coral color morphs and their differential responses to climate change. Video Abstract.
Additional Links: PMID-41923171
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PubMed:
Citation:
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@article {pmid41923171,
year = {2026},
author = {Delgadillo-Ordoñez, N and Schwarzenberg, A and Zhang, H and Beenham, L and Bensaddek, D and Raimundo, I and Terraneo, T and Benzoni, F and Peixoto, RS},
title = {Coral color morphs exhibit distinct microbial and proteomic profiles linked to stress and immune mechanisms in a changing ocean.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02391-z},
pmid = {41923171},
issn = {2049-2618},
abstract = {BACKGROUND: Coral phenotypic plasticity facilitates acclimation and adaptation to environmental variability. Coral species often display a variety of color morphs, yet key biological and ecological implications of such phenotypic variation remain underexplored. Here, we present the first proteomic and untargeted lipidomic and metabolomic survey to explore the biological characteristics and potential ecological significance of different color morphs (pink and brown) of healthy Pocillopora verrucosa sampled along a latitudinal gradient.
RESULTS: Our multi-omic approach elucidated distinct mechanisms associated with these dominant color morphs. We discovered bacterial indicators specific to each morph: putative pathogens such as Salmonella, Escherichia-Shigella, and carotenoid-producing Gemmatimonas were notably associated with the pink morph, whereas the brown morph was associated with potentially beneficial bacteria, such as Lysobacter, Acinetobacter, and Endozoicomonas. Despite these microbiome differences, the lipidome and metabolome of P. verrucosa were surprisingly homogeneous across colors and locations, suggesting similar metabolic performances during summer conditions. Key polar and apolar lipid classes, such as fatty acids, glycerophosphocholines, and retinoids, were prevalent. Notably, our proteomic analysis revealed morph-specific expressions, with pink morphs exhibiting enhanced levels of GFP-like proteins, Ankyrin, and the enzyme pullulanase, suggesting novel putative protective roles. In contrast, the brown morphs showed a higher abundance of heat shock proteins, indicating putative differential stress response capabilities.
CONCLUSION: This comprehensive study provides the first proteomic survey of P. verrucosa and identifies key physiological pathways and trade-offs linked to color morphs, which can further contribute to enhancing our understanding of coral resilience in the face of climate change.
SIGNIFICANCE STATEMENT: Understanding the phenotypic plasticity of corals is crucial for uncovering mechanisms of resilience in warming oceans, yet the biological significance of coral color morphs still needs to be explored. Using an innovative multi-omic approach (proteomics, lipidomics, and metabolomics), we provide the first comprehensive analysis of differences between pink and brown morphs of Pocillopora verrucosa. Our data reveal key taxa, potentially pathogenic or beneficial, associated with each morph, and suggest different strategies for each color morph to cope with heat stress, either expressing proteins involved in UV protection and heterotrophic activity or enhanced levels of heat stress resilience and DNA repair. These findings offer insights into the phenotypic plasticity of coral color morphs and their differential responses to climate change. Video Abstract.},
}
RevDate: 2026-04-02
EXPRESS: Oral administration of Enterococcus lactis strain SF68 speeds the recovery of amoxicillin-clavulanate-induced dysbiosis in cats.
Journal of feline medicine and surgery [Epub ahead of print].
OBJECTIVES: In a previous study, Torres-Henderson et al. (2017), the probiotic Enterococcus lactis strain SF68 was clinically shown to lessen amoxicillin-clavulanate associated diarrhea. The cause or mechanism as to why this clinical benefit occurred, however, was unknown. The cause or mechanism as to why this clinical benefit occurred, however, was not apparent in that study. Since the completion of that work, a new feline dysbiosis index (DI) has been developed and new information concerning the microbiome and bile acid metabolism has been published. The objective of this study was to assess changes in the feline DI and fecal bile acid metabolism to explain how this probiotic lessened amoxicillin-clavulanate-associated diarrhea.
METHODS: Prospective, randomized, placebo-controlled, double-blinded study. 27 healthy, young, adult, purpose-bred cats were used for a previous study. Cats were randomized into the probiotic (13 cats) or placebo (14 cats) group. Each cat received amoxicillin-clavulanate for 7 days at a standard dose and either the probiotic or placebo for 14 days. Fecal samples from all cats were obtained at baseline, day 7 and day 14. All samples were frozen at -80°C until assessed. Targeted qPCR assays were then used to determine the fecal feline DI and unconjugated fecal bile acid concentrations were measured at each time point.
RESULTS: An antibiotic-induced shift in fecal microbiota and unconjugated bile acids was observed, with the probiotic group showing normalization of the feline DI and increased secondary bile acids on Day 14 compared to the placebo group (P = 0.0322).
CONCLUSIONS AND RELEVANCE: The probiotic E. lactis strain SF68 lessened amoxicillin-clavulanate-associated clinical signs of disease at least in part from the positive effects on the selected microbiota and bile acid metabolism. These findings support supplementing this probiotic to cats that have a clinical need for amoxicillin-clavulanate treatment.
Additional Links: PMID-41923274
Publisher:
PubMed:
Citation:
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@article {pmid41923274,
year = {2026},
author = {Slaughter, M and Sung, CH and Suchodolski, JS and Pilla, R and Torres, C and Lappin, MR},
title = {EXPRESS: Oral administration of Enterococcus lactis strain SF68 speeds the recovery of amoxicillin-clavulanate-induced dysbiosis in cats.},
journal = {Journal of feline medicine and surgery},
volume = {},
number = {},
pages = {1098612X261441923},
doi = {10.1177/1098612X261441923},
pmid = {41923274},
issn = {1532-2750},
abstract = {OBJECTIVES: In a previous study, Torres-Henderson et al. (2017), the probiotic Enterococcus lactis strain SF68 was clinically shown to lessen amoxicillin-clavulanate associated diarrhea. The cause or mechanism as to why this clinical benefit occurred, however, was unknown. The cause or mechanism as to why this clinical benefit occurred, however, was not apparent in that study. Since the completion of that work, a new feline dysbiosis index (DI) has been developed and new information concerning the microbiome and bile acid metabolism has been published. The objective of this study was to assess changes in the feline DI and fecal bile acid metabolism to explain how this probiotic lessened amoxicillin-clavulanate-associated diarrhea.
METHODS: Prospective, randomized, placebo-controlled, double-blinded study. 27 healthy, young, adult, purpose-bred cats were used for a previous study. Cats were randomized into the probiotic (13 cats) or placebo (14 cats) group. Each cat received amoxicillin-clavulanate for 7 days at a standard dose and either the probiotic or placebo for 14 days. Fecal samples from all cats were obtained at baseline, day 7 and day 14. All samples were frozen at -80°C until assessed. Targeted qPCR assays were then used to determine the fecal feline DI and unconjugated fecal bile acid concentrations were measured at each time point.
RESULTS: An antibiotic-induced shift in fecal microbiota and unconjugated bile acids was observed, with the probiotic group showing normalization of the feline DI and increased secondary bile acids on Day 14 compared to the placebo group (P = 0.0322).
CONCLUSIONS AND RELEVANCE: The probiotic E. lactis strain SF68 lessened amoxicillin-clavulanate-associated clinical signs of disease at least in part from the positive effects on the selected microbiota and bile acid metabolism. These findings support supplementing this probiotic to cats that have a clinical need for amoxicillin-clavulanate treatment.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Network Pharmacology Combined With Gut Microbiome and Serum Metabolomics Reveals the Therapeutic Mechanisms of Hydroxysafflor Yellow A in Diabetic Kidney Disease.
Journal of diabetes research, 2026(1):e2131566.
Diabetic kidney disease (DKD) is a severe complication of diabetes, primarily driven by chronic inflammation, oxidative stress, and gut microbiota dysbiosis. Hydroxysafflor yellow A (HSY), a bioactive compound derived from Carthamus tinctorius L., demonstrates promising renoprotective effects. However, its mechanisms, especially through modulation of the gut-kidney axis, remain poorly understood. This study employed a combination of network pharmacology, a high-fat diet/streptozotocin-induced type 2 diabetic mouse model, 16S rRNA sequencing, and serum metabolomics to explore the therapeutic mechanisms of HSY. Renal function, oxidative stress, inflammation, and gut microbiota composition were evaluated. HSY significantly alleviated renal injury by reducing blood glucose, creatinine, and urea nitrogen levels (p < 0.05), while enhancing renal antioxidant enzyme activity (GSH, SOD, CAT). Inflammatory markers (TNF-α, IL-1β) and AGE-RAGE signaling were suppressed. Analysis of the gut microbiota revealed that HSY enriched SCFA-producing genera (e.g., Lactobacillus, Alloprevotella) and decreased the abundance of Schaedlerella. Serum metabolomics further indicated that HSY modulated riboflavin metabolism, linoleic acid metabolism, and steroid hormone biosynthesis, thereby linking microbial metabolites to renal protection. Spearman correlation analysis revealed strong associations between specific gut microbiota (e.g., Prevotella) and serum metabolites (e.g., eicosapentaenoic acid). HSY mitigates DKD by targeting AGE-RAGE-mediated inflammation, oxidative stress, and gut microbiota dysbiosis while correcting metabolic disturbances. This study offers a novel multi-omics approach to understanding HSY's renoprotective effects, highlighting its potential as a therapeutic agent for DKD.
Additional Links: PMID-41923440
PubMed:
Citation:
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@article {pmid41923440,
year = {2026},
author = {Wang, P and Liu, X and Sun, W and Dong, X and Tan, J and Chen, M and He, J and Ali, A and Wu, L and Shao, K},
title = {Network Pharmacology Combined With Gut Microbiome and Serum Metabolomics Reveals the Therapeutic Mechanisms of Hydroxysafflor Yellow A in Diabetic Kidney Disease.},
journal = {Journal of diabetes research},
volume = {2026},
number = {1},
pages = {e2131566},
pmid = {41923440},
issn = {2314-6753},
support = {SH2023073//Zhenjiang Science and Technology Innovation Fund (Key R&D Program-Social Development) Project/ ; YK2024116//Scientific Research Project of Yancheng Municipal Health Commission/ ; MS2022126//Project of Jiangsu Provincial Science and Technology Development Plan for Traditional Chinese Medicine/ ; },
mesh = {*Gastrointestinal Microbiome/drug effects ; Animals ; *Diabetic Nephropathies/drug therapy/metabolism/blood/microbiology ; Metabolomics ; *Chalcone/analogs & derivatives/pharmacology/therapeutic use ; *Quinones/pharmacology/therapeutic use ; Male ; Mice ; Oxidative Stress/drug effects ; *Network Pharmacology ; Kidney/drug effects/metabolism ; *Diabetes Mellitus, Experimental/drug therapy/metabolism/complications ; Mice, Inbred C57BL ; },
abstract = {Diabetic kidney disease (DKD) is a severe complication of diabetes, primarily driven by chronic inflammation, oxidative stress, and gut microbiota dysbiosis. Hydroxysafflor yellow A (HSY), a bioactive compound derived from Carthamus tinctorius L., demonstrates promising renoprotective effects. However, its mechanisms, especially through modulation of the gut-kidney axis, remain poorly understood. This study employed a combination of network pharmacology, a high-fat diet/streptozotocin-induced type 2 diabetic mouse model, 16S rRNA sequencing, and serum metabolomics to explore the therapeutic mechanisms of HSY. Renal function, oxidative stress, inflammation, and gut microbiota composition were evaluated. HSY significantly alleviated renal injury by reducing blood glucose, creatinine, and urea nitrogen levels (p < 0.05), while enhancing renal antioxidant enzyme activity (GSH, SOD, CAT). Inflammatory markers (TNF-α, IL-1β) and AGE-RAGE signaling were suppressed. Analysis of the gut microbiota revealed that HSY enriched SCFA-producing genera (e.g., Lactobacillus, Alloprevotella) and decreased the abundance of Schaedlerella. Serum metabolomics further indicated that HSY modulated riboflavin metabolism, linoleic acid metabolism, and steroid hormone biosynthesis, thereby linking microbial metabolites to renal protection. Spearman correlation analysis revealed strong associations between specific gut microbiota (e.g., Prevotella) and serum metabolites (e.g., eicosapentaenoic acid). HSY mitigates DKD by targeting AGE-RAGE-mediated inflammation, oxidative stress, and gut microbiota dysbiosis while correcting metabolic disturbances. This study offers a novel multi-omics approach to understanding HSY's renoprotective effects, highlighting its potential as a therapeutic agent for DKD.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Gastrointestinal Microbiome/drug effects
Animals
*Diabetic Nephropathies/drug therapy/metabolism/blood/microbiology
Metabolomics
*Chalcone/analogs & derivatives/pharmacology/therapeutic use
*Quinones/pharmacology/therapeutic use
Male
Mice
Oxidative Stress/drug effects
*Network Pharmacology
Kidney/drug effects/metabolism
*Diabetes Mellitus, Experimental/drug therapy/metabolism/complications
Mice, Inbred C57BL
RevDate: 2026-04-02
CmpDate: 2026-04-02
Comparative Amplicon and Shotgun Metagenome Profiling of Soil Microbial Communities in Kauri Forests Affected by Phytophthora agathidicida.
Environmental microbiology reports, 18(2):e70324.
Soil-borne pathogens can influence microbial communities and ecosystem function, making it important to understand their broader ecological impacts. We investigated interactions between Phytophthora agathidicida (the causal agent of kauri tree dieback) and soil microbial communities, while also comparing detection and community-profiling methods. Soils from 60 kauri trees across three sites in the Waitākere Ranges, New Zealand, were analysed using loop-mediated isothermal amplification (LAMP) for pathogen detection, and 16S rRNA gene/ITS gene amplicon sequencing alongside shotgun metagenomics for community characterisation. LAMP detected P. agathidicida in 39/60 samples, while shotgun sequencing detected Phytophthora-associated DNA at low abundance across all samples. Microbial community structure and functional potential showed weak association with pathogen presence, though differential abundance testing identified several genera enriched in pathogen-detected soils, including taxa previously linked to disease suppression. Amplicon and shotgun profiles indicated broadly comparable patterns at higher taxonomic and functional levels, while differences between approaches emerged primarily at finer taxonomic resolution. Importantly, functional predictions from PICRUSt2 closely matched shotgun-derived profiles at broader scales, indicating its suitability as a cost-effective tool for broad-scale monitoring. These findings suggest limited direct pathogen effects on microbial communities and highlight how integrating molecular approaches provides complementary insights into soil microbiome-pathogen interactions.
Additional Links: PMID-41923466
PubMed:
Citation:
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@article {pmid41923466,
year = {2026},
author = {King, Z and Buckley, HL and Lear, G and Seale, B and Lee, KC and Schwendenmann, L and Lacap-Bugler, DC},
title = {Comparative Amplicon and Shotgun Metagenome Profiling of Soil Microbial Communities in Kauri Forests Affected by Phytophthora agathidicida.},
journal = {Environmental microbiology reports},
volume = {18},
number = {2},
pages = {e70324},
pmid = {41923466},
issn = {1758-2229},
support = {C09X1817//New Zealand's Biological Heritage/ ; //Ministry of Business, Innovation and Employment/ ; },
mesh = {*Phytophthora/genetics/isolation & purification ; *Soil Microbiology ; New Zealand ; RNA, Ribosomal, 16S/genetics ; *Metagenome ; Forests ; *Microbiota ; Plant Diseases/microbiology/parasitology ; Metagenomics ; Bacteria/classification/genetics/isolation & purification ; Nucleic Acid Amplification Techniques ; Phylogeny ; },
abstract = {Soil-borne pathogens can influence microbial communities and ecosystem function, making it important to understand their broader ecological impacts. We investigated interactions between Phytophthora agathidicida (the causal agent of kauri tree dieback) and soil microbial communities, while also comparing detection and community-profiling methods. Soils from 60 kauri trees across three sites in the Waitākere Ranges, New Zealand, were analysed using loop-mediated isothermal amplification (LAMP) for pathogen detection, and 16S rRNA gene/ITS gene amplicon sequencing alongside shotgun metagenomics for community characterisation. LAMP detected P. agathidicida in 39/60 samples, while shotgun sequencing detected Phytophthora-associated DNA at low abundance across all samples. Microbial community structure and functional potential showed weak association with pathogen presence, though differential abundance testing identified several genera enriched in pathogen-detected soils, including taxa previously linked to disease suppression. Amplicon and shotgun profiles indicated broadly comparable patterns at higher taxonomic and functional levels, while differences between approaches emerged primarily at finer taxonomic resolution. Importantly, functional predictions from PICRUSt2 closely matched shotgun-derived profiles at broader scales, indicating its suitability as a cost-effective tool for broad-scale monitoring. These findings suggest limited direct pathogen effects on microbial communities and highlight how integrating molecular approaches provides complementary insights into soil microbiome-pathogen interactions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Phytophthora/genetics/isolation & purification
*Soil Microbiology
New Zealand
RNA, Ribosomal, 16S/genetics
*Metagenome
Forests
*Microbiota
Plant Diseases/microbiology/parasitology
Metagenomics
Bacteria/classification/genetics/isolation & purification
Nucleic Acid Amplification Techniques
Phylogeny
RevDate: 2026-04-02
CmpDate: 2026-04-02
Gut Microbiota and Dyslipidemia in Type 2 Diabetes: A Pilot Study of 16S rRNA Profiles and Predicted Functional Shifts.
Journal of diabetes research, 2026(1):e9317962.
Hyperlipidemia is a major, modifiable driver of global cardiovascular risk. The intestinal microbiota, comprising bacteria, archaea, fungi, and viruses, modulates lipid metabolism through bile acid transformation, energy harvest, and inflammatory signaling. This study profiled the gut microbiota of 15 adults with type 2 diabetes mellitus (T2DM) and explored associations with fasting lipid measures using 16S rRNA gene sequencing (V3-V4 region) on the Illumina MiSeq platform and PICRUSt2 functional prediction. Overall α-diversity was reduced, and community composition was dominated by Firmicutes and Actinobacteria with relative depletion of Bacteroidetes. At lower taxonomic ranks, enrichment of Prevotella copri, Collinsella spp., Ruminococcus spp., and selected Bifidobacterium spp. was observed, alongside depletion of short-chain fatty acid (SCFA)-linked taxa, including Akkermansia muciniphila, Lactobacillus plantarum, and members of the Bacteroides and Parabacteroides lineages. Exploratory within-cohort trends indicated that higher triglycerides (TGs) and lower HDL-C tended to co-occur with increased Collinsella and clostridial signals and reduced SCFA-associated taxa. Predicted Kyoto Encyclopedia of Genes and Genomes (KEGG) ortholog functions suggested shifts in lipid, carbohydrate, and secondary bile acid metabolism, consistent with a metabolically activated and proinflammatory intestinal milieu. In this single-arm cohort of adults with T2DM, a low-diversity, Firmicutes/Actinobacteria-weighted microbiome with depletion of SCFA-linked taxa paralleled an atherogenic lipid profile, supporting an association between gut microbial dysbiosis and lipid abnormalities in adults with T2DM. These findings suggest the potential of microbiota-informed adjuncts, including dietary fermentable fiber, targeted probiotics and next-generation biotherapeutics, and bile-acid-modulating strategies as supportive approaches to lipid management in T2DM. This was a pilot, single-arm, exploratory study without a nondiabetic control group, and findings should be interpreted as hypothesis-generating. Nevertheless, the cross-sectional design, small sample size, and 16S-based taxonomic resolution limit causal interpretation. Larger, longitudinal studies integrating shotgun metagenomics and metabolomics are needed to confirm these associations, validate biomarkers, and elucidate mechanistic pathways that could guide precision interventions for diabetic dyslipidemia.
Additional Links: PMID-41923582
PubMed:
Citation:
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@article {pmid41923582,
year = {2026},
author = {Menezes, GA and Sekar, P and Akhter, A and Tayade, KD and Fathima, S and Hussain, ZFZ and Nigam, A},
title = {Gut Microbiota and Dyslipidemia in Type 2 Diabetes: A Pilot Study of 16S rRNA Profiles and Predicted Functional Shifts.},
journal = {Journal of diabetes research},
volume = {2026},
number = {1},
pages = {e9317962},
pmid = {41923582},
issn = {2314-6753},
mesh = {Humans ; *Gastrointestinal Microbiome/genetics ; *Diabetes Mellitus, Type 2/microbiology/complications/blood ; Pilot Projects ; Middle Aged ; *Dyslipidemias/microbiology/blood ; Male ; *RNA, Ribosomal, 16S/genetics ; Female ; Aged ; Adult ; Bacteria/genetics/classification ; },
abstract = {Hyperlipidemia is a major, modifiable driver of global cardiovascular risk. The intestinal microbiota, comprising bacteria, archaea, fungi, and viruses, modulates lipid metabolism through bile acid transformation, energy harvest, and inflammatory signaling. This study profiled the gut microbiota of 15 adults with type 2 diabetes mellitus (T2DM) and explored associations with fasting lipid measures using 16S rRNA gene sequencing (V3-V4 region) on the Illumina MiSeq platform and PICRUSt2 functional prediction. Overall α-diversity was reduced, and community composition was dominated by Firmicutes and Actinobacteria with relative depletion of Bacteroidetes. At lower taxonomic ranks, enrichment of Prevotella copri, Collinsella spp., Ruminococcus spp., and selected Bifidobacterium spp. was observed, alongside depletion of short-chain fatty acid (SCFA)-linked taxa, including Akkermansia muciniphila, Lactobacillus plantarum, and members of the Bacteroides and Parabacteroides lineages. Exploratory within-cohort trends indicated that higher triglycerides (TGs) and lower HDL-C tended to co-occur with increased Collinsella and clostridial signals and reduced SCFA-associated taxa. Predicted Kyoto Encyclopedia of Genes and Genomes (KEGG) ortholog functions suggested shifts in lipid, carbohydrate, and secondary bile acid metabolism, consistent with a metabolically activated and proinflammatory intestinal milieu. In this single-arm cohort of adults with T2DM, a low-diversity, Firmicutes/Actinobacteria-weighted microbiome with depletion of SCFA-linked taxa paralleled an atherogenic lipid profile, supporting an association between gut microbial dysbiosis and lipid abnormalities in adults with T2DM. These findings suggest the potential of microbiota-informed adjuncts, including dietary fermentable fiber, targeted probiotics and next-generation biotherapeutics, and bile-acid-modulating strategies as supportive approaches to lipid management in T2DM. This was a pilot, single-arm, exploratory study without a nondiabetic control group, and findings should be interpreted as hypothesis-generating. Nevertheless, the cross-sectional design, small sample size, and 16S-based taxonomic resolution limit causal interpretation. Larger, longitudinal studies integrating shotgun metagenomics and metabolomics are needed to confirm these associations, validate biomarkers, and elucidate mechanistic pathways that could guide precision interventions for diabetic dyslipidemia.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/genetics
*Diabetes Mellitus, Type 2/microbiology/complications/blood
Pilot Projects
Middle Aged
*Dyslipidemias/microbiology/blood
Male
*RNA, Ribosomal, 16S/genetics
Female
Aged
Adult
Bacteria/genetics/classification
RevDate: 2026-04-02
CmpDate: 2026-04-02
Emerging synthetic biology-assisted technologies for overcoming antibiotic resistance: CRISPR-Cas, bacteriophage, microbiome, and metabolic engineering-based solutions.
Journal of microbiology (Seoul, Korea), 64(3):e2512002.
Antibiotic resistance has become a critical global health challenge due to the decreased efficacy of existing antibiotics and the emergence of multidrug-resistant pathogens. In particular, the rapid horizontal transfer of resistance genes and the diverse mechanisms by which bacteria acquire resistance have significantly undermined the effectiveness of conventional therapeutic strategies, revealing fundamental limitations in current infectious disease management. In this context, synthetic biology provides a promising framework to overcome the limitations of conventional antibiotics by integrating engineering principles with bioengineering approaches, thereby enabling precise and programmable control of biological processes. These synthetic biology-based approaches offer substantial potential for developing sustainable and highly specific antimicrobial strategies. This review comprehensively examines recent advances in synthetic biology-assisted antimicrobial strategies, including CRISPR-Cas systems, bacteriophage engineering, microbiome engineering, and metabolic engineering-driven antibiotic discovery. Collectively, these approaches represent a precision antimicrobial paradigm that enables selective targeting of resistant bacteria while preserving microbiome homeostasis. These strategies also provide new directions for limiting resistance dissemination and guiding the development of next-generation therapeutics.
Additional Links: PMID-41923586
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PubMed:
Citation:
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@article {pmid41923586,
year = {2026},
author = {Oh, Y and Lee, H and Jang, S},
title = {Emerging synthetic biology-assisted technologies for overcoming antibiotic resistance: CRISPR-Cas, bacteriophage, microbiome, and metabolic engineering-based solutions.},
journal = {Journal of microbiology (Seoul, Korea)},
volume = {64},
number = {3},
pages = {e2512002},
doi = {10.71150/jm.2512002},
pmid = {41923586},
issn = {1976-3794},
support = {//National Research Foundation of Korea/ ; RS-2025-02214910//Ministry of Science and ICT/ ; //Incheon National University/ ; },
mesh = {*CRISPR-Cas Systems ; *Synthetic Biology/methods ; *Bacteriophages/genetics ; *Metabolic Engineering/methods ; *Anti-Bacterial Agents/pharmacology ; *Microbiota/genetics ; *Bacteria/drug effects/genetics ; Humans ; *Drug Resistance, Bacterial/genetics ; *Drug Resistance, Microbial/genetics ; },
abstract = {Antibiotic resistance has become a critical global health challenge due to the decreased efficacy of existing antibiotics and the emergence of multidrug-resistant pathogens. In particular, the rapid horizontal transfer of resistance genes and the diverse mechanisms by which bacteria acquire resistance have significantly undermined the effectiveness of conventional therapeutic strategies, revealing fundamental limitations in current infectious disease management. In this context, synthetic biology provides a promising framework to overcome the limitations of conventional antibiotics by integrating engineering principles with bioengineering approaches, thereby enabling precise and programmable control of biological processes. These synthetic biology-based approaches offer substantial potential for developing sustainable and highly specific antimicrobial strategies. This review comprehensively examines recent advances in synthetic biology-assisted antimicrobial strategies, including CRISPR-Cas systems, bacteriophage engineering, microbiome engineering, and metabolic engineering-driven antibiotic discovery. Collectively, these approaches represent a precision antimicrobial paradigm that enables selective targeting of resistant bacteria while preserving microbiome homeostasis. These strategies also provide new directions for limiting resistance dissemination and guiding the development of next-generation therapeutics.},
}
MeSH Terms:
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*CRISPR-Cas Systems
*Synthetic Biology/methods
*Bacteriophages/genetics
*Metabolic Engineering/methods
*Anti-Bacterial Agents/pharmacology
*Microbiota/genetics
*Bacteria/drug effects/genetics
Humans
*Drug Resistance, Bacterial/genetics
*Drug Resistance, Microbial/genetics
RevDate: 2026-04-02
Tanshinones from Salvia miltiorrhiza alleviate ulcerative colitis via reprogramming the gut microbiota-metabolite axis.
Acta biochimica et biophysica Sinica [Epub ahead of print].
The anti-inflammatory properties of the traditional herb Salvia miltiorrhiza Bunge are well-established, yet its precise mechanism of action in ulcerative colitis (UC) remains unclear. Herein, we evaluate the therapeutic potential of four major tanshinones-tanshinone IIA (Tan IIA), miltirone, neocryptotanshinone, and dihydrotanshinone I-in a murine dextran sulfate sodium (DSS)-induced colitis model. Our results show that tanshinones effectively alleviate disease severity, suppress systemic and local inflammation, and restore intestinal barrier integrity. Integrated multi-omics analysis reveals that the therapeutic efficacy originates from a comprehensive reprogramming of the gut microbiota-metabolite axis. Specifically, tanshinones reverse colitis-associated dysbiosis and rectify metabolic disturbances in linoleic acid metabolism, bile acid biosynthesis, and amino acid utilization. Correlation network analysis identifies key functional modules linking beneficial microbes (e. g., Akkermansia) to anti-inflammatory lipid mediators and associating pathobionts (e . g., Desulfovibrio) with disrupted bile acid metabolism. Notably, supplementation with Akkermansia muciniphila synergizes with Tan IIA to amplify barrier restoration and metabolic normalization. Our findings establish that tanshinones ameliorate UC through microbiota-driven metabolic reprogramming, wherein the restructured microbial community actively shapes a therapeutic metabolic output. This work elucidates a metabolite-mediated mechanism of action and positions tanshinones as promising microbiome-targeting therapeutics for inflammatory bowel disease.
Additional Links: PMID-41923590
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@article {pmid41923590,
year = {2026},
author = {Liu, Z and Hui, C and Zhang, G and Yang, H and Wang, Y and Shi, Y and Wang, C and Liu, Y and Gao, X and Wen, Y},
title = {Tanshinones from Salvia miltiorrhiza alleviate ulcerative colitis via reprogramming the gut microbiota-metabolite axis.},
journal = {Acta biochimica et biophysica Sinica},
volume = {},
number = {},
pages = {},
doi = {10.3724/abbs.2026054},
pmid = {41923590},
issn = {1745-7270},
abstract = {The anti-inflammatory properties of the traditional herb Salvia miltiorrhiza Bunge are well-established, yet its precise mechanism of action in ulcerative colitis (UC) remains unclear. Herein, we evaluate the therapeutic potential of four major tanshinones-tanshinone IIA (Tan IIA), miltirone, neocryptotanshinone, and dihydrotanshinone I-in a murine dextran sulfate sodium (DSS)-induced colitis model. Our results show that tanshinones effectively alleviate disease severity, suppress systemic and local inflammation, and restore intestinal barrier integrity. Integrated multi-omics analysis reveals that the therapeutic efficacy originates from a comprehensive reprogramming of the gut microbiota-metabolite axis. Specifically, tanshinones reverse colitis-associated dysbiosis and rectify metabolic disturbances in linoleic acid metabolism, bile acid biosynthesis, and amino acid utilization. Correlation network analysis identifies key functional modules linking beneficial microbes (e. g., Akkermansia) to anti-inflammatory lipid mediators and associating pathobionts (e . g., Desulfovibrio) with disrupted bile acid metabolism. Notably, supplementation with Akkermansia muciniphila synergizes with Tan IIA to amplify barrier restoration and metabolic normalization. Our findings establish that tanshinones ameliorate UC through microbiota-driven metabolic reprogramming, wherein the restructured microbial community actively shapes a therapeutic metabolic output. This work elucidates a metabolite-mediated mechanism of action and positions tanshinones as promising microbiome-targeting therapeutics for inflammatory bowel disease.},
}
RevDate: 2026-04-02
Soil microbial diversity associates with lower prevalence of human bacterial pathogens across global soils.
Cell host & microbe pii:S1931-3128(26)00119-8 [Epub ahead of print].
Soil-inhabiting pathogens threaten human health, but their biogeography and associations with soil biodiversity remain poorly understood. Here, we present global patterns of dominant human bacterial pathogens by integrating 1,602 soil metagenomes from 59 countries across continents. We show that dominant human pathogens are more prevalent (i.e., relative abundance) in wet (tropical and temperate) ecosystems and are particularly abundant in cropland soils. We find a global negative association between soil microbiome diversity and pathogen prevalence. We further reveal a significant and positive correlation between the abundance of dominant human pathogens and both disease virulence and global patterns of mortality associated with infectious diseases. Many dominant pathogens are likely to increase their proportion under global change scenarios. Our work provides a global atlas of dominant soil-inhabiting human pathogens and reveals their biogeography and ecology. These findings can guide the development of effective surveillance and risk management strategies to reduce outbreaks and pandemics.
Additional Links: PMID-41923636
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@article {pmid41923636,
year = {2026},
author = {Xiong, C and Delgado-Baquerizo, M and Liang, J and Wang, J and Yan, Z and Jensen, SO and Gao, M and Sáez-Sandino, T and Guirado, E and Muñoz-Rojas, M and Román, R and Maestre, FT and Singh, BK},
title = {Soil microbial diversity associates with lower prevalence of human bacterial pathogens across global soils.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.03.011},
pmid = {41923636},
issn = {1934-6069},
abstract = {Soil-inhabiting pathogens threaten human health, but their biogeography and associations with soil biodiversity remain poorly understood. Here, we present global patterns of dominant human bacterial pathogens by integrating 1,602 soil metagenomes from 59 countries across continents. We show that dominant human pathogens are more prevalent (i.e., relative abundance) in wet (tropical and temperate) ecosystems and are particularly abundant in cropland soils. We find a global negative association between soil microbiome diversity and pathogen prevalence. We further reveal a significant and positive correlation between the abundance of dominant human pathogens and both disease virulence and global patterns of mortality associated with infectious diseases. Many dominant pathogens are likely to increase their proportion under global change scenarios. Our work provides a global atlas of dominant soil-inhabiting human pathogens and reveals their biogeography and ecology. These findings can guide the development of effective surveillance and risk management strategies to reduce outbreaks and pandemics.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Clostridioides difficile Colonization and Infection in Pediatric Oncology and Stem Cell Transplant Patients.
Open forum infectious diseases, 13(4):ofag149.
BACKGROUND: Pediatric oncology and hematopoietic stem cell transplant (HSCT) patients have elevated risk for Clostridioides difficile infection (CDI), which can prolong hospitalization and delay chemotherapy. Colonization is an important prelude to symptomatic CDI. We sought to characterize colonization status in these patients.
METHODS: We retrospectively studied 276 stools longitudinally collected over 34 months from 32 HSCT and 12 oncology patients treated at a single tertiary center. Specimens were cultured for C difficile and compared by whole genome sequencing. The fecal microbiome was characterized by 16S rRNA gene sequencing.
RESULTS: Baseline cultures were positive in 16 (50%) HSCT patients and 2 (12%) oncology. On subsequent samples, 64% of patients who were initially negative acquired colonization: 8 of 15 (53%) HSCT and 8 of 10 (80%) oncology. Nine clonal strains and 25 multilocus sequence types were identified by whole genome sequencing, with 4 clones found in both cohorts. Nine patients had different strains at different time points. Seven clonal strains were found in multiple patients. Seven (15.9%) patients had symptomatic CDI. C difficile-positive stools had greater microbial diversity than negative stools in both the oncology cohort (Simpson diversity index, 0.07; 95% CI, .01-.14; P = .03) and the HSCT cohort (0.15; 95% CI, .07-.24; P < .001).
CONCLUSIONS: C difficile acquisition and colonization are common in pediatric oncology and HSCT patients. The high prevalence of clonally related strains in multiple patients suggests that asymptomatic patients may be important reservoirs of this pathogen and lead to symptomatic CDI in some patients. Gut microbial composition may influence the risk of colonization.
Additional Links: PMID-41923890
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Citation:
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@article {pmid41923890,
year = {2026},
author = {Willis, DN and Dubberke, ER and Hayashi, RJ and Tarr, PI and Haslam, DB and Hink, T and Luo, J and Tao, Y and Padhye, A and Hall, EM and Storch, GA},
title = {Clostridioides difficile Colonization and Infection in Pediatric Oncology and Stem Cell Transplant Patients.},
journal = {Open forum infectious diseases},
volume = {13},
number = {4},
pages = {ofag149},
pmid = {41923890},
issn = {2328-8957},
abstract = {BACKGROUND: Pediatric oncology and hematopoietic stem cell transplant (HSCT) patients have elevated risk for Clostridioides difficile infection (CDI), which can prolong hospitalization and delay chemotherapy. Colonization is an important prelude to symptomatic CDI. We sought to characterize colonization status in these patients.
METHODS: We retrospectively studied 276 stools longitudinally collected over 34 months from 32 HSCT and 12 oncology patients treated at a single tertiary center. Specimens were cultured for C difficile and compared by whole genome sequencing. The fecal microbiome was characterized by 16S rRNA gene sequencing.
RESULTS: Baseline cultures were positive in 16 (50%) HSCT patients and 2 (12%) oncology. On subsequent samples, 64% of patients who were initially negative acquired colonization: 8 of 15 (53%) HSCT and 8 of 10 (80%) oncology. Nine clonal strains and 25 multilocus sequence types were identified by whole genome sequencing, with 4 clones found in both cohorts. Nine patients had different strains at different time points. Seven clonal strains were found in multiple patients. Seven (15.9%) patients had symptomatic CDI. C difficile-positive stools had greater microbial diversity than negative stools in both the oncology cohort (Simpson diversity index, 0.07; 95% CI, .01-.14; P = .03) and the HSCT cohort (0.15; 95% CI, .07-.24; P < .001).
CONCLUSIONS: C difficile acquisition and colonization are common in pediatric oncology and HSCT patients. The high prevalence of clonally related strains in multiple patients suggests that asymptomatic patients may be important reservoirs of this pathogen and lead to symptomatic CDI in some patients. Gut microbial composition may influence the risk of colonization.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
The microbiome: regulating anti-tumor immunity.
Frontiers in immunology, 17:1781872.
Microorganisms distributed throughout the human body have always been a complex ecosystem that has long coexisted with other organisms. They are involved in essential key links, such as nutrient absorption, energy regulation, metabolism, toxin clearance, and immune regulation. With a deeper understanding of the microbiome, many studies have shown that the microbiome is also actively involved in the occurrence and development of tumors. The core mechanism of dysregulated microorganisms and their derivatives in the treatment response and toxicity management of tumors is the regulation of the immune function. This article explores the evolution of the microbiome and its impact on the immune function during tumor progression, and focuses on analyzing cutting-edge treatment strategies targeting the microbiome, as well as future research directions and challenges in clinical translation.
Additional Links: PMID-41924284
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@article {pmid41924284,
year = {2026},
author = {Tao, YL and Wu, XX and Wang, JR and Liu, M and Liu, YN and Lian, YQ and Liang, ZY and Zhu, SF},
title = {The microbiome: regulating anti-tumor immunity.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1781872},
pmid = {41924284},
issn = {1664-3224},
mesh = {Humans ; *Neoplasms/immunology/microbiology/therapy ; Animals ; *Microbiota/immunology ; *Gastrointestinal Microbiome/immunology ; Tumor Microenvironment/immunology ; },
abstract = {Microorganisms distributed throughout the human body have always been a complex ecosystem that has long coexisted with other organisms. They are involved in essential key links, such as nutrient absorption, energy regulation, metabolism, toxin clearance, and immune regulation. With a deeper understanding of the microbiome, many studies have shown that the microbiome is also actively involved in the occurrence and development of tumors. The core mechanism of dysregulated microorganisms and their derivatives in the treatment response and toxicity management of tumors is the regulation of the immune function. This article explores the evolution of the microbiome and its impact on the immune function during tumor progression, and focuses on analyzing cutting-edge treatment strategies targeting the microbiome, as well as future research directions and challenges in clinical translation.},
}
MeSH Terms:
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Humans
*Neoplasms/immunology/microbiology/therapy
Animals
*Microbiota/immunology
*Gastrointestinal Microbiome/immunology
Tumor Microenvironment/immunology
RevDate: 2026-04-02
CmpDate: 2026-04-02
The gut microbiota and sleep in infants: a focus on diurnal rhythmicity patterns.
Gut microbes reports, 3(1):2649096.
Emerging evidence supports a bidirectional relationship between the gut microbiome and sleep, which is partly mediated by the microbiota‒gut‒brain axis. Infancy is a critical window for the establishment of both the gut microbiome and sleep regulation, which we hypothesize to be linked across both short (diurnal) and long (monthly) time scales. In this longitudinal study, we investigated associations between gut microbiota development and sleep patterns in 20 infants at 2, 4, and 6 months of age (n = 163 samples). Infants were continuously monitored across 48-h sampling periods. The gut microbiota profiles were characterized using 16S rRNA gene sequencing; gut melatonin concentrations were measured; sleep data were collected via wearable actimetry, 24-h parent-reported sleep diaries, and the Brief Infant Sleep Questionnaire; and parenting style and behavioral development were assessed. In some infants, bacterial diversity followed diurnal rhythmic patterns. While bacterial rhythmicity was not significantly associated with sleep rhythmicity, infants with higher microbial alpha diversity showed more robust sleep patterns. Infant age emerged as the strongest predictor of gut microbial diversity and melatonin levels. Our findings suggest that gut microbial establishment may support the maturation of sleep‒wake rhythms in early infancy. Further research is needed to elucidate mechanistic roles of the gut microbiome in sleep development.
Additional Links: PMID-41924305
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Citation:
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@article {pmid41924305,
year = {2026},
author = {Kerff, F and Mühlematter, C and Adamov, A and Fast, D and Plüss, S and Zimmermann, P and Kurth, S and Bokulich, NA},
title = {The gut microbiota and sleep in infants: a focus on diurnal rhythmicity patterns.},
journal = {Gut microbes reports},
volume = {3},
number = {1},
pages = {2649096},
pmid = {41924305},
issn = {2993-3935},
abstract = {Emerging evidence supports a bidirectional relationship between the gut microbiome and sleep, which is partly mediated by the microbiota‒gut‒brain axis. Infancy is a critical window for the establishment of both the gut microbiome and sleep regulation, which we hypothesize to be linked across both short (diurnal) and long (monthly) time scales. In this longitudinal study, we investigated associations between gut microbiota development and sleep patterns in 20 infants at 2, 4, and 6 months of age (n = 163 samples). Infants were continuously monitored across 48-h sampling periods. The gut microbiota profiles were characterized using 16S rRNA gene sequencing; gut melatonin concentrations were measured; sleep data were collected via wearable actimetry, 24-h parent-reported sleep diaries, and the Brief Infant Sleep Questionnaire; and parenting style and behavioral development were assessed. In some infants, bacterial diversity followed diurnal rhythmic patterns. While bacterial rhythmicity was not significantly associated with sleep rhythmicity, infants with higher microbial alpha diversity showed more robust sleep patterns. Infant age emerged as the strongest predictor of gut microbial diversity and melatonin levels. Our findings suggest that gut microbial establishment may support the maturation of sleep‒wake rhythms in early infancy. Further research is needed to elucidate mechanistic roles of the gut microbiome in sleep development.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Oleoylethanolamide supplementation enriches Akkermansia muciniphila and modulates intestinal barrier function in adults with obesity: A randomized, double-blind, placebo-controlled trial.
Gut microbes reports, 3(1):2622259.
Targeted modulation of the gut microbiome represents a promising nutritional strategy to support metabolic and intestinal health in overweight and obese adults. Oleoylethanolamide (OEA) is an endogenous lipid mediator that regulates satiety, lipid metabolism, and inflammation, but its effects on the human microbiome are not well defined. In this randomized, double-blind, placebo-controlled trial, 57 adults with obesity (BMI 30-40 kg/m[2]) received either 300 mg of TRPTI, providing 250 mg/day of OEA (n = 28), or placebo (n = 29) for 12 weeks. Outcomes included shotgun metagenomics, microbiome profiling, intestinal barrier and inflammatory biomarkers, and safety measures. OEA was safe and well-tolerated with no adverse changes in clinical biomarkers. Although overall microbial diversity remained stable, OEA induced selective, health-relevant compositional shifts. Notably, Faecalibacterium prausnitzii and Akkermansia muciniphila were enriched. These changes coincided with functional host benefits, including increased occludin at Week 12 and interleukin-2 at Week 6, while reducing interleukin-1β, consistent with improved epithelial barrier dynamics and reduced inflammation. Functional pathway analysis suggested enhanced microbial metabolic and redox capacity. These findings indicate OEA supplementation selectively enriches beneficial gut bacteria - particularly A. muciniphila, while improving gut barrier biomarkers and immune function without disrupting microbiome stability. These findings position OEA as a safe, targeted microbiome-modulating ingredient with potential applications for supporting gut and metabolic health.
Additional Links: PMID-41924306
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Citation:
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@article {pmid41924306,
year = {2026},
author = {Batacan, R and Rao, A and Bajagai, YS and Stanley, D and Briskey, D},
title = {Oleoylethanolamide supplementation enriches Akkermansia muciniphila and modulates intestinal barrier function in adults with obesity: A randomized, double-blind, placebo-controlled trial.},
journal = {Gut microbes reports},
volume = {3},
number = {1},
pages = {2622259},
pmid = {41924306},
issn = {2993-3935},
abstract = {Targeted modulation of the gut microbiome represents a promising nutritional strategy to support metabolic and intestinal health in overweight and obese adults. Oleoylethanolamide (OEA) is an endogenous lipid mediator that regulates satiety, lipid metabolism, and inflammation, but its effects on the human microbiome are not well defined. In this randomized, double-blind, placebo-controlled trial, 57 adults with obesity (BMI 30-40 kg/m[2]) received either 300 mg of TRPTI, providing 250 mg/day of OEA (n = 28), or placebo (n = 29) for 12 weeks. Outcomes included shotgun metagenomics, microbiome profiling, intestinal barrier and inflammatory biomarkers, and safety measures. OEA was safe and well-tolerated with no adverse changes in clinical biomarkers. Although overall microbial diversity remained stable, OEA induced selective, health-relevant compositional shifts. Notably, Faecalibacterium prausnitzii and Akkermansia muciniphila were enriched. These changes coincided with functional host benefits, including increased occludin at Week 12 and interleukin-2 at Week 6, while reducing interleukin-1β, consistent with improved epithelial barrier dynamics and reduced inflammation. Functional pathway analysis suggested enhanced microbial metabolic and redox capacity. These findings indicate OEA supplementation selectively enriches beneficial gut bacteria - particularly A. muciniphila, while improving gut barrier biomarkers and immune function without disrupting microbiome stability. These findings position OEA as a safe, targeted microbiome-modulating ingredient with potential applications for supporting gut and metabolic health.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Cafeteria diet exposure, and not weight gain propensity, impacts gut microbiota of rats - a within laboratory meta-analysis.
Gut microbes reports, 3(1):2649442.
Preclinical studies have implicated the microbiota in body weight control, but its translation to humans remains uncertain, partly owing to methodological variability in assessing the relationship between diet-induced obesity and microbiota composition. We performed an internal meta-analysis to determine whether the propensity for diet-induced obesity, defined by relative weight gain due to a high-fat, high-sugar "cafeteria" diet, is associated with changes in microbiota composition. We collated fecal microbiome data from 12 studies using our validated model of diet-induced obesity (208 male and 74 female Sprague-Dawley rats; 3.5-13 weeks of chow (control) or cafeteria diet) and determined whether the alpha diversity and composition of the gut microbiota differed between obese-prone and obese-resistant rats. We found consistent effects of cafeteria diet exposure on the microbiota, with marked changes in overall composition, and reduced microbial richness and evenness. Furthermore, specific obesity-associated microbial genera, such as Bacteroides and Blautia, were enriched by the cafeteria diet. Critically, alpha diversity measures and the gut microbiota composition did not differ between obese-prone and obese-resistant rats in either diet group. Our findings suggest that while the microbiota is substantially altered by cafeteria diet intake, these changes appear unrelated to individual susceptibility to weight gain, highlighting the role of additional host factors in modulating diet-induced obesity.
Additional Links: PMID-41924307
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@article {pmid41924307,
year = {2026},
author = {Bhagavata Srinivasan, SP and Kendig, MD and Hasebe, K and Kaakoush, NO and Morris, MJ and Leigh, SJ},
title = {Cafeteria diet exposure, and not weight gain propensity, impacts gut microbiota of rats - a within laboratory meta-analysis.},
journal = {Gut microbes reports},
volume = {3},
number = {1},
pages = {2649442},
pmid = {41924307},
issn = {2993-3935},
abstract = {Preclinical studies have implicated the microbiota in body weight control, but its translation to humans remains uncertain, partly owing to methodological variability in assessing the relationship between diet-induced obesity and microbiota composition. We performed an internal meta-analysis to determine whether the propensity for diet-induced obesity, defined by relative weight gain due to a high-fat, high-sugar "cafeteria" diet, is associated with changes in microbiota composition. We collated fecal microbiome data from 12 studies using our validated model of diet-induced obesity (208 male and 74 female Sprague-Dawley rats; 3.5-13 weeks of chow (control) or cafeteria diet) and determined whether the alpha diversity and composition of the gut microbiota differed between obese-prone and obese-resistant rats. We found consistent effects of cafeteria diet exposure on the microbiota, with marked changes in overall composition, and reduced microbial richness and evenness. Furthermore, specific obesity-associated microbial genera, such as Bacteroides and Blautia, were enriched by the cafeteria diet. Critically, alpha diversity measures and the gut microbiota composition did not differ between obese-prone and obese-resistant rats in either diet group. Our findings suggest that while the microbiota is substantially altered by cafeteria diet intake, these changes appear unrelated to individual susceptibility to weight gain, highlighting the role of additional host factors in modulating diet-induced obesity.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Systems analysis of the HPV-microbiome-biofilm triad.
Frontiers in cellular and infection microbiology, 16:1767224.
BACKGROUND: Human papillomavirus (HPV) remains the leading cause of cervical cancer worldwide, however, its pathogenesis cannot be sufficiently explained by viral factors alone. Accumulating evidence highlights the critical role of cervicovaginal microbiome composition and biofilm formation in shaping viral persistence, epithelial barrier disruption and carcinogenic progression.
METHODS: This systems-based integrative synthesis analyzed peer-reviewed literature published between January 2000 and July 2025, retrieved from PubMed and Google Scholar with additional records identified through backward citation screening. The collected data were synthesized to construct a conceptual model of the HPV-microbiome-biofilm triad and to evaluate its clinical and biological implications.
RESULTS: The analysis indicates that depletion of Lactobacillus-dominated communities and expansion of anaerobic taxa, particularly Gardnerella vaginalis, are associated with biofilm development, chronic inflammation and immune modulation. These interrelated processes form self-reinforcing feedback loops that promote HPV persistence and reduce therapeutic efficacy. Microbiome dysbiosis and biofilm formation were further linked to impaired epithelial integrity, altered cytokine signaling pathways and clinically relevant phenotypes including immune escape, metabolic shifts and treatment non-responsiveness.
DISCUSSION: This systems perspective challenges reductionist pathogen-centered models and emphasizes the importance of integrating microbiome profiling and biofilm dynamics into cervical cancer risk stratification and therapeutic strategies. The coupled interactions between microbial communities, host immunity and viral persistence underscore the cervicovaginal ecosystem as an active regulator of disease progression rather than a passive bystander. Incorporating ecosystem-based parameters into clinical decision-making may enhance prognostic assessment and improve treatment outcomes, particularly in low- and middle-income countries where high HPV prevalence coincides with increased microbiome vulnerability.
https://www.crd.york.ac.uk/PROSPERO/, identifier CRD420251208178.
Additional Links: PMID-41924422
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Citation:
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@article {pmid41924422,
year = {2026},
author = {Nazarova, V and Kamzayeva, N and Ukybassova, T and Kozhakhmetov, S and Kushugulova, A},
title = {Systems analysis of the HPV-microbiome-biofilm triad.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1767224},
pmid = {41924422},
issn = {2235-2988},
mesh = {*Biofilms/growth & development ; Humans ; *Microbiota ; Female ; *Papillomavirus Infections/microbiology/virology/immunology ; Dysbiosis/microbiology ; *Papillomaviridae/physiology ; Vagina/microbiology/virology ; Uterine Cervical Neoplasms/virology/microbiology ; },
abstract = {BACKGROUND: Human papillomavirus (HPV) remains the leading cause of cervical cancer worldwide, however, its pathogenesis cannot be sufficiently explained by viral factors alone. Accumulating evidence highlights the critical role of cervicovaginal microbiome composition and biofilm formation in shaping viral persistence, epithelial barrier disruption and carcinogenic progression.
METHODS: This systems-based integrative synthesis analyzed peer-reviewed literature published between January 2000 and July 2025, retrieved from PubMed and Google Scholar with additional records identified through backward citation screening. The collected data were synthesized to construct a conceptual model of the HPV-microbiome-biofilm triad and to evaluate its clinical and biological implications.
RESULTS: The analysis indicates that depletion of Lactobacillus-dominated communities and expansion of anaerobic taxa, particularly Gardnerella vaginalis, are associated with biofilm development, chronic inflammation and immune modulation. These interrelated processes form self-reinforcing feedback loops that promote HPV persistence and reduce therapeutic efficacy. Microbiome dysbiosis and biofilm formation were further linked to impaired epithelial integrity, altered cytokine signaling pathways and clinically relevant phenotypes including immune escape, metabolic shifts and treatment non-responsiveness.
DISCUSSION: This systems perspective challenges reductionist pathogen-centered models and emphasizes the importance of integrating microbiome profiling and biofilm dynamics into cervical cancer risk stratification and therapeutic strategies. The coupled interactions between microbial communities, host immunity and viral persistence underscore the cervicovaginal ecosystem as an active regulator of disease progression rather than a passive bystander. Incorporating ecosystem-based parameters into clinical decision-making may enhance prognostic assessment and improve treatment outcomes, particularly in low- and middle-income countries where high HPV prevalence coincides with increased microbiome vulnerability.
https://www.crd.york.ac.uk/PROSPERO/, identifier CRD420251208178.},
}
MeSH Terms:
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*Biofilms/growth & development
Humans
*Microbiota
Female
*Papillomavirus Infections/microbiology/virology/immunology
Dysbiosis/microbiology
*Papillomaviridae/physiology
Vagina/microbiology/virology
Uterine Cervical Neoplasms/virology/microbiology
RevDate: 2026-04-02
CmpDate: 2026-04-02
Jinzhi and fecal microbiota transplantation: a comparative review of historical and modern microbial therapeutics.
Frontiers in microbiology, 17:1700764.
Since its formal introduction in 1958, fecal microbiota transplantation (FMT) has gained prominence. However, challenges remain in standardizing protocols and optimizing efficacy. This review provides a systematic comparison between the historical practice of Jinzhi and modern FMT, focusing on their preparation methodologies. We hypothesize that specific, underexplored features of Jinzhi preparation could inform and refine current FMT practices. Specifically, we propose that the utilization of adolescent donors, underground low-temperature fermentation, and the careful consideration of seasonal timing, all integral to Jinzhi's traditional protocol, may offer novel insights and testable hypotheses for enhancing microbial diversity, functionality, and therapeutic stability in FMT. By bridging this ancient wisdom with modern microbiome science, we aim to outline a novel and actionable framework for developing the next generation of microbiota-based therapeutics, urging future research to empirically test these historically inspired hypotheses.
Additional Links: PMID-41924474
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Citation:
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@article {pmid41924474,
year = {2026},
author = {Li, M and Dai, L and Yang, Y and Chen, S and Ma, J and Feng, P},
title = {Jinzhi and fecal microbiota transplantation: a comparative review of historical and modern microbial therapeutics.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1700764},
pmid = {41924474},
issn = {1664-302X},
abstract = {Since its formal introduction in 1958, fecal microbiota transplantation (FMT) has gained prominence. However, challenges remain in standardizing protocols and optimizing efficacy. This review provides a systematic comparison between the historical practice of Jinzhi and modern FMT, focusing on their preparation methodologies. We hypothesize that specific, underexplored features of Jinzhi preparation could inform and refine current FMT practices. Specifically, we propose that the utilization of adolescent donors, underground low-temperature fermentation, and the careful consideration of seasonal timing, all integral to Jinzhi's traditional protocol, may offer novel insights and testable hypotheses for enhancing microbial diversity, functionality, and therapeutic stability in FMT. By bridging this ancient wisdom with modern microbiome science, we aim to outline a novel and actionable framework for developing the next generation of microbiota-based therapeutics, urging future research to empirically test these historically inspired hypotheses.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Multi-omics insights into triticale silage as a sustainable alternative to corn silage in heifer diets.
Frontiers in microbiology, 17:1761287.
BACKGROUND: Intensive ruminant production systems rely heavily on corn silage (CS) as a primary forage source; however, its resource-intensive cultivation and environmental constraints necessitate the development of sustainable alternatives.
METHODS: In a 90-day feeding trial, 24 growing heifers were assigned to diets in which CS was replaced by triticale silage (TS) at 0, 25, 50%, or 100% (DM basis). Growth performance, rumen fermentation, ruminal fatty acid (FA) profiles, and integrated rumen microbiome-metabolome interactions were evaluated.
RESULTS: A 25% substitution (TS25) as the optimal level, maintaining growth performance comparable to the control while achieving the lowest feed cost of gain. TS25 improved rumen fermentation (lower A: P and high total VFA), promoted more efficient nitrogen utilization (higher MCP with lower ammonia N), and enriched functionally relevant bacteria associated with fiber degradation and fermentation (e.g., Ruminococcus, Prevotella, and Rikenellaceae_RC9_gut_group). Consistently, TS inclusion shifted ruminal lipid metabolism, increasing UFA proportions and elevating PUFA (TS25 and TS50 increased PUFA by 15.2 and 23.7% vs. control), alongside metabolomic signals indicating upregulation of linoleic acid metabolism and aromatic amino acid biosynthesis pathways. In contrast, TS substitution ≥50% reduced DMI and ADG, impairing feed utilization.
CONCLUSION: Partial replacement of CS with TS at 25% provides a practical, data-supported strategy to improve economic efficiency while maintaining productivity and promoting favorable rumen microbial-metabolic features. This feeding approach may be applicable in water-limited or double-cropping regions, where TS can enhance forage system sustainability without compromising heifer growth.
Additional Links: PMID-41924483
PubMed:
Citation:
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@article {pmid41924483,
year = {2026},
author = {Niu, Y and Wang, C and Kuang, Y and Ma, X and Nan, S and Zhang, P and Lu, Q and Qi, Y and Nie, C and Wu, Y and Zhang, W},
title = {Multi-omics insights into triticale silage as a sustainable alternative to corn silage in heifer diets.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1761287},
pmid = {41924483},
issn = {1664-302X},
abstract = {BACKGROUND: Intensive ruminant production systems rely heavily on corn silage (CS) as a primary forage source; however, its resource-intensive cultivation and environmental constraints necessitate the development of sustainable alternatives.
METHODS: In a 90-day feeding trial, 24 growing heifers were assigned to diets in which CS was replaced by triticale silage (TS) at 0, 25, 50%, or 100% (DM basis). Growth performance, rumen fermentation, ruminal fatty acid (FA) profiles, and integrated rumen microbiome-metabolome interactions were evaluated.
RESULTS: A 25% substitution (TS25) as the optimal level, maintaining growth performance comparable to the control while achieving the lowest feed cost of gain. TS25 improved rumen fermentation (lower A: P and high total VFA), promoted more efficient nitrogen utilization (higher MCP with lower ammonia N), and enriched functionally relevant bacteria associated with fiber degradation and fermentation (e.g., Ruminococcus, Prevotella, and Rikenellaceae_RC9_gut_group). Consistently, TS inclusion shifted ruminal lipid metabolism, increasing UFA proportions and elevating PUFA (TS25 and TS50 increased PUFA by 15.2 and 23.7% vs. control), alongside metabolomic signals indicating upregulation of linoleic acid metabolism and aromatic amino acid biosynthesis pathways. In contrast, TS substitution ≥50% reduced DMI and ADG, impairing feed utilization.
CONCLUSION: Partial replacement of CS with TS at 25% provides a practical, data-supported strategy to improve economic efficiency while maintaining productivity and promoting favorable rumen microbial-metabolic features. This feeding approach may be applicable in water-limited or double-cropping regions, where TS can enhance forage system sustainability without compromising heifer growth.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Editorial: Role of endophytic/symbiotic fungi in plant growth promotion and disease suppression.
Frontiers in fungal biology, 7:1820241.
Additional Links: PMID-41924563
PubMed:
Citation:
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@article {pmid41924563,
year = {2026},
author = {Santoyo, G and Kumar, A and Orozco-Mosqueda, MDC and de Oliveira Mendes, G},
title = {Editorial: Role of endophytic/symbiotic fungi in plant growth promotion and disease suppression.},
journal = {Frontiers in fungal biology},
volume = {7},
number = {},
pages = {1820241},
pmid = {41924563},
issn = {2673-6128},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Vaginal microbial community state types fail to predict IVF outcomes, whereas Ureaplasma parvum and Lactobacillus iners are negative predictors of implantation, clinical pregnancy, and live birth.
Human reproduction open, 2026(2):hoag018.
STUDY QUESTION: Are previously proposed vaginal microbial community state types (CSTs) valid predictors of IVF success, or do alternative microbial signatures provide stronger associations?
SUMMARY ANSWER: Previously proposed CSTs as predictors of implantation, clinical pregnancy, and live birth were not confirmed, while an interaction between Ureaplasma parvum and Lactobacillus iners emerged as a strong negative predictor.
WHAT IS KNOWN ALREADY: Infertility affects 17% of the global population. Only one-third of treatment cycles of assisted reproductive technologies result in embryo implantation, and even fewer lead to clinical pregnancy or live births. While early findings have spurred the development of microbiome-based tests for success prediction, evidence on supporting their reliability remains inconclusive.
STUDY DESIGN SIZE DURATION: This prospective, single-centre study aimed to validate existing, and identify better, microbial predictors of infertility treatment outcomes. A cohort of 266 infertile female patients (age 18-45 years) undergoing a frozen-thawed embryo transfer cycle in an anovulatory regimen (i.e. a cycle with transfer of an embryo following a previous oocyte retrieval, fertilization, and freezing of embryos) was recruited for the study within a timeframe from May 2017 to March 2019.
The female, infertile patients, aged 18-45 years, were undergoing routine care. Vaginal swabs were taken prior to embryo transfer and subjected to DNA isolation for 16S-based microbiota analysis. Extended demographic and treatment data were recorded. Clinical outcomes were defined as: (i) implantation, confirmed by a positive hCG test, (ii) clinical pregnancy, and (iii) live birth (defined as the birth of a viable infant). Sequencing data were processed in mothur following established pipelines, and microbial composition (taxonomy) as well as microbial diversity (dissimilarity analyses) were determined using the open-source software R. A prediction model for implantation success was built using binary logistic regression based on abundance of putatively predictive microbial taxa.
This study suggests that vaginal microbial CSTs, alpha-diversity, and the ratio of dominant Lactobacillus species do not correlate in statistical terms or in a clinically meaningful manner with implantation and clinical pregnancy (as a surrogate for endometrial receptivity) or with live birth (as a surrogate for ongoing pregnancy viability). However, Ureaplasma parvum and Lactobacillus iners abundances were identified as negative predictors of embryo implantation, clinical pregnancy, and live birth. A subset of women colonized by these taxa experienced drastically reduced embryo implantation and completely failed to achieve clinical pregnancy or give birth to live offspring, suggesting a potential role of these organisms in implantation failure and reproductive outcome, independent of other influencing factors such as age, oestradiol levels, endometrial thickness etc.
LARGE SCALE DATA: The raw sequencing data used for this manuscript are publicly available at the European Nucleotide Archive under accession number PRJEB107113.
This study is a single-centre study warranting further validation cohorts. Given the variable nature of the vaginal microbiota, sample sizes need to be enlarged for better refinement of the analyses. Further, the underlying mechanistical basis of our findings is yet elusive and clinical translation has yet to be established.
While this novel association warrants confirmation, the results caution against reliance on previously suggested CSTs as predictors, and highlight the need for refined, reproducible microbiome-based diagnostics in reproductive medicine.
Financial support was received from the University of Lübeck and the German Center of Infection Research. M.L., A.M., I.P., M.D., and J.R. declare no conflicts of interest. S.G. discloses personal fees from Organon outside the submitted work. T.K.E. discloses honoraria from Ferring; travel support from Ferring, Merck, Theramex, and Gedeon-Richter; and receipt of equipment/materials/laboratory analyses (to institution) from Arthrex, Besins, Merck, and Abbott outside the submitted work. N.H. discloses personal fees from Gedeon Richter, Ferring, and Merck. G.G. reports that his institution received grants or contracts from Besins, Merck, Abbott, Ferring, and Theramex. He has received personal consulting fees, support for travel fees and meeting attendance, and honoraria for lectures or educational events from Organon, Ferring, Merck, Gedeon-Richter, Theramex, Abbott, ReproNovo, Igyxos, OxoLife, Philipps, ReprodWissen, PregLem, Guerbet, Roche, IBSA, and Besins. He also received support for travel and meeting attendance from Merck, Organon, Ferring, Theramex, Gedeon-Richter, and Abbott. Additionally, he holds unpaid leadership positions as a member of the ESHRE Working Group on RIF, the ESHRE Working Group on clinical KPI, and the ESHRE guideline development group on ovarian stimulation. A.S.-M. reports consulting fees and speaker's fees from Merck, Theramex, and Gedeon-Richter as well as travel support from Merck, Theramex, Gedeon-Richter, IBSA, Ferring, and MSD.
Additional Links: PMID-41924635
PubMed:
Citation:
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@article {pmid41924635,
year = {2026},
author = {Graspeuntner, S and Lupatsii, M and Hamala, N and Masuch, A and Depenbusch, M and Pfeffer, I and Schultze-Mosgau, A and Eggersmann, TK and Rupp, J and Griesinger, G},
title = {Vaginal microbial community state types fail to predict IVF outcomes, whereas Ureaplasma parvum and Lactobacillus iners are negative predictors of implantation, clinical pregnancy, and live birth.},
journal = {Human reproduction open},
volume = {2026},
number = {2},
pages = {hoag018},
pmid = {41924635},
issn = {2399-3529},
abstract = {STUDY QUESTION: Are previously proposed vaginal microbial community state types (CSTs) valid predictors of IVF success, or do alternative microbial signatures provide stronger associations?
SUMMARY ANSWER: Previously proposed CSTs as predictors of implantation, clinical pregnancy, and live birth were not confirmed, while an interaction between Ureaplasma parvum and Lactobacillus iners emerged as a strong negative predictor.
WHAT IS KNOWN ALREADY: Infertility affects 17% of the global population. Only one-third of treatment cycles of assisted reproductive technologies result in embryo implantation, and even fewer lead to clinical pregnancy or live births. While early findings have spurred the development of microbiome-based tests for success prediction, evidence on supporting their reliability remains inconclusive.
STUDY DESIGN SIZE DURATION: This prospective, single-centre study aimed to validate existing, and identify better, microbial predictors of infertility treatment outcomes. A cohort of 266 infertile female patients (age 18-45 years) undergoing a frozen-thawed embryo transfer cycle in an anovulatory regimen (i.e. a cycle with transfer of an embryo following a previous oocyte retrieval, fertilization, and freezing of embryos) was recruited for the study within a timeframe from May 2017 to March 2019.
The female, infertile patients, aged 18-45 years, were undergoing routine care. Vaginal swabs were taken prior to embryo transfer and subjected to DNA isolation for 16S-based microbiota analysis. Extended demographic and treatment data were recorded. Clinical outcomes were defined as: (i) implantation, confirmed by a positive hCG test, (ii) clinical pregnancy, and (iii) live birth (defined as the birth of a viable infant). Sequencing data were processed in mothur following established pipelines, and microbial composition (taxonomy) as well as microbial diversity (dissimilarity analyses) were determined using the open-source software R. A prediction model for implantation success was built using binary logistic regression based on abundance of putatively predictive microbial taxa.
This study suggests that vaginal microbial CSTs, alpha-diversity, and the ratio of dominant Lactobacillus species do not correlate in statistical terms or in a clinically meaningful manner with implantation and clinical pregnancy (as a surrogate for endometrial receptivity) or with live birth (as a surrogate for ongoing pregnancy viability). However, Ureaplasma parvum and Lactobacillus iners abundances were identified as negative predictors of embryo implantation, clinical pregnancy, and live birth. A subset of women colonized by these taxa experienced drastically reduced embryo implantation and completely failed to achieve clinical pregnancy or give birth to live offspring, suggesting a potential role of these organisms in implantation failure and reproductive outcome, independent of other influencing factors such as age, oestradiol levels, endometrial thickness etc.
LARGE SCALE DATA: The raw sequencing data used for this manuscript are publicly available at the European Nucleotide Archive under accession number PRJEB107113.
This study is a single-centre study warranting further validation cohorts. Given the variable nature of the vaginal microbiota, sample sizes need to be enlarged for better refinement of the analyses. Further, the underlying mechanistical basis of our findings is yet elusive and clinical translation has yet to be established.
While this novel association warrants confirmation, the results caution against reliance on previously suggested CSTs as predictors, and highlight the need for refined, reproducible microbiome-based diagnostics in reproductive medicine.
Financial support was received from the University of Lübeck and the German Center of Infection Research. M.L., A.M., I.P., M.D., and J.R. declare no conflicts of interest. S.G. discloses personal fees from Organon outside the submitted work. T.K.E. discloses honoraria from Ferring; travel support from Ferring, Merck, Theramex, and Gedeon-Richter; and receipt of equipment/materials/laboratory analyses (to institution) from Arthrex, Besins, Merck, and Abbott outside the submitted work. N.H. discloses personal fees from Gedeon Richter, Ferring, and Merck. G.G. reports that his institution received grants or contracts from Besins, Merck, Abbott, Ferring, and Theramex. He has received personal consulting fees, support for travel fees and meeting attendance, and honoraria for lectures or educational events from Organon, Ferring, Merck, Gedeon-Richter, Theramex, Abbott, ReproNovo, Igyxos, OxoLife, Philipps, ReprodWissen, PregLem, Guerbet, Roche, IBSA, and Besins. He also received support for travel and meeting attendance from Merck, Organon, Ferring, Theramex, Gedeon-Richter, and Abbott. Additionally, he holds unpaid leadership positions as a member of the ESHRE Working Group on RIF, the ESHRE Working Group on clinical KPI, and the ESHRE guideline development group on ovarian stimulation. A.S.-M. reports consulting fees and speaker's fees from Merck, Theramex, and Gedeon-Richter as well as travel support from Merck, Theramex, Gedeon-Richter, IBSA, Ferring, and MSD.},
}
RevDate: 2026-04-02
Response of the mTOR signaling pathway to the reproductive dysfunction of dysbiosis-induced male mice.
Reproductive biology, 26(2):101213 pii:S1642-431X(26)00035-5 [Epub ahead of print].
The mammalian target of rapamycin (mTOR) signaling pathway plays a key role in coordinating several cellular activities in response to environmental signals, thereby influencing metabolism and reproduction. This study aimed to determine the role of mTOR signaling pathway in testicular dysfunction caused by intestinal microbiome imbalance. An antibiotic mixture containing ampicillin, neomycin sulfate, vancomycin, and metronidazole was administered orally to mice for four weeks, and subsequently serum, and tissues were obtained following sacrifice. Glucose, cholesterol, and sex hormone levels were measured in the serum, and real-time PCR was performed using extracts of the ileum and testis to determine the expression of genes associated with pro-inflammatory cytokines, mTOR signals and testosterone synthesis. The levels of glucose and sex hormones in the serum of antibiotic-induced dysbiosis (WD) mice were significantly decreased, while the cholesterol levels were elevated (p < 0.05). The mRNA expression of IL-1β, IL-6 and TNF-α significantly increased in the testis of the WD group (p < 0.05 & p < 0.01), while testosterone synthesis, such as the expression of 3β-HSD and P450scc decreased (p < 0.05). Immunofluorescence revealed the localization of mTOR in the mid-piece and tail of the epididymal spermatozoa. The mRNA expression of mTOR signaling pathway, including Mtor, Raptor, p53, PI3K, Akt1, P70s6k, and Rheb, was significantly upregulated in the testis of the WD group (p < 0.05). Consequently, antibiotic-induced dysbiosis in male mice led to increased secretion of pro-inflammatory cytokines in the testis, decreased serum sex hormone levels, and impaired sperm quality, all of which could be associated with altered regulation of the mTOR signaling pathway.
Additional Links: PMID-41924822
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PubMed:
Citation:
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@article {pmid41924822,
year = {2026},
author = {Gamage, MAGNDMA and Dissanayake, WMN and Yi, YJ},
title = {Response of the mTOR signaling pathway to the reproductive dysfunction of dysbiosis-induced male mice.},
journal = {Reproductive biology},
volume = {26},
number = {2},
pages = {101213},
doi = {10.1016/j.repbio.2026.101213},
pmid = {41924822},
issn = {2300-732X},
abstract = {The mammalian target of rapamycin (mTOR) signaling pathway plays a key role in coordinating several cellular activities in response to environmental signals, thereby influencing metabolism and reproduction. This study aimed to determine the role of mTOR signaling pathway in testicular dysfunction caused by intestinal microbiome imbalance. An antibiotic mixture containing ampicillin, neomycin sulfate, vancomycin, and metronidazole was administered orally to mice for four weeks, and subsequently serum, and tissues were obtained following sacrifice. Glucose, cholesterol, and sex hormone levels were measured in the serum, and real-time PCR was performed using extracts of the ileum and testis to determine the expression of genes associated with pro-inflammatory cytokines, mTOR signals and testosterone synthesis. The levels of glucose and sex hormones in the serum of antibiotic-induced dysbiosis (WD) mice were significantly decreased, while the cholesterol levels were elevated (p < 0.05). The mRNA expression of IL-1β, IL-6 and TNF-α significantly increased in the testis of the WD group (p < 0.05 & p < 0.01), while testosterone synthesis, such as the expression of 3β-HSD and P450scc decreased (p < 0.05). Immunofluorescence revealed the localization of mTOR in the mid-piece and tail of the epididymal spermatozoa. The mRNA expression of mTOR signaling pathway, including Mtor, Raptor, p53, PI3K, Akt1, P70s6k, and Rheb, was significantly upregulated in the testis of the WD group (p < 0.05). Consequently, antibiotic-induced dysbiosis in male mice led to increased secretion of pro-inflammatory cytokines in the testis, decreased serum sex hormone levels, and impaired sperm quality, all of which could be associated with altered regulation of the mTOR signaling pathway.},
}
RevDate: 2026-04-03
Caenorhabditis elegans fed native gut microbiota have altered bioenergetic pathway utilization impacting mitochondrial function and susceptibility to pollutants.
Environmental science. Processes & impacts [Epub ahead of print].
The gut microbiome can influence host health by facilitating digestion, immune function, and xenobiotic metabolism. Microbial metabolites can influence mitochondrial function by shifting bioenergetic pathways, potentially altering sensitivity to mitochondrial toxicants. However, mechanisms through which the gut microbiota can alter mitochondrial function and susceptibility to mitochondrial toxicity are not well characterized. We used the model organism Caenorhabditis elegans and the microbiome kit CeMbio, a characterized collection of native gut commensals, to explore the interactions between gut microbiota, mitochondrial function, and chemical susceptibility. C. elegans grown on selected bacterial strains had varying levels of steady-state whole-body ATP, with an ∼3 fold difference between the highest and lowest strains, as well as 2- and 3-fold changes in antioxidant and mitochondrial unfolded protein gene induction. Further, C. elegans grown on selected bacterial strains showed differential sensitivity to short-term exposure to chemicals that inhibit mitochondrial electron transport chain Complexes I, II, and V, and fatty acid oxidation. To test mechanistically how microbiome-mediated sensitivities could result in chemical susceptibility, we carried out follow-up experiments using the Complex I inhibitor rotenone. We found that C. elegans grown on BIGb0170 (Sphingobacterium multivorum) had much higher lethality after 24- and 48-hour exposures than when grown on MYb10 (Acinetobacter guillouiae), MYb11 (Pseudomonas lurida), and OP50 (Escherichia coli) strains. Metabolomic analysis revealed that C. elegans grown on BIGb0170 had lower amounts of triglycerides and acylcarnitines. ATP levels were partially rescued by supplementing BIGb0170 with pyruvate. This work suggests that BIGb0170 can impact mitochondrial function through changes in metabolite abundance, which can increase sensitivity to the Complex I inhibitor rotenone.
Additional Links: PMID-41925161
PubMed:
Citation:
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@article {pmid41925161,
year = {2026},
author = {Bergemann, CM and Jameson, LE and Kenny-Ganzert, IW and Huayta, J and Castellano-Escuder, P and Sarkar, A and Ilkayeva, OR and Sherwood, DR and Hirschey, MD and Meyer, JN},
title = {Caenorhabditis elegans fed native gut microbiota have altered bioenergetic pathway utilization impacting mitochondrial function and susceptibility to pollutants.},
journal = {Environmental science. Processes & impacts},
volume = {},
number = {},
pages = {},
pmid = {41925161},
issn = {2050-7895},
support = {P42 ES010356/ES/NIEHS NIH HHS/United States ; R01 ES034270/ES/NIEHS NIH HHS/United States ; R35 GM118049/GM/NIGMS NIH HHS/United States ; T32 ES021432/ES/NIEHS NIH HHS/United States ; },
abstract = {The gut microbiome can influence host health by facilitating digestion, immune function, and xenobiotic metabolism. Microbial metabolites can influence mitochondrial function by shifting bioenergetic pathways, potentially altering sensitivity to mitochondrial toxicants. However, mechanisms through which the gut microbiota can alter mitochondrial function and susceptibility to mitochondrial toxicity are not well characterized. We used the model organism Caenorhabditis elegans and the microbiome kit CeMbio, a characterized collection of native gut commensals, to explore the interactions between gut microbiota, mitochondrial function, and chemical susceptibility. C. elegans grown on selected bacterial strains had varying levels of steady-state whole-body ATP, with an ∼3 fold difference between the highest and lowest strains, as well as 2- and 3-fold changes in antioxidant and mitochondrial unfolded protein gene induction. Further, C. elegans grown on selected bacterial strains showed differential sensitivity to short-term exposure to chemicals that inhibit mitochondrial electron transport chain Complexes I, II, and V, and fatty acid oxidation. To test mechanistically how microbiome-mediated sensitivities could result in chemical susceptibility, we carried out follow-up experiments using the Complex I inhibitor rotenone. We found that C. elegans grown on BIGb0170 (Sphingobacterium multivorum) had much higher lethality after 24- and 48-hour exposures than when grown on MYb10 (Acinetobacter guillouiae), MYb11 (Pseudomonas lurida), and OP50 (Escherichia coli) strains. Metabolomic analysis revealed that C. elegans grown on BIGb0170 had lower amounts of triglycerides and acylcarnitines. ATP levels were partially rescued by supplementing BIGb0170 with pyruvate. This work suggests that BIGb0170 can impact mitochondrial function through changes in metabolite abundance, which can increase sensitivity to the Complex I inhibitor rotenone.},
}
RevDate: 2026-04-02
Phage-display immunoprecipitation sequencing reveals distinct antibody signatures against bacterial flagellins associated with treatment response in Crohn's disease.
Clinical and translational gastroenterology pii:01720094-990000000-00569 [Epub ahead of print].
OBJECTIVES: Enhanced immune response against bacterial flagellins among patients with Crohn's disease (CD) is associated with aggressive disease course. However, its association with response to biologic treatment is unknown. We aimed to assess whether treatment response among patients with CD is associated with antibody reaction to bacterial flagellins and related microbial alterations.
METHODS: Thirty-nine patients with active CD (Harvey-Bradshaw Index [HBI]>4 or fecal calprotectin [FCP]>150μg/g) commencing biologic treatment were included. Serum and stool samples were collected at baseline and during treatment at weeks 14, 22 and 52. Serum samples were analyzed using high-throughput phage-display immunoprecipitation sequencing (PhIP-Seq) and fecal samples by DNA shotgun metagenomic sequencing.
RESULTS: Using PhIP-Seq analysis, only the anti-flagellin antibodies library showed consistently attenuated antibody responses against bacterial flagellins in patients achieving remission (HBI≤4 and FCP≤150) versus non-remission at all time points (p<0.05). Of the 55 anti-flagellin antibodies analyzed, 15 showed consistent >1.5-fold over-representation in non-remission samples, with high conservation of amino-acid sequences and targeting of Clostridiales, Lachnospiraceae, or Roseburia species. Remission was associated with increased abundance of flagellin-target taxa including Roseburia intestinalis and decreased Ruminococcus_B gnavus and pathways involved in cellular oxidative stress, while non-remission showed increased Bacteroides species and pathways involved in 5-aminoimidazole ribonucleotide and semi-essential amino acids biosynthesis (q<0.05).
CONCLUSIONS: PhIP-Seq revealed that biologic treatment response in patients with CD associates with consistently decreased antibody responses against specific bacterial flagellins with conserved sequences. These findings identify potential biomarkers and therapeutic targets for improving treatment outcomes.
Additional Links: PMID-41925202
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PubMed:
Citation:
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@article {pmid41925202,
year = {2026},
author = {Leibovitzh, H and Krongauz, D and Schlesinger, Y and Cohen, NA and Hirsch, A and Ron, Y and Thurm, T and Godneva, A and Weinberger, A and Segal, E and Maharshak, N},
title = {Phage-display immunoprecipitation sequencing reveals distinct antibody signatures against bacterial flagellins associated with treatment response in Crohn's disease.},
journal = {Clinical and translational gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.14309/ctg.0000000000001030},
pmid = {41925202},
issn = {2155-384X},
abstract = {OBJECTIVES: Enhanced immune response against bacterial flagellins among patients with Crohn's disease (CD) is associated with aggressive disease course. However, its association with response to biologic treatment is unknown. We aimed to assess whether treatment response among patients with CD is associated with antibody reaction to bacterial flagellins and related microbial alterations.
METHODS: Thirty-nine patients with active CD (Harvey-Bradshaw Index [HBI]>4 or fecal calprotectin [FCP]>150μg/g) commencing biologic treatment were included. Serum and stool samples were collected at baseline and during treatment at weeks 14, 22 and 52. Serum samples were analyzed using high-throughput phage-display immunoprecipitation sequencing (PhIP-Seq) and fecal samples by DNA shotgun metagenomic sequencing.
RESULTS: Using PhIP-Seq analysis, only the anti-flagellin antibodies library showed consistently attenuated antibody responses against bacterial flagellins in patients achieving remission (HBI≤4 and FCP≤150) versus non-remission at all time points (p<0.05). Of the 55 anti-flagellin antibodies analyzed, 15 showed consistent >1.5-fold over-representation in non-remission samples, with high conservation of amino-acid sequences and targeting of Clostridiales, Lachnospiraceae, or Roseburia species. Remission was associated with increased abundance of flagellin-target taxa including Roseburia intestinalis and decreased Ruminococcus_B gnavus and pathways involved in cellular oxidative stress, while non-remission showed increased Bacteroides species and pathways involved in 5-aminoimidazole ribonucleotide and semi-essential amino acids biosynthesis (q<0.05).
CONCLUSIONS: PhIP-Seq revealed that biologic treatment response in patients with CD associates with consistently decreased antibody responses against specific bacterial flagellins with conserved sequences. These findings identify potential biomarkers and therapeutic targets for improving treatment outcomes.},
}
RevDate: 2026-04-02
Microoxic conditions promote Escherichia-associated cellulase expression in the giant panda gut.
The ISME journal pii:8572364 [Epub ahead of print].
Giant pandas possess a carnivore-like gastrointestinal tract yet subsist on bamboo, and their gut communities contain few canonical cellulolytic taxa. We investigated how fiber processing proceeds in this setting by building a species-resolved reference and linking community features to cellular transcriptional profiles and isolate phenotypes. Using culturomics and PacBio HiFi metagenomics, we assembled a species-resolved reference catalog for the panda gut microbiome (Pbac v2; 466 species-level genomes). Community profiling across 142 samples resolved three enterotypes dominated by Escherichia coli (ET-Ecoli), Clostridium SGBP116 (ET-Clos), and Streptococcus alactolyticus (ET-StreA), with ET-Ecoli enriched for tricarboxylic-acid and respiratory-chain modules and showing higher abundance of an endo-β-1,4-glucanase marker. Droplet-based microbial single-cell RNA-seq from four samples (16 659 cells) assigned a substantial share of cellulase-associated transcripts (GH1/GH3/GH5/GH9) in situ to Escherichia and revealed within-species heterogeneity: E. coli subpopulations segregated into respiration-enriched versus three-carbon/anaerobic-like programs, with cellulase/LPMO-linked transcripts concentrated in the former. Guided by these associations, panda-derived E. coli isolates assayed under defined atmospheres showed oxygen-dependent cellulolytic readouts in vitro. Although in vivo oxygen levels were not measured, the convergence of species-resolved community signatures, single-cell attribution and isolate phenotypes indicates that E. coli can contribute to cellulose processing under microoxic conditions in this cohort. The Pbac v2 resource and the integrated workflow (culturomics + HiFi metagenomes, multi-omics, microbial scRNA-seq) provide a template for species-level assignment of microbiome functions in hosts with unconventional diet-physiology combinations.
Additional Links: PMID-41925227
Publisher:
PubMed:
Citation:
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@article {pmid41925227,
year = {2026},
author = {Deng, F and Han, Y and Peng, Y and Xu, Z and Yang, J and He, J and Li, D and Dong, G and Zhang, P and Jiang, H and Chai, J and Wang, C and Zhao, J and Li, Y},
title = {Microoxic conditions promote Escherichia-associated cellulase expression in the giant panda gut.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag068},
pmid = {41925227},
issn = {1751-7370},
abstract = {Giant pandas possess a carnivore-like gastrointestinal tract yet subsist on bamboo, and their gut communities contain few canonical cellulolytic taxa. We investigated how fiber processing proceeds in this setting by building a species-resolved reference and linking community features to cellular transcriptional profiles and isolate phenotypes. Using culturomics and PacBio HiFi metagenomics, we assembled a species-resolved reference catalog for the panda gut microbiome (Pbac v2; 466 species-level genomes). Community profiling across 142 samples resolved three enterotypes dominated by Escherichia coli (ET-Ecoli), Clostridium SGBP116 (ET-Clos), and Streptococcus alactolyticus (ET-StreA), with ET-Ecoli enriched for tricarboxylic-acid and respiratory-chain modules and showing higher abundance of an endo-β-1,4-glucanase marker. Droplet-based microbial single-cell RNA-seq from four samples (16 659 cells) assigned a substantial share of cellulase-associated transcripts (GH1/GH3/GH5/GH9) in situ to Escherichia and revealed within-species heterogeneity: E. coli subpopulations segregated into respiration-enriched versus three-carbon/anaerobic-like programs, with cellulase/LPMO-linked transcripts concentrated in the former. Guided by these associations, panda-derived E. coli isolates assayed under defined atmospheres showed oxygen-dependent cellulolytic readouts in vitro. Although in vivo oxygen levels were not measured, the convergence of species-resolved community signatures, single-cell attribution and isolate phenotypes indicates that E. coli can contribute to cellulose processing under microoxic conditions in this cohort. The Pbac v2 resource and the integrated workflow (culturomics + HiFi metagenomes, multi-omics, microbial scRNA-seq) provide a template for species-level assignment of microbiome functions in hosts with unconventional diet-physiology combinations.},
}
RevDate: 2026-04-02
Harnessing the lung microbiome for precision management of fibrotic lung disease.
Trends in molecular medicine pii:S1471-4914(26)00032-8 [Epub ahead of print].
Interstitial lung diseases, particularly idiopathic pulmonary fibrosis (IPF), have dismal prognoses, with a median survival of 3-5 years, owing to a lack of early biomarkers or effective treatments. This review highlights the lung microbiome as a key biological factor in IPF pathogenesis and a promising therapeutic target. Elevated burdens of pathogenic bacteria, including Streptococcus and Staphylococcus, in bronchoalveolar lavage fluid correlate with accelerated progression and higher mortality. These bacteria release toxins and activate Th17-driven inflammation, providing mechanistic links to alveolar injury and fibrosis. Host genetics and systemic factors, including oral-gut-lung interactions, further shape disease progression. Although antibiotic trials have been unsuccessful, embracing the microbiome as an active participant in IPF may open unprecedented opportunities for personalized interventions.
Additional Links: PMID-41925420
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@article {pmid41925420,
year = {2026},
author = {Leroy, S and Roméo, B and Belaid, A and Brest, P and Marquette, CH and Vouret-Craviari, V and Hofman, V and Hofman, P and Mograbi, B},
title = {Harnessing the lung microbiome for precision management of fibrotic lung disease.},
journal = {Trends in molecular medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.molmed.2026.02.002},
pmid = {41925420},
issn = {1471-499X},
abstract = {Interstitial lung diseases, particularly idiopathic pulmonary fibrosis (IPF), have dismal prognoses, with a median survival of 3-5 years, owing to a lack of early biomarkers or effective treatments. This review highlights the lung microbiome as a key biological factor in IPF pathogenesis and a promising therapeutic target. Elevated burdens of pathogenic bacteria, including Streptococcus and Staphylococcus, in bronchoalveolar lavage fluid correlate with accelerated progression and higher mortality. These bacteria release toxins and activate Th17-driven inflammation, providing mechanistic links to alveolar injury and fibrosis. Host genetics and systemic factors, including oral-gut-lung interactions, further shape disease progression. Although antibiotic trials have been unsuccessful, embracing the microbiome as an active participant in IPF may open unprecedented opportunities for personalized interventions.},
}
RevDate: 2026-04-02
The rhizosphere microbiome as a decentralized immune system.
Trends in microbiology pii:S0966-842X(26)00065-X [Epub ahead of print].
Plant immunity should be reconsidered beyond the boundaries of the plant genome. We propose that the rhizosphere microbiome may function analogously to a decentralized immune system, contributing adaptive defenselike properties and memory effects. In this forum article, we discuss how this perspective reframes immunity as an emergent property of plant-microbiome interactions, shifting the focus from a solitary host toward an integrated holobiont.
Additional Links: PMID-41925447
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@article {pmid41925447,
year = {2026},
author = {Araujo, ASF and Pereira, APA and de Medeiros, EV and Mendes, LW},
title = {The rhizosphere microbiome as a decentralized immune system.},
journal = {Trends in microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tim.2026.03.006},
pmid = {41925447},
issn = {1878-4380},
abstract = {Plant immunity should be reconsidered beyond the boundaries of the plant genome. We propose that the rhizosphere microbiome may function analogously to a decentralized immune system, contributing adaptive defenselike properties and memory effects. In this forum article, we discuss how this perspective reframes immunity as an emergent property of plant-microbiome interactions, shifting the focus from a solitary host toward an integrated holobiont.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
The Gut Microbiome in Amyotrophic Lateral Sclerosis: Emerging Mechanisms and Therapeutic Potential.
Molecular neurobiology, 63(1):.
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder marked by progressive loss of motor neurons and a median survival of 2 to 3 years after symptom onset. Despite advances in genetics, particularly the identification of mutations in C9ORF72, SOD1, and TDP 43, substantial variability in disease onset and progression remains unexplained. Mounting evidence points to the gut microbiome as a potential modifier of ALS biology. Microbial communities within the intestine influence systemic and central immune responses, energy metabolism, and the bioavailability of nutrients and therapeutic agents. Animal studies reveal that dysbiosis contributes to intestinal barrier dysfunction, immune activation, and altered metabolite production, while supplementation with beneficial metabolites such as butyrate or nicotinamide can delay disease progression and extend survival. Human studies, though inconsistent in their findings, consistently identify microbial imbalances and loss of diversity in subsets of patients. The gut-brain axis provides a plausible framework for these effects, as microbial products can signal through endocrine, neural, and immune pathways to influence central nervous system function. Beyond motor decline, microbiota alterations may also contribute to non-motor symptoms such as depression, anxiety, and gastrointestinal dysfunction, further shaping quality of life. While methodological variability complicates interpretation, integration of microbiome research with host genomics and metabolomics offers a path toward precision medicine. Targeting microbial composition and function may ultimately represent a novel therapeutic approach capable of modifying both disease biology and patient outcomes in ALS.
Additional Links: PMID-41925964
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@article {pmid41925964,
year = {2026},
author = {Oriquat, G and H, M and Maharana, L and Dhyani, A and Al-Hasnaawei, S and Singh-Chauhan, A and Arora, V and Sharma, J and Sadeghi-Samarjan, R},
title = {The Gut Microbiome in Amyotrophic Lateral Sclerosis: Emerging Mechanisms and Therapeutic Potential.},
journal = {Molecular neurobiology},
volume = {63},
number = {1},
pages = {},
pmid = {41925964},
issn = {1559-1182},
mesh = {*Amyotrophic Lateral Sclerosis/microbiology/therapy ; Humans ; *Gastrointestinal Microbiome/physiology ; Animals ; Dysbiosis ; },
abstract = {Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder marked by progressive loss of motor neurons and a median survival of 2 to 3 years after symptom onset. Despite advances in genetics, particularly the identification of mutations in C9ORF72, SOD1, and TDP 43, substantial variability in disease onset and progression remains unexplained. Mounting evidence points to the gut microbiome as a potential modifier of ALS biology. Microbial communities within the intestine influence systemic and central immune responses, energy metabolism, and the bioavailability of nutrients and therapeutic agents. Animal studies reveal that dysbiosis contributes to intestinal barrier dysfunction, immune activation, and altered metabolite production, while supplementation with beneficial metabolites such as butyrate or nicotinamide can delay disease progression and extend survival. Human studies, though inconsistent in their findings, consistently identify microbial imbalances and loss of diversity in subsets of patients. The gut-brain axis provides a plausible framework for these effects, as microbial products can signal through endocrine, neural, and immune pathways to influence central nervous system function. Beyond motor decline, microbiota alterations may also contribute to non-motor symptoms such as depression, anxiety, and gastrointestinal dysfunction, further shaping quality of life. While methodological variability complicates interpretation, integration of microbiome research with host genomics and metabolomics offers a path toward precision medicine. Targeting microbial composition and function may ultimately represent a novel therapeutic approach capable of modifying both disease biology and patient outcomes in ALS.},
}
MeSH Terms:
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*Amyotrophic Lateral Sclerosis/microbiology/therapy
Humans
*Gastrointestinal Microbiome/physiology
Animals
Dysbiosis
RevDate: 2026-04-02
Integrative Dermatology for Longevity: The Synergy of Topical and Internal Approaches.
Dermatology and therapy [Epub ahead of print].
Skin aging reflects both intrinsic biological decline and extrinsic influences collectively known as the skin exposome, including ultraviolet (UV) radiation, air pollution, psychosocial stress, fatigue, sleep disruption, and suboptimal lifestyle behaviors. These factors contribute to cumulative molecular and structural damage, positioning the skin as both a visible marker of whole-body aging and a target for longevity strategies. This review examines the validity of an integrative "In and Out" approach, combining topical treatments, such as retinoids, peptides, antioxidants, and exosome-based formulations, with internal nutraceuticals including NAD[+] precursors, collagen peptides, polyphenols, and microbiome modulators. By targeting key hallmarks of aging, oxidative stress, inflammation, and epigenetic changes, this dual-modality model has the potential to promote skin regeneration, enhance aesthetic and functional outcomes, and contribute to broader health span optimization. Emerging tools such as skin aging clocks, biomarker-driven personalization, and artificial intelligence (AI)-guided interventions further strengthen this paradigm, establishing a scientifically grounded, preventive, and personalized framework that redefines the role of dermatology in the context of longevity. Personalized strategies that integrate diagnostic tools, lifestyle coaching, and tracking technologies allow for adaptive, dynamic strategies both internally and externally.
Additional Links: PMID-41926038
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@article {pmid41926038,
year = {2026},
author = {Haykal, D and Flament, F and Balooch, G and Mora, P and Kovylkina, N and Calixto, LS and Mercurio, DG and Sachdev, M and Sundaram, H},
title = {Integrative Dermatology for Longevity: The Synergy of Topical and Internal Approaches.},
journal = {Dermatology and therapy},
volume = {},
number = {},
pages = {},
pmid = {41926038},
issn = {2193-8210},
abstract = {Skin aging reflects both intrinsic biological decline and extrinsic influences collectively known as the skin exposome, including ultraviolet (UV) radiation, air pollution, psychosocial stress, fatigue, sleep disruption, and suboptimal lifestyle behaviors. These factors contribute to cumulative molecular and structural damage, positioning the skin as both a visible marker of whole-body aging and a target for longevity strategies. This review examines the validity of an integrative "In and Out" approach, combining topical treatments, such as retinoids, peptides, antioxidants, and exosome-based formulations, with internal nutraceuticals including NAD[+] precursors, collagen peptides, polyphenols, and microbiome modulators. By targeting key hallmarks of aging, oxidative stress, inflammation, and epigenetic changes, this dual-modality model has the potential to promote skin regeneration, enhance aesthetic and functional outcomes, and contribute to broader health span optimization. Emerging tools such as skin aging clocks, biomarker-driven personalization, and artificial intelligence (AI)-guided interventions further strengthen this paradigm, establishing a scientifically grounded, preventive, and personalized framework that redefines the role of dermatology in the context of longevity. Personalized strategies that integrate diagnostic tools, lifestyle coaching, and tracking technologies allow for adaptive, dynamic strategies both internally and externally.},
}
RevDate: 2026-04-02
The Maternal Brain in Context: Systemic Physiological Changes Across Pregnancy.
Annual review of neuroscience [Epub ahead of print].
During pregnancy, the maternal body undergoes profound, coordinated physiological adaptations to support the developing fetus, including major shifts in immune regulation and dramatic changes in the vascular system. Accompanying these peripheral adaptations, recent longitudinal studies in humans point to significant remodeling of the nervous system, occurring in lockstep with increases in gonadal hormone production. To understand the neural adaptations tied to pregnancy and the postpartum period, a holistic approach is essential-one that accounts for changes across multiple peripheral systems. In this review, we consider the impact of the endocrine, cardiovascular, microbiome, and immune systems on the maternal brain. By adopting this integrative approach, we aim to better understand the biological pathways that shape the maternal brain during normative pregnancies and those marked by adverse events.
Additional Links: PMID-41926198
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@article {pmid41926198,
year = {2026},
author = {Grotzinger, H and Martínez-García, M and Miller, EC and Stelzer, IA and Collado, MC and Jacobs, EG},
title = {The Maternal Brain in Context: Systemic Physiological Changes Across Pregnancy.},
journal = {Annual review of neuroscience},
volume = {},
number = {},
pages = {},
doi = {10.1146/annurev-neuro-102124-043515},
pmid = {41926198},
issn = {1545-4126},
abstract = {During pregnancy, the maternal body undergoes profound, coordinated physiological adaptations to support the developing fetus, including major shifts in immune regulation and dramatic changes in the vascular system. Accompanying these peripheral adaptations, recent longitudinal studies in humans point to significant remodeling of the nervous system, occurring in lockstep with increases in gonadal hormone production. To understand the neural adaptations tied to pregnancy and the postpartum period, a holistic approach is essential-one that accounts for changes across multiple peripheral systems. In this review, we consider the impact of the endocrine, cardiovascular, microbiome, and immune systems on the maternal brain. By adopting this integrative approach, we aim to better understand the biological pathways that shape the maternal brain during normative pregnancies and those marked by adverse events.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Analysis of the Impact of Preterm Premature Rupture of Membranes (PPROM) on Maternal and Infant Outcomes and Countermeasures.
International journal of women's health, 18:534571.
OBJECTIVE: This study aimed to analyze the risk factors for Preterm Premature Rupture of Membranes (PPROM) and evaluate the impact of the timing of antibiotic administration on maternal and neonatal outcomes.
METHODS: A retrospective cohort study was conducted involving 480 pregnant women (240 with PPROM and 240 without PPROM) hospitalized between January 2021 and December 2022. Maternal data, genital microbiome profiles, and pregnancy outcomes were collected and compared. Within the PPROM group, patients were subdivided into an Early Treatment group (received intravenous cefuroxime sodium within 12 hours of membrane rupture, n=120) and a Late Treatment group (received antibiotics after 12 hours, n=120). Statistical analyses were performed using SPSS 22.0.
RESULTS: Genital infections (73.8% vs 20.4%, p<0.001) and gestational diabetes mellitus (GDM; 53.3% vs 22.9%, p<0.001) were significantly more prevalent in the PPROM group and were identified as independent risk factors (Genital infections: OR=3.895; GDM: OR=11.166). The PPROM group had worse outcomes, including a higher cesarean section rate (39.2% vs 25.8%, p=0.002) and higher incidences of neonatal asphyxia (4.2% vs 0.4%, p=0.006) and sepsis (2.5% vs 0%, p=0.040). Compared to the Late Treatment group, the Early Treatment group demonstrated significantly lower rates of intrauterine infection (1.67% vs 7.50%, p<0.05), cesarean section (30.0% vs 48.3%, p<0.05), neonatal asphyxia (0.83% vs 7.50%, p<0.01), and neonatal sepsis (0% vs 5.00%, p<0.05).
CONCLUSION: Genital tract infections and GDM are significant risk factors for PPROM. Early administration of antibiotics within 12 hours of membrane rupture is associated with substantially improved maternal and neonatal outcomes, underscoring its critical importance in clinical management.
Additional Links: PMID-41926522
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Citation:
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@article {pmid41926522,
year = {2026},
author = {Chen, Y and Zhou, D and Tu, Y and Wang, Y},
title = {Analysis of the Impact of Preterm Premature Rupture of Membranes (PPROM) on Maternal and Infant Outcomes and Countermeasures.},
journal = {International journal of women's health},
volume = {18},
number = {},
pages = {534571},
pmid = {41926522},
issn = {1179-1411},
abstract = {OBJECTIVE: This study aimed to analyze the risk factors for Preterm Premature Rupture of Membranes (PPROM) and evaluate the impact of the timing of antibiotic administration on maternal and neonatal outcomes.
METHODS: A retrospective cohort study was conducted involving 480 pregnant women (240 with PPROM and 240 without PPROM) hospitalized between January 2021 and December 2022. Maternal data, genital microbiome profiles, and pregnancy outcomes were collected and compared. Within the PPROM group, patients were subdivided into an Early Treatment group (received intravenous cefuroxime sodium within 12 hours of membrane rupture, n=120) and a Late Treatment group (received antibiotics after 12 hours, n=120). Statistical analyses were performed using SPSS 22.0.
RESULTS: Genital infections (73.8% vs 20.4%, p<0.001) and gestational diabetes mellitus (GDM; 53.3% vs 22.9%, p<0.001) were significantly more prevalent in the PPROM group and were identified as independent risk factors (Genital infections: OR=3.895; GDM: OR=11.166). The PPROM group had worse outcomes, including a higher cesarean section rate (39.2% vs 25.8%, p=0.002) and higher incidences of neonatal asphyxia (4.2% vs 0.4%, p=0.006) and sepsis (2.5% vs 0%, p=0.040). Compared to the Late Treatment group, the Early Treatment group demonstrated significantly lower rates of intrauterine infection (1.67% vs 7.50%, p<0.05), cesarean section (30.0% vs 48.3%, p<0.05), neonatal asphyxia (0.83% vs 7.50%, p<0.01), and neonatal sepsis (0% vs 5.00%, p<0.05).
CONCLUSION: Genital tract infections and GDM are significant risk factors for PPROM. Early administration of antibiotics within 12 hours of membrane rupture is associated with substantially improved maternal and neonatal outcomes, underscoring its critical importance in clinical management.},
}
RevDate: 2026-04-02
Maternal Preconception Antibiotic Exposure Disrupts Microbial Succession: A Transgenerational Risk for Offspring Gut Mucosal Immaturity and Colitis Susceptibility.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
The early-life microbiome plays a pivotal role in host development and lifelong health. Maternal factors are increasingly recognized as crucial in shaping offspring microbiome. However, how maternal preconception perturbations affects offspring health remain unclear. Thus, we combined animal and clinical data to elucidate whether preconception microbial perturbations disrupt microbial succession and increase offspring susceptibility to colitis. In animals, preconception antibiotic exposure induced long-lasting disruptions in offspring microbial ecology, through enhanced maternal-offspring microbial transmission, altered microbial developmental trajectories, and increased selective pressures during microbial community assembly. Ultimately, these alterations resulted in persistent gut mucosal immaturity and heightened susceptibility to colitis in adulthood. Complementary clinical studies revealed concordant alterations in gut microbiome and metabolome of children with inflammatory bowel disease (IBD) and their seemingly healthy mothers, characterized by pro-inflammatory taxa and metabolites. Notably, mothers of IBD children reported significantly higher antibiotic exposure than controls, which was also associated with enhanced maternal-offspring microbial transmission and increased selective pressures during microbial community assembly. Our findings reveal a potential intergenerational mechanism in which preconception perturbations are associated with disrupted microbial succession, transgenerational propagation of gut mucosal immaturity, and susceptibility to colitis. These results underscore the importance of judicious antibiotic use during the often-overlooked preconception period.
Additional Links: PMID-41926667
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PubMed:
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@article {pmid41926667,
year = {2026},
author = {Chen, Y and Duan, R and Zhang, C and Li, G and Ji, X and Zhang, Q and Pei, F and Wang, K and Duan, L},
title = {Maternal Preconception Antibiotic Exposure Disrupts Microbial Succession: A Transgenerational Risk for Offspring Gut Mucosal Immaturity and Colitis Susceptibility.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e16931},
doi = {10.1002/advs.202516931},
pmid = {41926667},
issn = {2198-3844},
support = {2021YFA1301300//National Key R&D Program of China/ ; 82470578//National Natural Science Foundation of China/ ; 7254451//Beijing Natural Science Foundation/ ; },
abstract = {The early-life microbiome plays a pivotal role in host development and lifelong health. Maternal factors are increasingly recognized as crucial in shaping offspring microbiome. However, how maternal preconception perturbations affects offspring health remain unclear. Thus, we combined animal and clinical data to elucidate whether preconception microbial perturbations disrupt microbial succession and increase offspring susceptibility to colitis. In animals, preconception antibiotic exposure induced long-lasting disruptions in offspring microbial ecology, through enhanced maternal-offspring microbial transmission, altered microbial developmental trajectories, and increased selective pressures during microbial community assembly. Ultimately, these alterations resulted in persistent gut mucosal immaturity and heightened susceptibility to colitis in adulthood. Complementary clinical studies revealed concordant alterations in gut microbiome and metabolome of children with inflammatory bowel disease (IBD) and their seemingly healthy mothers, characterized by pro-inflammatory taxa and metabolites. Notably, mothers of IBD children reported significantly higher antibiotic exposure than controls, which was also associated with enhanced maternal-offspring microbial transmission and increased selective pressures during microbial community assembly. Our findings reveal a potential intergenerational mechanism in which preconception perturbations are associated with disrupted microbial succession, transgenerational propagation of gut mucosal immaturity, and susceptibility to colitis. These results underscore the importance of judicious antibiotic use during the often-overlooked preconception period.},
}
RevDate: 2026-04-02
Immune Checkpoint Inhibitors and Immunomodulators for Cancer Immunotherapy: Insights Into Resistance and Therapeutic Strategies.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
Cancer immunotherapy has redefined cancer treatment. However, the molecular and cellular basis of immune evasion and therapeutic resistance remains incompletely understood. Early immune checkpoint inhibitors have delivered significant clinical benefit, but their efficacy and durability remain limited in many patients. These limitations have driven the exploration of next-generation immune checkpoints and additional regulatory pathways that shape tumor-immune interactions. Recent advances have broadened the immune checkpoint landscape and revealed new targets. These targets operate within interconnected networks shaped by tumor-intrinsic alterations, microenvironmental cues, the microbiome, and neuroimmune crosstalk. The application of emerging technologies has enabled high-resolution dissection of immune-tumor dynamics, providing a technological foundation for improving clinical outcomes through precise patient stratification and intervention. Furthermore, distinct regulated cell deaths, including apoptosis, ferroptosis, pyroptosis, necroptosis, and alkaliptosis, are increasingly recognized as critical modulators of antitumor immunity. Harnessing these mechanisms offers a rational path toward designing targeted and controllable therapeutic strategies that enhance the efficacy and durability of cancer immunotherapy.
Additional Links: PMID-41926670
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@article {pmid41926670,
year = {2026},
author = {Chen, F and Yu, Y and Cai, X and Lin, J and Liang, R and Kang, R and Tang, D and Liu, J},
title = {Immune Checkpoint Inhibitors and Immunomodulators for Cancer Immunotherapy: Insights Into Resistance and Therapeutic Strategies.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e21355},
doi = {10.1002/advs.202521355},
pmid = {41926670},
issn = {2198-3844},
support = {32500653//National Natural Science Foundation of China/ ; 20261A031076//Guangzhou Health Science and Technology Young Talents Cultivation Program/ ; 2025M782596//China Postdoctoral Science Foundation/ ; GZC20251317//Postdoctoral Fellowship Program of China Postdoctoral Science Foundation/ ; 2024A03J0895//Guangzhou Municipal Science and Technology Bureau/ ; },
abstract = {Cancer immunotherapy has redefined cancer treatment. However, the molecular and cellular basis of immune evasion and therapeutic resistance remains incompletely understood. Early immune checkpoint inhibitors have delivered significant clinical benefit, but their efficacy and durability remain limited in many patients. These limitations have driven the exploration of next-generation immune checkpoints and additional regulatory pathways that shape tumor-immune interactions. Recent advances have broadened the immune checkpoint landscape and revealed new targets. These targets operate within interconnected networks shaped by tumor-intrinsic alterations, microenvironmental cues, the microbiome, and neuroimmune crosstalk. The application of emerging technologies has enabled high-resolution dissection of immune-tumor dynamics, providing a technological foundation for improving clinical outcomes through precise patient stratification and intervention. Furthermore, distinct regulated cell deaths, including apoptosis, ferroptosis, pyroptosis, necroptosis, and alkaliptosis, are increasingly recognized as critical modulators of antitumor immunity. Harnessing these mechanisms offers a rational path toward designing targeted and controllable therapeutic strategies that enhance the efficacy and durability of cancer immunotherapy.},
}
RevDate: 2026-04-02
Humic acid supplementation modulates ruminal and fecal microbial communities in lamb.
Research in veterinary science, 205:106166 pii:S0034-5288(26)00119-0 [Epub ahead of print].
The gastrointestinal microbiome affects the health and productivity of animals. Modifying these traits with additives may enhance their effects, making it a relevant strategy. This study investigated the effects of humic acids (HA) on the ruminal and fecal microbiomes of lambs and its potential adherence to ruminal mucosa. Twenty weaned Hampshire Down crossbred lambs aged 102.1 ± 6.6 days with an average body weight of 24.2 ± 3.5 kg were randomly allocated into two groups. Control group was fed a basal diet without HA, and treatment group was fed a basal diet with commercial HA at a dose of 500 mg/kg BW/day for 56 days. At the end of the experiment, ruminal and fecal samples were analyzed using 16S rRNA gene sequencing, and ruminal mucosal tissue from the slaughtered lambs was evaluated using histology and scanning electron microscopy (SEM). The addition of HA to the feed of lambs increased the relative abundance of the genus Bifidobacterium and decreased the genus Lachnospiraceae CAG-127 in the ruminal microbiome of lambs. Furthermore, an increase in the relative abundance of the genera Acutalibacteraceae UBA5905 and Lachnospiraceae VUNI01, along with a reduction in the order Campylobacterales and the genus Acutalibacteraceae CAG-180 was observed in the fecal microbiome. HA was not found in the ruminal mucosa of lambs, as determined by histology or SEM. HA supplementation modulated the ruminal and fecal microbiomes of lambs by reducing harmful and increasing beneficial bacteria, highlighting its potential as a functional feed additive to support ovine gut health.
Additional Links: PMID-41926812
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@article {pmid41926812,
year = {2026},
author = {Santana, DAD and Rolinski, F and Trombetta, LG and Göhringer, RMD and Lipinski, LC and Weber, SH and Sotomaior, CS and Ollhoff, RD},
title = {Humic acid supplementation modulates ruminal and fecal microbial communities in lamb.},
journal = {Research in veterinary science},
volume = {205},
number = {},
pages = {106166},
doi = {10.1016/j.rvsc.2026.106166},
pmid = {41926812},
issn = {1532-2661},
abstract = {The gastrointestinal microbiome affects the health and productivity of animals. Modifying these traits with additives may enhance their effects, making it a relevant strategy. This study investigated the effects of humic acids (HA) on the ruminal and fecal microbiomes of lambs and its potential adherence to ruminal mucosa. Twenty weaned Hampshire Down crossbred lambs aged 102.1 ± 6.6 days with an average body weight of 24.2 ± 3.5 kg were randomly allocated into two groups. Control group was fed a basal diet without HA, and treatment group was fed a basal diet with commercial HA at a dose of 500 mg/kg BW/day for 56 days. At the end of the experiment, ruminal and fecal samples were analyzed using 16S rRNA gene sequencing, and ruminal mucosal tissue from the slaughtered lambs was evaluated using histology and scanning electron microscopy (SEM). The addition of HA to the feed of lambs increased the relative abundance of the genus Bifidobacterium and decreased the genus Lachnospiraceae CAG-127 in the ruminal microbiome of lambs. Furthermore, an increase in the relative abundance of the genera Acutalibacteraceae UBA5905 and Lachnospiraceae VUNI01, along with a reduction in the order Campylobacterales and the genus Acutalibacteraceae CAG-180 was observed in the fecal microbiome. HA was not found in the ruminal mucosa of lambs, as determined by histology or SEM. HA supplementation modulated the ruminal and fecal microbiomes of lambs by reducing harmful and increasing beneficial bacteria, highlighting its potential as a functional feed additive to support ovine gut health.},
}
RevDate: 2026-04-02
Microbial community dynamics and functional potential in response to organic micropollutants in river sediments.
Marine pollution bulletin, 229:119679 pii:S0025-326X(26)00466-2 [Epub ahead of print].
Freshwater river sediments are increasingly exposed to complex mixtures of anthropogenic contaminants, yet the ecological repercussions on indigenous microbial communities -the main drivers of biogeochemical cycling- remain poorly understood. Previous investigations have focused primarily on contaminant occurrence, with no integrated assessment linking sediment contamination to microbial community structure and function. The objective of this study is to characterize the microbiome of the Upper Litani River Basin and to determine how chronic inputs of pharmaceuticals and aromatic hydrocarbons influence taxonomic composition, diversity, and predicted metabolic functions. 54 sediment samples were collected across nine locations during consecutive wet and dry seasons. Target organic micropollutants were quantified in the river sediments using validated analytical methods, and spatiotemporal patterns in microbial composition and metabolic functional potential were determined using amplicon sequencing. Across all samples, 45 phyla were identified, with Pseudomonadota, Bacillota, and Actinomycetota consistently being the dominant taxa. At the genus level, microbial communities were dominated by Acinetobacter, Exiguobacterium, Proteiniclasticum, Planococcus, and Clostridium sensu stricto. Variations in microbial community structure were correlated with the occurrence and concentrations of specific organic micropollutants detected in the sediments, namely with the pharmaceuticals ibuprofen, clomipramine and atenolol, as well as the hydrocarbons o-xylene and toluene. Functional predictions revealed a microbiome highly oriented toward chemoheterotrophic metabolism, underscoring the community's response to persistent organic enrichment. Collectively, these results demonstrate that pollutant concentrations and chemical profiles act as a major ecological force that shapes sediment microbial community dynamics and metabolic function in impacted freshwater ecosystems.
Additional Links: PMID-41926825
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PubMed:
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@article {pmid41926825,
year = {2026},
author = {Ali Ahmad, F and Salam, DA},
title = {Microbial community dynamics and functional potential in response to organic micropollutants in river sediments.},
journal = {Marine pollution bulletin},
volume = {229},
number = {},
pages = {119679},
doi = {10.1016/j.marpolbul.2026.119679},
pmid = {41926825},
issn = {1879-3363},
abstract = {Freshwater river sediments are increasingly exposed to complex mixtures of anthropogenic contaminants, yet the ecological repercussions on indigenous microbial communities -the main drivers of biogeochemical cycling- remain poorly understood. Previous investigations have focused primarily on contaminant occurrence, with no integrated assessment linking sediment contamination to microbial community structure and function. The objective of this study is to characterize the microbiome of the Upper Litani River Basin and to determine how chronic inputs of pharmaceuticals and aromatic hydrocarbons influence taxonomic composition, diversity, and predicted metabolic functions. 54 sediment samples were collected across nine locations during consecutive wet and dry seasons. Target organic micropollutants were quantified in the river sediments using validated analytical methods, and spatiotemporal patterns in microbial composition and metabolic functional potential were determined using amplicon sequencing. Across all samples, 45 phyla were identified, with Pseudomonadota, Bacillota, and Actinomycetota consistently being the dominant taxa. At the genus level, microbial communities were dominated by Acinetobacter, Exiguobacterium, Proteiniclasticum, Planococcus, and Clostridium sensu stricto. Variations in microbial community structure were correlated with the occurrence and concentrations of specific organic micropollutants detected in the sediments, namely with the pharmaceuticals ibuprofen, clomipramine and atenolol, as well as the hydrocarbons o-xylene and toluene. Functional predictions revealed a microbiome highly oriented toward chemoheterotrophic metabolism, underscoring the community's response to persistent organic enrichment. Collectively, these results demonstrate that pollutant concentrations and chemical profiles act as a major ecological force that shapes sediment microbial community dynamics and metabolic function in impacted freshwater ecosystems.},
}
RevDate: 2026-04-02
The vaginal microbiome and HIV acquisition risk.
The lancet. HIV pii:S2352-3018(26)00032-9 [Epub ahead of print].
Non-optimal vaginal bacteriomes, vulvovaginal candidiasis, and sexually transmitted infections have been associated with increased risk of HIV acquisition in multiple clinical studies. However, there are still major gaps in our understanding of the role of the vaginal microbiome in HIV acquisition risk and non-bacterial components of the vaginal microbiome are not well characterised. Additionally, the functional interactions between the vaginal microbiome and its host that can result in increased risk of HIV acquisition are not fully understood. Better vaginal microbiome diagnostics and therapeutics feasible for implementation in settings with insufficient financial, human, and infrastructural resources are needed, and the effects of vaginal microbiome interventions on HIV risk need to be clinically evaluated. Progress is being made towards effective interventions through advanced omics technologies and improved in-vitro models that more accurately represent the complexity of the female genital tract. However, continued research and investments are needed to address this important women's health issue.
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@article {pmid41926978,
year = {2026},
author = {Masson, L and Radzey, N and Abrahams, AG and Ngcapu, S and McKinnon, L and Jaspan, HB},
title = {The vaginal microbiome and HIV acquisition risk.},
journal = {The lancet. HIV},
volume = {},
number = {},
pages = {},
doi = {10.1016/S2352-3018(26)00032-9},
pmid = {41926978},
issn = {2352-3018},
abstract = {Non-optimal vaginal bacteriomes, vulvovaginal candidiasis, and sexually transmitted infections have been associated with increased risk of HIV acquisition in multiple clinical studies. However, there are still major gaps in our understanding of the role of the vaginal microbiome in HIV acquisition risk and non-bacterial components of the vaginal microbiome are not well characterised. Additionally, the functional interactions between the vaginal microbiome and its host that can result in increased risk of HIV acquisition are not fully understood. Better vaginal microbiome diagnostics and therapeutics feasible for implementation in settings with insufficient financial, human, and infrastructural resources are needed, and the effects of vaginal microbiome interventions on HIV risk need to be clinically evaluated. Progress is being made towards effective interventions through advanced omics technologies and improved in-vitro models that more accurately represent the complexity of the female genital tract. However, continued research and investments are needed to address this important women's health issue.},
}
RevDate: 2026-04-02
Increased gastrointestinal cancer risk in cystic fibrosis: Screening, prevention, and future directions.
Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society pii:S1569-1993(26)00092-5 [Epub ahead of print].
The marked improvement in life expectancy from advances in treatment for cystic fibrosis has focused attention on diseases of aging. Cystic fibrosis (CF) is associated with increased risk for digestive system malignancies, including colorectal cancer and pancreaticobiliary cancers. Although risk factors for gastrointestinal malignancy include solid organ transplant and older age, people with CF may present with cancer at a younger age than the general population. Potential mechanisms for increased digestive cancer susceptibility include the underlying genetic defect, dietary patterns, or alterations in the gut microbiome. The impact of cystic fibrosis transmembrane regulator modulator therapies on gastrointestinal cancer risk remains unclear. Our review summarizes the previously published consensus screening recommendations for colorectal cancer, which endorsed starting colonoscopy at age 30 in patients with history of transplant and at age 40 in patients without a transplant. Recent work evaluating the use of non invasive testing for colorectal cancer is reviewed. We propose screening practices for non-colorectal cancers based on the limited evidence to date. We discuss potential preventative approaches and conclude with future directions to improve our ability to address this growing problem. Future work should focus on a greater understanding of the underlying mechanisms of pathogenesis at a molecular level, clinical risk factors for gastrointestinal malignancies at a population level, and preventative strategies.
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@article {pmid41927358,
year = {2026},
author = {Cummings, LC and Freedman, SD},
title = {Increased gastrointestinal cancer risk in cystic fibrosis: Screening, prevention, and future directions.},
journal = {Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jcf.2026.03.024},
pmid = {41927358},
issn = {1873-5010},
abstract = {The marked improvement in life expectancy from advances in treatment for cystic fibrosis has focused attention on diseases of aging. Cystic fibrosis (CF) is associated with increased risk for digestive system malignancies, including colorectal cancer and pancreaticobiliary cancers. Although risk factors for gastrointestinal malignancy include solid organ transplant and older age, people with CF may present with cancer at a younger age than the general population. Potential mechanisms for increased digestive cancer susceptibility include the underlying genetic defect, dietary patterns, or alterations in the gut microbiome. The impact of cystic fibrosis transmembrane regulator modulator therapies on gastrointestinal cancer risk remains unclear. Our review summarizes the previously published consensus screening recommendations for colorectal cancer, which endorsed starting colonoscopy at age 30 in patients with history of transplant and at age 40 in patients without a transplant. Recent work evaluating the use of non invasive testing for colorectal cancer is reviewed. We propose screening practices for non-colorectal cancers based on the limited evidence to date. We discuss potential preventative approaches and conclude with future directions to improve our ability to address this growing problem. Future work should focus on a greater understanding of the underlying mechanisms of pathogenesis at a molecular level, clinical risk factors for gastrointestinal malignancies at a population level, and preventative strategies.},
}
RevDate: 2026-04-02
Letter to the Editor re: "Age-related changes in the urinary microbiome of healthy Japanese children".
Additional Links: PMID-41927378
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@article {pmid41927378,
year = {2026},
author = {Cai, Z and Han, C},
title = {Letter to the Editor re: "Age-related changes in the urinary microbiome of healthy Japanese children".},
journal = {Journal of pediatric urology},
volume = {},
number = {},
pages = {105884},
doi = {10.1016/j.jpurol.2026.105884},
pmid = {41927378},
issn = {1873-4898},
}
RevDate: 2026-04-01
Terracing influences soil microbial assembly in citrus orchards: stochastic processes dominate community dynamics in a karst sloping land.
BMC microbiology, 26(1):.
BACKGROUND: Terracing is a key soil conservation practice in karst citrus orchards, yet its long-term effects on rhizosphere microbial community assembly remain poorly understood, especially the relative influence of deterministic (e.g., environmental filtering) versus stochastic processes (e.g., dispersal limitation).
RESULTS: We investigated rhizosphere soil microbial communities along a terrace chronosequence (0–12 years) in the Lijiang River Basin using MiSeq sequencing and metabolomics, with null model analysis employed to assess community assembly processes. Terrace age did not significantly affect microbial α-diversity, but was associated with subtle changes in community composition: Proteobacteria, a copiotrophic group, decreased slightly, while Chloroflexi, an oligotrophic group, increased modestly. These shifts suggest a weak trend toward lower soil nutrient availability rather than a clear successional reorganization. Microbial diversity and structure were significantly correlated with soil stoichiometric ratios and available phosphorus (p < 0.05). Terracing also affected microbial network complexity and potential function. Potential functional profiling and metabolome data revealed that L-glutamine, a key nitrogen source, was negatively correlated with potential catabolic nitrate reduction (p < 0.05). This relationship was most pronounced at the Y5 phase (peak diversity/network complexity), suggesting accelerated L-glutamine utilization tightly coupled with enhanced potential for dissimilatory nitrate reduction to maximize nitrogen-use efficiency during the successional climax. Notably, stochastic processes explained over 96% of the microbial assembly. Bacterial communities were primarily driven by homogenizing dispersal, while fungal communities followed undominated processes.
CONCLUSION: The prominence of stochasticity in our results complements current understanding of agricultural microbiome assembly, particularly emphasizing its vital role in fragile karst environments. We propose that optimizing terrace rotation intervals (e.g., every 5-year) could be a practical strategy to enhance nitrogen-cycling efficiency and support sustainable nutrient management in karst citrus cultivation.
GRAPHICAL ABSTRACT: [Image: see text]
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-026-04811-4.
Additional Links: PMID-41742032
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@article {pmid41742032,
year = {2026},
author = {Zhang, J and Dai, Y and Mustafa, A and Li, L and Li, Y and Sun, T and Chen, M and Yang, H and Ma, J},
title = {Terracing influences soil microbial assembly in citrus orchards: stochastic processes dominate community dynamics in a karst sloping land.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {},
pmid = {41742032},
issn = {1471-2180},
support = {GUIKE AB22080071//Guangxi Key Research and Development Program/ ; AA20161002//Science and Technology Major Project of Guangxi/ ; },
abstract = {BACKGROUND: Terracing is a key soil conservation practice in karst citrus orchards, yet its long-term effects on rhizosphere microbial community assembly remain poorly understood, especially the relative influence of deterministic (e.g., environmental filtering) versus stochastic processes (e.g., dispersal limitation).
RESULTS: We investigated rhizosphere soil microbial communities along a terrace chronosequence (0–12 years) in the Lijiang River Basin using MiSeq sequencing and metabolomics, with null model analysis employed to assess community assembly processes. Terrace age did not significantly affect microbial α-diversity, but was associated with subtle changes in community composition: Proteobacteria, a copiotrophic group, decreased slightly, while Chloroflexi, an oligotrophic group, increased modestly. These shifts suggest a weak trend toward lower soil nutrient availability rather than a clear successional reorganization. Microbial diversity and structure were significantly correlated with soil stoichiometric ratios and available phosphorus (p < 0.05). Terracing also affected microbial network complexity and potential function. Potential functional profiling and metabolome data revealed that L-glutamine, a key nitrogen source, was negatively correlated with potential catabolic nitrate reduction (p < 0.05). This relationship was most pronounced at the Y5 phase (peak diversity/network complexity), suggesting accelerated L-glutamine utilization tightly coupled with enhanced potential for dissimilatory nitrate reduction to maximize nitrogen-use efficiency during the successional climax. Notably, stochastic processes explained over 96% of the microbial assembly. Bacterial communities were primarily driven by homogenizing dispersal, while fungal communities followed undominated processes.
CONCLUSION: The prominence of stochasticity in our results complements current understanding of agricultural microbiome assembly, particularly emphasizing its vital role in fragile karst environments. We propose that optimizing terrace rotation intervals (e.g., every 5-year) could be a practical strategy to enhance nitrogen-cycling efficiency and support sustainable nutrient management in karst citrus cultivation.
GRAPHICAL ABSTRACT: [Image: see text]
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-026-04811-4.},
}
RevDate: 2026-04-02
Functional potential of archaeal KEGG enzymes in the Moringa oleifera rhizosphere revealed by metagenomic analysis.
BMC genomics, 27(1):.
BACKGROUND: Archaea are a major domain of life that inhabit diverse and often extreme environments, contributing to biogeochemical cycles and participating in nutrient cycling within plant rhizospheric soils. This study applies metagenomic whole-genome shotgun sequencing to characterize the archaeal component of the rhizospheric microbiome associated with the wild plant species Moringa oleifera in Saudi Arabia.
RESULTS: Based on KEGG-annotated enzymes, Thaumarchaeota and Euryarchaeota emerged as the predominant archaeal phyla in the rhizosphere, with higher abundance than in bulk soil. The most abundant archaeal enzymes were assigned to metabolic pathways related to nitrogen and sulfur metabolism, carbon transformations, and responses to oxidative stress, indicating a putative contribution to nutrient turnover and stress-related functions. Network analysis further identified archaeal chemotaxis-related regulators and two-component sensor kinases linked to the root–soil interface. Key enzymes detected included urease, glutamine synthetase, thiosulfate sulfurtransferase, and catalase-peroxidase.
CONCLUSIONS: These findings suggest that archaeal communities form a distinct functional module within the M. oleifera rhizosphere, potentially influencing soil nutrient dynamics and plant performance. The chief limitation is reliance on DNA-based metagenomic data from a single site and time point, without multi-omics or detailed soil characterization, restricting temporal and ecological generalization. Nonetheless, the dataset provides a genome-scale view of archaeal functional potential and offers testable directions for future experimental and process-oriented studies.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12864-026-12700-3.
Additional Links: PMID-41749104
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@article {pmid41749104,
year = {2026},
author = {Baz, L},
title = {Functional potential of archaeal KEGG enzymes in the Moringa oleifera rhizosphere revealed by metagenomic analysis.},
journal = {BMC genomics},
volume = {27},
number = {1},
pages = {},
pmid = {41749104},
issn = {1471-2164},
abstract = {BACKGROUND: Archaea are a major domain of life that inhabit diverse and often extreme environments, contributing to biogeochemical cycles and participating in nutrient cycling within plant rhizospheric soils. This study applies metagenomic whole-genome shotgun sequencing to characterize the archaeal component of the rhizospheric microbiome associated with the wild plant species Moringa oleifera in Saudi Arabia.
RESULTS: Based on KEGG-annotated enzymes, Thaumarchaeota and Euryarchaeota emerged as the predominant archaeal phyla in the rhizosphere, with higher abundance than in bulk soil. The most abundant archaeal enzymes were assigned to metabolic pathways related to nitrogen and sulfur metabolism, carbon transformations, and responses to oxidative stress, indicating a putative contribution to nutrient turnover and stress-related functions. Network analysis further identified archaeal chemotaxis-related regulators and two-component sensor kinases linked to the root–soil interface. Key enzymes detected included urease, glutamine synthetase, thiosulfate sulfurtransferase, and catalase-peroxidase.
CONCLUSIONS: These findings suggest that archaeal communities form a distinct functional module within the M. oleifera rhizosphere, potentially influencing soil nutrient dynamics and plant performance. The chief limitation is reliance on DNA-based metagenomic data from a single site and time point, without multi-omics or detailed soil characterization, restricting temporal and ecological generalization. Nonetheless, the dataset provides a genome-scale view of archaeal functional potential and offers testable directions for future experimental and process-oriented studies.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12864-026-12700-3.},
}
RevDate: 2026-04-01
Characteristics of gut microbiota and metabolites in patients with metabolic dysfunction-associated steatotic liver disease and colorectal adenoma.
Scientific reports, 16(1):.
UNLABELLED: Metabolic dysfunction-associated steatotic liver disease (MASLD) has become one of the most prevalent chronic liver conditions worldwide, with its incidence steadily rising. However, the underlying mechanisms linking MASLD to colorectal adenoma remain unclear, and the role of gut microbiota and metabolites in this association requires further investigation. This study aims to characterise the gut microbiota and metabolites in patients with MASLD and colorectal adenoma. A cohort of 58 MASLD patients was enrolled and stratified into two groups based on colorectal adenoma status: the MASLD with colorectal adenoma group (M-CA group, n = 30) and the MASLD without colorectal adenoma group (M-NCA group, n = 28). The gut microbial ecosystem in the M-CA group showed significant dysregulation, evidenced by a decreased Gut Microbiome Health Index (GMHI) and significantly increased Microbiome Dysbiosis Index (MDI). Linear Discriminant Analysis Effect Size (LEfSe) identified 75 differentially abundant microbial taxa between groups, with Bacteroides vulgatus, Bacteroides ovatus, uncultured bacterium of norank genus of Muribaculaceae family, Muribaculaceae, and norank of Muribaculaceae family being significantly enriched in the M-CA group, representing potential microbial biomarkers for this cohort. Partial Least Squares Discriminant Analysis (PLS-DA) screened 116 differential metabolites. When combined with Random Forest (RF), Support Vector Machine (SVM) and Least Absolute Shrinkage and Selection Operator (LASSO) machine learning algorithms, 16 significantly identified biomarkers were discovered. The joint analysis of both omics revealed that variations in differential metabolite levels were associated with changes in specific microbiota abundances. Kyoto encyclopedia of genes and genomes (KEGG) functional prediction analysis indicated that the coordinated alterations in metabolites and microbiota may collectively influence multiple metabolic pathways, including lipid metabolism, xenobiotics biodegradation and metabolism, amino acid metabolism, carbohydrate metabolism, biosynthesis of other secondary metabolites and nucleotide metabolism. This study revealed that patients with MASLD and colorectal adenoma exhibited significant alterations in the gut microbiota composition and metabolic profile, indicating potential impacts on associated metabolic pathways. These findings provided novel insights and a foundation for future research into potential intervention strategies for this clinical complication.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-45782-w.
Additional Links: PMID-41896654
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@article {pmid41896654,
year = {2026},
author = {Li, Y and Fu, W and Xiang, Z and Zhao, M and Xie, X and Guo, W and Zhou, Y and Zheng, M and Yang, J},
title = {Characteristics of gut microbiota and metabolites in patients with metabolic dysfunction-associated steatotic liver disease and colorectal adenoma.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {41896654},
issn = {2045-2322},
support = {2021J0252//Scientific Research Fund Project of Yunnan Provincial Department of Education/ ; 2025J0270//Scientific Research Fund Project of Yunnan Provincial Department of Education/ ; 2024B010//Innovation Fund for Postgraduate Education of Kunming Medical University/ ; 202501AY070001-088//Science and Technology Plan Project of Yunnan Provincial Department of Science and Technology/ ; 82160106//National Natural Science Foundation of China/ ; },
abstract = {UNLABELLED: Metabolic dysfunction-associated steatotic liver disease (MASLD) has become one of the most prevalent chronic liver conditions worldwide, with its incidence steadily rising. However, the underlying mechanisms linking MASLD to colorectal adenoma remain unclear, and the role of gut microbiota and metabolites in this association requires further investigation. This study aims to characterise the gut microbiota and metabolites in patients with MASLD and colorectal adenoma. A cohort of 58 MASLD patients was enrolled and stratified into two groups based on colorectal adenoma status: the MASLD with colorectal adenoma group (M-CA group, n = 30) and the MASLD without colorectal adenoma group (M-NCA group, n = 28). The gut microbial ecosystem in the M-CA group showed significant dysregulation, evidenced by a decreased Gut Microbiome Health Index (GMHI) and significantly increased Microbiome Dysbiosis Index (MDI). Linear Discriminant Analysis Effect Size (LEfSe) identified 75 differentially abundant microbial taxa between groups, with Bacteroides vulgatus, Bacteroides ovatus, uncultured bacterium of norank genus of Muribaculaceae family, Muribaculaceae, and norank of Muribaculaceae family being significantly enriched in the M-CA group, representing potential microbial biomarkers for this cohort. Partial Least Squares Discriminant Analysis (PLS-DA) screened 116 differential metabolites. When combined with Random Forest (RF), Support Vector Machine (SVM) and Least Absolute Shrinkage and Selection Operator (LASSO) machine learning algorithms, 16 significantly identified biomarkers were discovered. The joint analysis of both omics revealed that variations in differential metabolite levels were associated with changes in specific microbiota abundances. Kyoto encyclopedia of genes and genomes (KEGG) functional prediction analysis indicated that the coordinated alterations in metabolites and microbiota may collectively influence multiple metabolic pathways, including lipid metabolism, xenobiotics biodegradation and metabolism, amino acid metabolism, carbohydrate metabolism, biosynthesis of other secondary metabolites and nucleotide metabolism. This study revealed that patients with MASLD and colorectal adenoma exhibited significant alterations in the gut microbiota composition and metabolic profile, indicating potential impacts on associated metabolic pathways. These findings provided novel insights and a foundation for future research into potential intervention strategies for this clinical complication.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-45782-w.},
}
RevDate: 2026-03-31
CmpDate: 2026-03-31
Lentinula edodes Cultured Extract Intake at Puberty Mitigates Inflammatory Signals at the Mammary Glands by the Involvement of Epigenetic Mechanisms in BALB/c Mice.
The breast journal, 2026(1):e2122220.
Exposure to immune stress or lipopolysaccharide (LPS) during critical developmental stages like puberty may lead to gut microbiome dysbiosis and epigenetic dysregulation in mammary glands, affecting gene expression and potentially elevating breast cancer susceptibility in adulthood. Although LPS's adverse impacts on intestinal and brain functions are well-documented, its effects on mammary glands remain underexplored. Using an immunocompetent BALB/c mouse model, we administered an acute LPS dose (1.5 mg/kg body weight) during puberty. The study evaluated the long-term consequences of LPS exposure alone and combined with AHCC (Lentinula edodes cultured extract, 2 g/kg body weight/day) on DNA methylation patterns, cytokine profiles, and microRNA expression in mammary glands at 9 weeks of age. Analyses included DNA methylation sequencing, multiplex immunoassays, quantitative PCR, and image processing. Pubertal LPS exposure produced persistent molecular dysregulation in mammary glands, including differential DNA methylation (> 5% change vs. control; FDR-adjusted p < 0.05), elevated inflammatory mediators, and altered microRNA expression. Differentially methylated regions were enriched in regulatory features, with decreased methylation at transcription start sites, promoters, and 5' UTRs of genes implicated in mammary development and oncogenic signaling (including Vav3, Pdgfa, Pdgfc, Jag2, Hras, Ksr1, Il2rb, Il17b, and Il17rb) in the LPS group, whereas the AHCC + LPS group exhibited a shift toward hypermethylation at these loci (approximately 5%-10% decrease). Inflammatory profiling showed increased IL-17A/F (∼2-fold vs. control; p < 0.05), while microRNA analyses indicated reduced let-7a/c (∼30% vs. control; p < 0.05). Notably, miR-130a and miR-34a increased ∼1.5-fold across all treatment groups relative to control. Pubertal LPS exposure induces enduring epigenetic and inflammatory changes in mammary glands that may heighten breast cancer risk. AHCC's mitigating role indicates potential for dietary interventions to counteract these effects.
Additional Links: PMID-41915463
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@article {pmid41915463,
year = {2026},
author = {Yasavoli-Sharahi, H and Shahbazi, R and Alsadi, N and Sahebi, NB and Cuenin, C and Cahais, V and Chung, FF and Herceg, Z and Matar, C},
title = {Lentinula edodes Cultured Extract Intake at Puberty Mitigates Inflammatory Signals at the Mammary Glands by the Involvement of Epigenetic Mechanisms in BALB/c Mice.},
journal = {The breast journal},
volume = {2026},
number = {1},
pages = {e2122220},
doi = {10.1155/tbj/2122220},
pmid = {41915463},
issn = {1524-4741},
support = {532223-18//Natural Sciences and Engineering Research Council of Canada/ ; 2019-01497//AHCC Research Association, and New Frontiers in Research Fund-Exploration (NFRF/ ; //University of Ottawa/ ; },
mesh = {Animals ; Female ; Mice ; Mice, Inbred BALB C ; *Epigenesis, Genetic/drug effects ; DNA Methylation/drug effects ; *Mammary Glands, Animal/drug effects/metabolism ; Lipopolysaccharides ; *Shiitake Mushrooms/chemistry ; Sexual Maturation ; MicroRNAs/metabolism ; *Inflammation ; },
abstract = {Exposure to immune stress or lipopolysaccharide (LPS) during critical developmental stages like puberty may lead to gut microbiome dysbiosis and epigenetic dysregulation in mammary glands, affecting gene expression and potentially elevating breast cancer susceptibility in adulthood. Although LPS's adverse impacts on intestinal and brain functions are well-documented, its effects on mammary glands remain underexplored. Using an immunocompetent BALB/c mouse model, we administered an acute LPS dose (1.5 mg/kg body weight) during puberty. The study evaluated the long-term consequences of LPS exposure alone and combined with AHCC (Lentinula edodes cultured extract, 2 g/kg body weight/day) on DNA methylation patterns, cytokine profiles, and microRNA expression in mammary glands at 9 weeks of age. Analyses included DNA methylation sequencing, multiplex immunoassays, quantitative PCR, and image processing. Pubertal LPS exposure produced persistent molecular dysregulation in mammary glands, including differential DNA methylation (> 5% change vs. control; FDR-adjusted p < 0.05), elevated inflammatory mediators, and altered microRNA expression. Differentially methylated regions were enriched in regulatory features, with decreased methylation at transcription start sites, promoters, and 5' UTRs of genes implicated in mammary development and oncogenic signaling (including Vav3, Pdgfa, Pdgfc, Jag2, Hras, Ksr1, Il2rb, Il17b, and Il17rb) in the LPS group, whereas the AHCC + LPS group exhibited a shift toward hypermethylation at these loci (approximately 5%-10% decrease). Inflammatory profiling showed increased IL-17A/F (∼2-fold vs. control; p < 0.05), while microRNA analyses indicated reduced let-7a/c (∼30% vs. control; p < 0.05). Notably, miR-130a and miR-34a increased ∼1.5-fold across all treatment groups relative to control. Pubertal LPS exposure induces enduring epigenetic and inflammatory changes in mammary glands that may heighten breast cancer risk. AHCC's mitigating role indicates potential for dietary interventions to counteract these effects.},
}
MeSH Terms:
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Animals
Female
Mice
Mice, Inbred BALB C
*Epigenesis, Genetic/drug effects
DNA Methylation/drug effects
*Mammary Glands, Animal/drug effects/metabolism
Lipopolysaccharides
*Shiitake Mushrooms/chemistry
Sexual Maturation
MicroRNAs/metabolism
*Inflammation
RevDate: 2026-03-31
Phage-related symbiosis and antagonism shape gut ecosystem dynamics in Lachnospiraceae and Bacteroidaceae.
Cell reports, 45(4):117166 pii:S2211-1247(26)00244-5 [Epub ahead of print].
The human gut microbiota is shaped by intricate, yet poorly resolved interactions among bacteria, as well as their relationship to bacteriophages. However, resolving this complex interaction and dynamics has been limited by the challenges in genome recovery and functional characterization. We develop culture-enriched metagenomic co-barcoding sequencing (cMECOS), obtain 5,006 high- or medium-quality (HMQ) metagenome-assembled genomes (MAGs) and reconstruct bacteria-phage interaction networks via CRISPR spacer mapping. This framework uncovers two ecologically distinct, inter-specific bacterial networks: a Lachnospiraceae-dominated community associates with temperate phages and is characterized by metabolic cross-feeding and a Bacteroidaceae-dominated community linked to virulent phages and marked by resource competition. Both network architectures are disrupted in both inflammatory bowel disease (IBD) and obesity (OB), underscoring their role in ecosystem stability. Our work establishes cMECOS as a powerful platform for deciphering complex microbiome interactions and identifies phage-related bacterial networks as critical regulators of gut homeostasis, providing a foundation for phage-informed therapeutic development.
Additional Links: PMID-41915473
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@article {pmid41915473,
year = {2026},
author = {Zhao, Y and Li, J and Han, K and Chen, L and Zhuang, Q and Li, S and Hua, M and Li, N and Yue, J and Gu, C and Rong, C and Yang, D and Deng, Z and Huang, J and He, L and Zeng, H and Yu, Z and Chen, C},
title = {Phage-related symbiosis and antagonism shape gut ecosystem dynamics in Lachnospiraceae and Bacteroidaceae.},
journal = {Cell reports},
volume = {45},
number = {4},
pages = {117166},
doi = {10.1016/j.celrep.2026.117166},
pmid = {41915473},
issn = {2211-1247},
abstract = {The human gut microbiota is shaped by intricate, yet poorly resolved interactions among bacteria, as well as their relationship to bacteriophages. However, resolving this complex interaction and dynamics has been limited by the challenges in genome recovery and functional characterization. We develop culture-enriched metagenomic co-barcoding sequencing (cMECOS), obtain 5,006 high- or medium-quality (HMQ) metagenome-assembled genomes (MAGs) and reconstruct bacteria-phage interaction networks via CRISPR spacer mapping. This framework uncovers two ecologically distinct, inter-specific bacterial networks: a Lachnospiraceae-dominated community associates with temperate phages and is characterized by metabolic cross-feeding and a Bacteroidaceae-dominated community linked to virulent phages and marked by resource competition. Both network architectures are disrupted in both inflammatory bowel disease (IBD) and obesity (OB), underscoring their role in ecosystem stability. Our work establishes cMECOS as a powerful platform for deciphering complex microbiome interactions and identifies phage-related bacterial networks as critical regulators of gut homeostasis, providing a foundation for phage-informed therapeutic development.},
}
RevDate: 2026-03-31
Gut Microbiome, Immune Cells, and Heart Failure: A Multi-Omics Mendelian Randomization Study.
Cardiology pii:000550655 [Epub ahead of print].
INTRODUCTION: The global burden of heart failure is escalating, marked by persistently rising prevalence, incidence, and mortality. The emerging hypothesis that the gut microbiome, as a modifiable factor, influences HF pathogenesis through immune modulation.
METHODS: To examine the causal relationship, we conducted two-sample Mendelian randomization (MR) analyses using summary genetic data, which was obtained from genome-wide association studies (GWASs) of gut microbial taxa, immune cells, and HF. Single-cell RNA sequencing data and single-nucleus RNA sequencing from chronic heart failure and healthy samples were extracted for investigation. Expression quantitative trait loci (eQTL) MR analysis was used to integrate HF GWAS with eQTL from heart to confirm potential genes. We performed functional enrichment analysis to enrich their functions.
RESULTS: The analysis revealed that genus Blautia (p = 0.0287), genus Corynebactrium (p = 0.022), genus Demequina (p = 0.0064), genus Enterococcus (p = 0.0307), genus Eubacterium (p = 0.0234), genus F0482 (p = 0.0107), genus Leclercia (p = 0.0026), genus Prevotellamassilia (p = 0.0444), and genus Ruminococcus were causally linked to a higher risk of HF, while genus CAG-125 (p = 0.0443), genus CAG-245 (p = 0.0116), genus Fournierella (p = 0.0326), genus Roseibacillus (p = 0.028) protective factors for HF. Among differential microflora, genus Leclercia was significantly related to higher level of HVEM on terminally differentiated CD4+T-cell count (p = 0.0058). Moreover, HF patients underwent obviously increased NK/T cells. We identified positive association of EIF3A, RPL5, SLC25A51, HERC5, SUSD3, ZNF292, ZNF655, and DNAJC9 with increased risk of HF, whereas the expression of RMC1, CAMK2G, RPS26, ATP5PO displayed protective effect against HF by eQTL MR analysis; they were mainly enriched in myc-Targets-V1, IFN-γ-response, IFN-α-response, PI3K/AKT/mTOR signaling, TGF-beta signaling, allograft rejection, notch signaling pathways, angiogenesis, epithelial mesenchymal transition, UV-response-DN, hedgehog signaling, myogenesis.
CONCLUSION: Our multi-omics MR study uncovered the causality of gut microbiome on immune cells and HF. Genus Leclercia-related changes in T cells may present as a viable focus for HF. This offers new insights into mechanisms and therapy of gut microbiome-mediated HF.
Additional Links: PMID-41915616
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@article {pmid41915616,
year = {2026},
author = {Wei, Y and Ji, X and Mao, Y and Liu, Y and Li, Y},
title = {Gut Microbiome, Immune Cells, and Heart Failure: A Multi-Omics Mendelian Randomization Study.},
journal = {Cardiology},
volume = {},
number = {},
pages = {1-14},
doi = {10.1159/000550655},
pmid = {41915616},
issn = {1421-9751},
abstract = {INTRODUCTION: The global burden of heart failure is escalating, marked by persistently rising prevalence, incidence, and mortality. The emerging hypothesis that the gut microbiome, as a modifiable factor, influences HF pathogenesis through immune modulation.
METHODS: To examine the causal relationship, we conducted two-sample Mendelian randomization (MR) analyses using summary genetic data, which was obtained from genome-wide association studies (GWASs) of gut microbial taxa, immune cells, and HF. Single-cell RNA sequencing data and single-nucleus RNA sequencing from chronic heart failure and healthy samples were extracted for investigation. Expression quantitative trait loci (eQTL) MR analysis was used to integrate HF GWAS with eQTL from heart to confirm potential genes. We performed functional enrichment analysis to enrich their functions.
RESULTS: The analysis revealed that genus Blautia (p = 0.0287), genus Corynebactrium (p = 0.022), genus Demequina (p = 0.0064), genus Enterococcus (p = 0.0307), genus Eubacterium (p = 0.0234), genus F0482 (p = 0.0107), genus Leclercia (p = 0.0026), genus Prevotellamassilia (p = 0.0444), and genus Ruminococcus were causally linked to a higher risk of HF, while genus CAG-125 (p = 0.0443), genus CAG-245 (p = 0.0116), genus Fournierella (p = 0.0326), genus Roseibacillus (p = 0.028) protective factors for HF. Among differential microflora, genus Leclercia was significantly related to higher level of HVEM on terminally differentiated CD4+T-cell count (p = 0.0058). Moreover, HF patients underwent obviously increased NK/T cells. We identified positive association of EIF3A, RPL5, SLC25A51, HERC5, SUSD3, ZNF292, ZNF655, and DNAJC9 with increased risk of HF, whereas the expression of RMC1, CAMK2G, RPS26, ATP5PO displayed protective effect against HF by eQTL MR analysis; they were mainly enriched in myc-Targets-V1, IFN-γ-response, IFN-α-response, PI3K/AKT/mTOR signaling, TGF-beta signaling, allograft rejection, notch signaling pathways, angiogenesis, epithelial mesenchymal transition, UV-response-DN, hedgehog signaling, myogenesis.
CONCLUSION: Our multi-omics MR study uncovered the causality of gut microbiome on immune cells and HF. Genus Leclercia-related changes in T cells may present as a viable focus for HF. This offers new insights into mechanisms and therapy of gut microbiome-mediated HF.},
}
RevDate: 2026-03-31
Beyond the crop: the role of medicinal and aromatic plants in soil carbon sequestration and nitrogen cycling.
International journal of environmental health research [Epub ahead of print].
Medicinal and aromatic plants (MAPs) play a critical yet underexplored role in enhancing soil functionality through their unique phytochemical interactions and ecological adaptability. This review synthesizes current research on how MAPs influence soil carbon sequestration and nitrogen cycling, positioning them as multifunctional agents in sustainable agroecosystems. Unlike conventional crops, MAPs release complex secondary metabolites, such as flavonoids, alkaloids, terpenoids, and phenolics, which modulate microbial diversity, enzymatic activity, and nutrient transformation. These compounds shape the rhizosphere microbial communities, facilitate nitrogen fixation and mineralization, and contribute to soil organic matter (SOM) stabilization through rhizosphere priming and humus formation. Integrated approaches, such as intercropping, agroforestry, and organic amendments, enhance these benefits, while mitigating allelopathic effects and improving carbon and nitrogen fluxes. This review further explores technological innovations including remote sensing (RS), biochar applications, and nanotechnology, which support MAP-based climate-resilient agriculture. Case studies across diverse geographies demonstrate MAPs' potential to restore degraded soils, reduce greenhouse gas emissions, and improve phytochemical yields. Overall, MAPs offer a promising model for regenerative, low-input farming systems that align ecological integrity with economic viability. By actively engineering the soil environment, MAPs emerge not only as botanical resources but also as ecological catalysts in the transition to sustainable agriculture.
Additional Links: PMID-41915730
Publisher:
PubMed:
Citation:
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@article {pmid41915730,
year = {2026},
author = {Negahban, M and Msaada, K},
title = {Beyond the crop: the role of medicinal and aromatic plants in soil carbon sequestration and nitrogen cycling.},
journal = {International journal of environmental health research},
volume = {},
number = {},
pages = {1-24},
doi = {10.1080/09603123.2026.2653197},
pmid = {41915730},
issn = {1369-1619},
abstract = {Medicinal and aromatic plants (MAPs) play a critical yet underexplored role in enhancing soil functionality through their unique phytochemical interactions and ecological adaptability. This review synthesizes current research on how MAPs influence soil carbon sequestration and nitrogen cycling, positioning them as multifunctional agents in sustainable agroecosystems. Unlike conventional crops, MAPs release complex secondary metabolites, such as flavonoids, alkaloids, terpenoids, and phenolics, which modulate microbial diversity, enzymatic activity, and nutrient transformation. These compounds shape the rhizosphere microbial communities, facilitate nitrogen fixation and mineralization, and contribute to soil organic matter (SOM) stabilization through rhizosphere priming and humus formation. Integrated approaches, such as intercropping, agroforestry, and organic amendments, enhance these benefits, while mitigating allelopathic effects and improving carbon and nitrogen fluxes. This review further explores technological innovations including remote sensing (RS), biochar applications, and nanotechnology, which support MAP-based climate-resilient agriculture. Case studies across diverse geographies demonstrate MAPs' potential to restore degraded soils, reduce greenhouse gas emissions, and improve phytochemical yields. Overall, MAPs offer a promising model for regenerative, low-input farming systems that align ecological integrity with economic viability. By actively engineering the soil environment, MAPs emerge not only as botanical resources but also as ecological catalysts in the transition to sustainable agriculture.},
}
RevDate: 2026-03-31
Influence of synbiotic supplementation on performance, fecal consistency, cecal microbiome, and egg quality of hens during late laying phase.
Poultry science, 105(6):106851 pii:S0032-5791(26)00480-3 [Epub ahead of print].
Hens in the late laying phase often experience age-related physiological constraints that may reduce production efficiency, eggshell quality, and welfare. This study evaluated the effects of dietary synbiotic supplementation on laying performance, egg quality, fecal characteristics, and the cecal microbiome of late-phase laying hens. A total of 240 Lohmann Brown hens (50 weeks old) were distributed into 20 replicates and randomly assigned to a corn-soybean control diet or the same diet supplemented with 100 mg/kg synbiotic (SYNLAC Prime®) for 22 weeks. Synbiotic supplementation did not affect egg production or egg mass but significantly reduced feed intake (P = 0.036). It also improved eggshell quality by decreasing the proportion of cracked eggs (P = 0.014) and increasing eggshell weight (P = 0.049) and shell thickness (P = 0.031). Fecal score and moisture content were not affected; however, synbiotic-fed hens showed lower fecal ammonia concentration (P = 0.033). Synbiotic supplementation increased both alpha and beta microbial diversity in the cecum. While microbial composition at higher taxonomic levels was largely unchanged, the relative abundances of Ruminococcaceae and Lachnospiraceae increased, whereas those of Bacteroidaceae and Clostridiaceae decreased. At the genus level, synbiotic supplementation increased Faecalibacterium, Ruminococcus, and Lactobacillus, while reducing Bacteroides and Alistipes. Functional prediction analysis indicated that synbiotic supplementation upregulated 12 cecal metabolic pathways and downregulated two pathways. Overall, synbiotic supplementation improved eggshell quality, promoted beneficial gut microbial populations, and reduced fecal ammonia emissions, suggesting its potential as a dietary strategy to support productivity and gut health in hens during the late laying phase.
Additional Links: PMID-41916054
Publisher:
PubMed:
Citation:
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@article {pmid41916054,
year = {2026},
author = {Pongmanee, K and Rassmidatta, K and Lee, TY and Lin, JS and Chaosap, C and Adeyemi, KD and Ruangpanit, Y},
title = {Influence of synbiotic supplementation on performance, fecal consistency, cecal microbiome, and egg quality of hens during late laying phase.},
journal = {Poultry science},
volume = {105},
number = {6},
pages = {106851},
doi = {10.1016/j.psj.2026.106851},
pmid = {41916054},
issn = {1525-3171},
abstract = {Hens in the late laying phase often experience age-related physiological constraints that may reduce production efficiency, eggshell quality, and welfare. This study evaluated the effects of dietary synbiotic supplementation on laying performance, egg quality, fecal characteristics, and the cecal microbiome of late-phase laying hens. A total of 240 Lohmann Brown hens (50 weeks old) were distributed into 20 replicates and randomly assigned to a corn-soybean control diet or the same diet supplemented with 100 mg/kg synbiotic (SYNLAC Prime®) for 22 weeks. Synbiotic supplementation did not affect egg production or egg mass but significantly reduced feed intake (P = 0.036). It also improved eggshell quality by decreasing the proportion of cracked eggs (P = 0.014) and increasing eggshell weight (P = 0.049) and shell thickness (P = 0.031). Fecal score and moisture content were not affected; however, synbiotic-fed hens showed lower fecal ammonia concentration (P = 0.033). Synbiotic supplementation increased both alpha and beta microbial diversity in the cecum. While microbial composition at higher taxonomic levels was largely unchanged, the relative abundances of Ruminococcaceae and Lachnospiraceae increased, whereas those of Bacteroidaceae and Clostridiaceae decreased. At the genus level, synbiotic supplementation increased Faecalibacterium, Ruminococcus, and Lactobacillus, while reducing Bacteroides and Alistipes. Functional prediction analysis indicated that synbiotic supplementation upregulated 12 cecal metabolic pathways and downregulated two pathways. Overall, synbiotic supplementation improved eggshell quality, promoted beneficial gut microbial populations, and reduced fecal ammonia emissions, suggesting its potential as a dietary strategy to support productivity and gut health in hens during the late laying phase.},
}
RevDate: 2026-03-31
Higher ultra-processed food consumption is associated with higher likelihood of paediatric-onset multiple sclerosis.
Multiple sclerosis and related disorders, 109:107159 pii:S2211-0348(26)00195-1 [Epub ahead of print].
BACKGROUND: Diets are increasingly dominated by ultra-processed foods, which have been linked to several chronic diseases. Emerging evidence suggests an association between ultra-processed food consumption and inflammatory diseases, including multiple sclerosis (MS).
OBJECTIVE: To assess associations between consumption of ultra-processed foods and paediatric-onset MS (PoMS).
METHODS: We used data from the microbiome sub-study of the Canadian Pediatric Demyelinating Disease Network Study for PoMS cases (symptom onset aged <18 years) and unaffected controls. Data on consumption of ultra-processed foods (defined within the Nova system) were derived from dietary intake data collected using the Block Kids Food Screener. Dietary contribution of ultra-processed foods (% of total grams consumed per day) was estimated. Logistic regression models were used to examine associations between ultra-processed food consumption (continuous and tertiles) and likelihood of PoMS. Models were adjusted for age at dietary data collection, sex, race, region of residence, and total energy intake.
RESULTS: Dietary data were collected from PoMS participants (females=57, males=23) aged 5-28 years and controls (females=30, males=16) aged 8-26 years. Each additional 10% in ultra-processed food consumption was associated with a 35% higher odds of being a PoMS participant (adjusted odds ratio [aOR]=1.35, 95% CI 1.05, 1.73). Participants in the highest (versus lowest) tertile for ultra-processed food consumption had over five times higher odds of being a PoMS participant (aOR=5.30, 95% CI 1.36, 20.70).
CONCLUSION: Participants with PoMS reported greater consumption of ultra-processed foods compared to unaffected peers. More comprehensive longitudinal dietary histories are required to better understand this observation.
Additional Links: PMID-41916081
Publisher:
PubMed:
Citation:
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hide bibtex listing
@article {pmid41916081,
year = {2026},
author = {Machado, P and Mazahery, H and Black, LJ and Tremlett, H and Daly, A and Pham, NM and Tessema, GA and Zhu, F and Banwell, B and Bar-Or, A and Marrie, RA and Bernstein, CN and Mirza, AI and Yeh, EA and Waubant, E and O'Mahony, J and Dunlop, E and , },
title = {Higher ultra-processed food consumption is associated with higher likelihood of paediatric-onset multiple sclerosis.},
journal = {Multiple sclerosis and related disorders},
volume = {109},
number = {},
pages = {107159},
doi = {10.1016/j.msard.2026.107159},
pmid = {41916081},
issn = {2211-0356},
abstract = {BACKGROUND: Diets are increasingly dominated by ultra-processed foods, which have been linked to several chronic diseases. Emerging evidence suggests an association between ultra-processed food consumption and inflammatory diseases, including multiple sclerosis (MS).
OBJECTIVE: To assess associations between consumption of ultra-processed foods and paediatric-onset MS (PoMS).
METHODS: We used data from the microbiome sub-study of the Canadian Pediatric Demyelinating Disease Network Study for PoMS cases (symptom onset aged <18 years) and unaffected controls. Data on consumption of ultra-processed foods (defined within the Nova system) were derived from dietary intake data collected using the Block Kids Food Screener. Dietary contribution of ultra-processed foods (% of total grams consumed per day) was estimated. Logistic regression models were used to examine associations between ultra-processed food consumption (continuous and tertiles) and likelihood of PoMS. Models were adjusted for age at dietary data collection, sex, race, region of residence, and total energy intake.
RESULTS: Dietary data were collected from PoMS participants (females=57, males=23) aged 5-28 years and controls (females=30, males=16) aged 8-26 years. Each additional 10% in ultra-processed food consumption was associated with a 35% higher odds of being a PoMS participant (adjusted odds ratio [aOR]=1.35, 95% CI 1.05, 1.73). Participants in the highest (versus lowest) tertile for ultra-processed food consumption had over five times higher odds of being a PoMS participant (aOR=5.30, 95% CI 1.36, 20.70).
CONCLUSION: Participants with PoMS reported greater consumption of ultra-processed foods compared to unaffected peers. More comprehensive longitudinal dietary histories are required to better understand this observation.},
}
RevDate: 2026-03-31
Ageing of the Oral Mucosa: Mechanisms and Consequences.
International dental journal, 76(3):109482 pii:S0020-6539(26)00078-X [Epub ahead of print].
Oral mucosal ageing represents a fundamental reprogramming of the tissue microenvironment, a dynamic process that underlies the functional decline and heightened disease susceptibility observed in the elderly. This review synthesises current evidence to reconceptualise oral mucosal ageing as an active reprogramming of the tissue microenvironment, delineating the interplay between structural, molecular, and immunological changes, and exploring how these alterations drive functional decline and increase susceptibility to age-related oral diseases. Through a comprehensive analysis of experimental and clinical studies from human and animal models, we demonstrate that the ageing process fundamentally transforms the oral mucosa. Key findings include structural changes such as epithelial atrophy, extracellular matrix remodelling, and salivary gland degeneration, driven molecularly by genomic instability, accumulation of proinflammatory senescent cells, stem cell exhaustion, and dysregulated stress responses. These are compounded by an immunological state of 'inflammaging' and functional decline in innate and adaptive immunity, further exacerbated by shifts in the oral microbiome. Collectively, these deficits lead to impaired regeneration, diminished sensory function, and reduced salivary secretion, creating a permissive landscape for chronic oral diseases. In conclusion, oral mucosal ageing is a dynamic process of microenvironmental reprogramming driven by cellular senescence, immunosenescence, and structural decay. This actively underpins the heightened vulnerability to oral disease in the elderly, providing a mechanistic foundation for developing targeted interventions to preserve oral health in ageing populations.
Additional Links: PMID-41916092
Publisher:
PubMed:
Citation:
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@article {pmid41916092,
year = {2026},
author = {Qiu, C and Jie, W and Qian, Y and Lu, X and Chen, Y and Si, M},
title = {Ageing of the Oral Mucosa: Mechanisms and Consequences.},
journal = {International dental journal},
volume = {76},
number = {3},
pages = {109482},
doi = {10.1016/j.identj.2026.109482},
pmid = {41916092},
issn = {1875-595X},
abstract = {Oral mucosal ageing represents a fundamental reprogramming of the tissue microenvironment, a dynamic process that underlies the functional decline and heightened disease susceptibility observed in the elderly. This review synthesises current evidence to reconceptualise oral mucosal ageing as an active reprogramming of the tissue microenvironment, delineating the interplay between structural, molecular, and immunological changes, and exploring how these alterations drive functional decline and increase susceptibility to age-related oral diseases. Through a comprehensive analysis of experimental and clinical studies from human and animal models, we demonstrate that the ageing process fundamentally transforms the oral mucosa. Key findings include structural changes such as epithelial atrophy, extracellular matrix remodelling, and salivary gland degeneration, driven molecularly by genomic instability, accumulation of proinflammatory senescent cells, stem cell exhaustion, and dysregulated stress responses. These are compounded by an immunological state of 'inflammaging' and functional decline in innate and adaptive immunity, further exacerbated by shifts in the oral microbiome. Collectively, these deficits lead to impaired regeneration, diminished sensory function, and reduced salivary secretion, creating a permissive landscape for chronic oral diseases. In conclusion, oral mucosal ageing is a dynamic process of microenvironmental reprogramming driven by cellular senescence, immunosenescence, and structural decay. This actively underpins the heightened vulnerability to oral disease in the elderly, providing a mechanistic foundation for developing targeted interventions to preserve oral health in ageing populations.},
}
RevDate: 2026-03-31
Aging enhances the ecological toxicity of polyethylene microplastics to marine medaka larvae (Oryzias melastigma).
Journal of environmental management, 404:129493 pii:S0301-4797(26)00953-9 [Epub ahead of print].
Microplastics (MPs), widely distributed in marine environments, pose urgent ecological risks as emerging contaminants. However, current ecological risk assessments are largely based on the commercially produced MPs, which poorly represent in natural settings. Here, we simulated the natural aging of polyethylene MPs (PE-MPs) using ultraviolet radiation (UV) and Fenton reactions, characterized the resultant physicochemical changes, and assessed their ecological toxicity in marine medaka larvae over a 30-day exposure experiment. Short-term aging via UV and Fenton reactions primarily altered the physical properties of PE, including surface morphology, hydrophobicity, and Zeta potential. Both original and aged PE induced intestinal damage and oxidative stress in the larvae, indicating that aged PE retains its toxicity. In contrast, aged PE significantly altered the microbial community structure in the fish intestines: Roseibacillus was significantly enriched in the UV-aged polyethylene (UVPE) exposure group, while Ruegeria and Pseudomonas were enriched in the Fenton-aged polyethylene (FPE) exposure group. Functional predictions of the intestinal microbial communities indicated that exposure to FPE resulted in the upregulation of metabolism-related functions, whereas exposure to UVPE significantly downregulated similar functions. Such upregulation likely reflects microbiome reprogramming under stress rather than improved health. Overall, our study demonstrated that aged PE exhibited pronounced toxicity to marine fish and their larvae by altering gut microbiota, and thus significantly impacting energy metabolism and nutrient absorption, leading to detrimental effects on their growth and development. These findings further underscore the enhanced ecological toxicity effects of aged MPs on marine organisms, highlighting the need for better assessments of the adverse impacts of MPs in marine environments.
Additional Links: PMID-41916240
Publisher:
PubMed:
Citation:
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@article {pmid41916240,
year = {2026},
author = {Wen, S and Liu, J and Lin, B and Li, N and Diao, X},
title = {Aging enhances the ecological toxicity of polyethylene microplastics to marine medaka larvae (Oryzias melastigma).},
journal = {Journal of environmental management},
volume = {404},
number = {},
pages = {129493},
doi = {10.1016/j.jenvman.2026.129493},
pmid = {41916240},
issn = {1095-8630},
abstract = {Microplastics (MPs), widely distributed in marine environments, pose urgent ecological risks as emerging contaminants. However, current ecological risk assessments are largely based on the commercially produced MPs, which poorly represent in natural settings. Here, we simulated the natural aging of polyethylene MPs (PE-MPs) using ultraviolet radiation (UV) and Fenton reactions, characterized the resultant physicochemical changes, and assessed their ecological toxicity in marine medaka larvae over a 30-day exposure experiment. Short-term aging via UV and Fenton reactions primarily altered the physical properties of PE, including surface morphology, hydrophobicity, and Zeta potential. Both original and aged PE induced intestinal damage and oxidative stress in the larvae, indicating that aged PE retains its toxicity. In contrast, aged PE significantly altered the microbial community structure in the fish intestines: Roseibacillus was significantly enriched in the UV-aged polyethylene (UVPE) exposure group, while Ruegeria and Pseudomonas were enriched in the Fenton-aged polyethylene (FPE) exposure group. Functional predictions of the intestinal microbial communities indicated that exposure to FPE resulted in the upregulation of metabolism-related functions, whereas exposure to UVPE significantly downregulated similar functions. Such upregulation likely reflects microbiome reprogramming under stress rather than improved health. Overall, our study demonstrated that aged PE exhibited pronounced toxicity to marine fish and their larvae by altering gut microbiota, and thus significantly impacting energy metabolism and nutrient absorption, leading to detrimental effects on their growth and development. These findings further underscore the enhanced ecological toxicity effects of aged MPs on marine organisms, highlighting the need for better assessments of the adverse impacts of MPs in marine environments.},
}
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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.
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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.
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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.
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Early support from the DOE component of the Human Genome Project was critically important for getting the ESP project on a firm foundation. Since that funding ended (nearly 20 years ago), the project has been operated as a purely volunteer effort. Anyone wishing to assist in these efforts should send an email to Robbins.
ESP Plans
With the development of methods for adding typeset side notes to PDF files, the ESP project now plans to add annotated versions of some classical papers to its holdings. We also plan to add new reference and pedagogical material. We have already started providing regularly updated, comprehensive bibliographies to the ESP.ORG site.
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Dinosaur tail, complete with feathers, found preserved in amber.
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