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Robert J. Robbins is a biologist, an educator, a science administrator, a publisher, an information technologist, and an IT leader and manager who specializes in advancing biomedical knowledge and supporting education through the application of information technology. More About: RJR | OUR TEAM | OUR SERVICES | THIS WEBSITE
RJR: Recommended Bibliography 14 Apr 2026 at 01:58 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: 2026-04-10
Artificial Intelligence in Functional Polysaccharides for Food Applications: Process Optimization, Structure-Function Decoding, and Rational Design.
Journal of agricultural and food chemistry [Epub ahead of print].
Functional polysaccharides are widely used as food ingredients but are hindered by extreme structural heterogeneity, poorly defined structure-function relationships, and inefficient trial-and-error production workflows. This review provides an integrative synthesis of how AI is reshaping functional polysaccharide research toward food-grade ingredients and formulations. We organize recent advances into a three-stage framework: (1) efficiency amplification, where machine-learning models improve extraction/fermentation optimization and enable rapid analysis when coupled with spectroscopic fingerprints; (2) mechanism-informed hypothesis generation, where deep Deep-QSAR, graph-based learning, and interpretable modeling begin to uncover quantitative links between structural motifs and functional properties, including microbiome-mediated effects relevant to health; and (3) design assistance, in which AI supports precision-guided polysaccharide engineering and formulation for targeted food functionalities. By bridging computational advances with experimental validation, this review provides a cohesive roadmap for polysaccharide discovery and discusses key translational barriers─data scarcity and standardization, model generalizability and interpretability, and regulatory acceptance─highlighting practical strategies for AI-guided polysaccharide discovery and application.
Additional Links: PMID-41961090
Publisher:
PubMed:
Citation:
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@article {pmid41961090,
year = {2026},
author = {Cao, Z and Chen, T and Xie, J and Xie, J},
title = {Artificial Intelligence in Functional Polysaccharides for Food Applications: Process Optimization, Structure-Function Decoding, and Rational Design.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.6c00806},
pmid = {41961090},
issn = {1520-5118},
abstract = {Functional polysaccharides are widely used as food ingredients but are hindered by extreme structural heterogeneity, poorly defined structure-function relationships, and inefficient trial-and-error production workflows. This review provides an integrative synthesis of how AI is reshaping functional polysaccharide research toward food-grade ingredients and formulations. We organize recent advances into a three-stage framework: (1) efficiency amplification, where machine-learning models improve extraction/fermentation optimization and enable rapid analysis when coupled with spectroscopic fingerprints; (2) mechanism-informed hypothesis generation, where deep Deep-QSAR, graph-based learning, and interpretable modeling begin to uncover quantitative links between structural motifs and functional properties, including microbiome-mediated effects relevant to health; and (3) design assistance, in which AI supports precision-guided polysaccharide engineering and formulation for targeted food functionalities. By bridging computational advances with experimental validation, this review provides a cohesive roadmap for polysaccharide discovery and discusses key translational barriers─data scarcity and standardization, model generalizability and interpretability, and regulatory acceptance─highlighting practical strategies for AI-guided polysaccharide discovery and application.},
}
RevDate: 2026-04-13
CmpDate: 2026-04-10
IBD risk locus rs1077773 enhances aryl hydrocarbon receptor activity and modulates immune cell function in vitro.
Inflammation research : official journal of the European Histamine Research Society ... [et al.], 75(1):.
INTRODUCTION: The inflammatory bowel diseases (IBD) Crohn's disease (CD) and ulcerative colitis (UC) are disorders that cause chronic inflammation of the gastrointestinal tract. Both genetic and environmental factors contribute to the pathogenesis of IBD. There are currently >200 known genetic susceptibility loci for the development of IBD. The physiological impact of the majority of these loci remain a gap in our knowledge. One such locus is the single nucleotide polymorphism rs1077773, located ~56 kbp downstream from the aryl hydrocarbon receptor (AHR) gene. AHR is a ligand-activated transcription factor that is crucial to maintaining intestinal homeostasis. We hypothesized that rs1077773 enhances AHR activity to regulate mucosal immune response and maintain intestinal homeostasis.
METHODS: All study procedures and reagents were approved by the Washington University Institutional Review Board (#202011003). Patient biopsies were collected at Barnes Jewish Hospital and genotyped using the IBD Genetics Consortium custom GSA SNP chip (Broad Institute) followed by imputation using TopMed Imputation Server at University of Michigan. Patient derived organoids (PDOs; N=3 G/G, N=4 G/A, N=5 A/A) were derived and maintained in 3D culture and supplemented with 50% L-WRN conditioned medium with passage every 3-4 days as previously described. PDOs were treated with AHR agonist 6-Formylindolo[3,2-b]carbazole (FICZ) or vehicle for 48 h. Expression of AHR and its transcriptional targets Cytochrome P450 1A1 (CYP1A1) and CYP1B1 was assessed by RT-qPCR. Blood was collected from pediatric patients undergoing intestinal resection at St. Louis Children's Hospital and was genotyped with custom TaqMan SNP assay (N=3 G/G, N=5 G/A). Peripheral blood monocyte-derived macrophages (MDMΦs) were treated with lipopolysaccharide in the presence or absence of AHR ligands FICZ or indole-3-carboxaldehyde for 24 h. Cytokine levels in culture supernatant were measured via using the ProcartaPlex human cytokine, chemokine, and growth factor 45-plex (ThermoFisher) on a Luminex FLEXMAP3D instrument.
RESULTS: AHR expression was similar across genotypes and treatments. PDOs homozygous for rs1077773 demonstrate enhanced CYP1A1 expression in response to AHR activation. In MDMΦs, cytokine secretion was stimulated by LPS treatment and was abrogated by FICZ treatment. MDMΦs with rs1077773 alternate allele demonstrated significant reduction in secretion of 12 cytokines and chemokines.
CONCLUSIONS: This work demonstrates that rs1077773 enhances AHR activity and modulates epithelial and immune cell function in vitro. Further mechanistic understanding of this locus and its correlates could improve our understanding of the molecular mechanisms of IBD susceptibility and may lead to novel personalized therapeutic approaches in IBD.
Additional Links: PMID-41961102
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41961102,
year = {2026},
author = {King, AC and Seiler, K and Swanson, K and Ciorba, MA and Alvarado, DM},
title = {IBD risk locus rs1077773 enhances aryl hydrocarbon receptor activity and modulates immune cell function in vitro.},
journal = {Inflammation research : official journal of the European Histamine Research Society ... [et al.]},
volume = {75},
number = {1},
pages = {},
pmid = {41961102},
issn = {1420-908X},
support = {R01-AI167285/DK/NIDDK NIH HHS/United States ; #648423//Crohn's and Colitis Foundation/ ; #UL1TR002345//Institute of Clinical and Translational Sciences/ ; },
mesh = {Humans ; *Receptors, Aryl Hydrocarbon/genetics ; Polymorphism, Single Nucleotide ; *Inflammatory Bowel Diseases/genetics/immunology ; *Basic Helix-Loop-Helix Proteins/genetics ; Cytochrome P-450 CYP1A1/genetics ; Genetic Predisposition to Disease ; Cytochrome P-450 CYP1B1/genetics ; Organoids ; Male ; Macrophages/immunology ; Female ; },
abstract = {INTRODUCTION: The inflammatory bowel diseases (IBD) Crohn's disease (CD) and ulcerative colitis (UC) are disorders that cause chronic inflammation of the gastrointestinal tract. Both genetic and environmental factors contribute to the pathogenesis of IBD. There are currently >200 known genetic susceptibility loci for the development of IBD. The physiological impact of the majority of these loci remain a gap in our knowledge. One such locus is the single nucleotide polymorphism rs1077773, located ~56 kbp downstream from the aryl hydrocarbon receptor (AHR) gene. AHR is a ligand-activated transcription factor that is crucial to maintaining intestinal homeostasis. We hypothesized that rs1077773 enhances AHR activity to regulate mucosal immune response and maintain intestinal homeostasis.
METHODS: All study procedures and reagents were approved by the Washington University Institutional Review Board (#202011003). Patient biopsies were collected at Barnes Jewish Hospital and genotyped using the IBD Genetics Consortium custom GSA SNP chip (Broad Institute) followed by imputation using TopMed Imputation Server at University of Michigan. Patient derived organoids (PDOs; N=3 G/G, N=4 G/A, N=5 A/A) were derived and maintained in 3D culture and supplemented with 50% L-WRN conditioned medium with passage every 3-4 days as previously described. PDOs were treated with AHR agonist 6-Formylindolo[3,2-b]carbazole (FICZ) or vehicle for 48 h. Expression of AHR and its transcriptional targets Cytochrome P450 1A1 (CYP1A1) and CYP1B1 was assessed by RT-qPCR. Blood was collected from pediatric patients undergoing intestinal resection at St. Louis Children's Hospital and was genotyped with custom TaqMan SNP assay (N=3 G/G, N=5 G/A). Peripheral blood monocyte-derived macrophages (MDMΦs) were treated with lipopolysaccharide in the presence or absence of AHR ligands FICZ or indole-3-carboxaldehyde for 24 h. Cytokine levels in culture supernatant were measured via using the ProcartaPlex human cytokine, chemokine, and growth factor 45-plex (ThermoFisher) on a Luminex FLEXMAP3D instrument.
RESULTS: AHR expression was similar across genotypes and treatments. PDOs homozygous for rs1077773 demonstrate enhanced CYP1A1 expression in response to AHR activation. In MDMΦs, cytokine secretion was stimulated by LPS treatment and was abrogated by FICZ treatment. MDMΦs with rs1077773 alternate allele demonstrated significant reduction in secretion of 12 cytokines and chemokines.
CONCLUSIONS: This work demonstrates that rs1077773 enhances AHR activity and modulates epithelial and immune cell function in vitro. Further mechanistic understanding of this locus and its correlates could improve our understanding of the molecular mechanisms of IBD susceptibility and may lead to novel personalized therapeutic approaches in IBD.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Receptors, Aryl Hydrocarbon/genetics
Polymorphism, Single Nucleotide
*Inflammatory Bowel Diseases/genetics/immunology
*Basic Helix-Loop-Helix Proteins/genetics
Cytochrome P-450 CYP1A1/genetics
Genetic Predisposition to Disease
Cytochrome P-450 CYP1B1/genetics
Organoids
Male
Macrophages/immunology
Female
RevDate: 2026-04-10
CmpDate: 2026-04-10
Metabolite sensing receptors in macrophage reprogramming: from inflammation to resolution.
Inflammation research : official journal of the European Histamine Research Society ... [et al.], 75(1):.
BACKGROUND: Macrophages are central to innate immunity, orchestrating both the inflammatory and resolution phases of host defense. Emerging evidence indicates that immunometabolic crosstalk critically dictates macrophage polarization and functions. Disruptions in cellular metabolism can impair these regulatory mechanisms, leading to dysfunctional immune responses associated with various disease pathologies. A key aspect of this regulation involves metabolite-sensing receptors that detect changes in intracellular metabolic intermediates and in extracellular metabolites derived from the diet, host tissues, and the microbiome.
METHODS: We have conducted a literature review of original research and review articles on metabolite-sensing receptors and their roles in immune cell function, drawn from central databases including PubMed and Google Scholar.
RESULTS AND CONCLUSION: A major class of extracellular metabolite-sensing receptors is G-protein-coupled receptors (GPCRs), which can directly or indirectly modulate macrophage activation, migration, cytokine production, and metabolic reprogramming. By fine-tuning macrophage-specific functions, metabolite-sensing receptors act as critical regulatory nodes in both inflammation and immune homeostasis, beyond their canonical role in sensing metabolic cues. This review provides a comprehensive overview of the metabolite-sensing receptor interactome, highlighting their central role in macrophage biology and underscoring their potential as therapeutic targets in inflammatory and metabolic diseases.
Additional Links: PMID-41961107
PubMed:
Citation:
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hide bibtex listing
@article {pmid41961107,
year = {2026},
author = {Rai, SK and Gupta, S and Sarangi, PP},
title = {Metabolite sensing receptors in macrophage reprogramming: from inflammation to resolution.},
journal = {Inflammation research : official journal of the European Histamine Research Society ... [et al.]},
volume = {75},
number = {1},
pages = {},
pmid = {41961107},
issn = {1420-908X},
support = {MoE-STARS/STARS-2/2023-0939//Ministry of Education, Govt. of India/ ; },
mesh = {Humans ; *Macrophages/immunology/metabolism ; Animals ; *Inflammation/immunology/metabolism ; *Receptors, G-Protein-Coupled/metabolism/immunology ; },
abstract = {BACKGROUND: Macrophages are central to innate immunity, orchestrating both the inflammatory and resolution phases of host defense. Emerging evidence indicates that immunometabolic crosstalk critically dictates macrophage polarization and functions. Disruptions in cellular metabolism can impair these regulatory mechanisms, leading to dysfunctional immune responses associated with various disease pathologies. A key aspect of this regulation involves metabolite-sensing receptors that detect changes in intracellular metabolic intermediates and in extracellular metabolites derived from the diet, host tissues, and the microbiome.
METHODS: We have conducted a literature review of original research and review articles on metabolite-sensing receptors and their roles in immune cell function, drawn from central databases including PubMed and Google Scholar.
RESULTS AND CONCLUSION: A major class of extracellular metabolite-sensing receptors is G-protein-coupled receptors (GPCRs), which can directly or indirectly modulate macrophage activation, migration, cytokine production, and metabolic reprogramming. By fine-tuning macrophage-specific functions, metabolite-sensing receptors act as critical regulatory nodes in both inflammation and immune homeostasis, beyond their canonical role in sensing metabolic cues. This review provides a comprehensive overview of the metabolite-sensing receptor interactome, highlighting their central role in macrophage biology and underscoring their potential as therapeutic targets in inflammatory and metabolic diseases.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Macrophages/immunology/metabolism
Animals
*Inflammation/immunology/metabolism
*Receptors, G-Protein-Coupled/metabolism/immunology
RevDate: 2026-04-13
Bacterial taxa associated with lung cancer cases in Southeast Asians: a pilot case-control study.
Cellular oncology (Dordrecht, Netherlands), 49(2):.
PURPOSE: Lung cancer is the leading cause of cancer-related mortality worldwide, yet its underlying mechanisms remain unclear. Disruptions in the respiratory microbiome may promote inflammation and carcinogenesis. This study aimed to comprehensively compare genus-level sputum microbiota between lung cancer patients and healthy controls in a multiethnic Southeast Asian population.
METHODS: Sputum samples were collected from lung cancer patients across three Singapore hospitals. Socio-demographic data were obtained via questionnaire. We analyzed 16S rRNA amplicon sequences from 70 lung cancer patients and 47 healthy controls from a separate local cohort, using identical sequencing protocols to minimize batch effects. Alpha- and beta-diversity metrics, random forest models, and ANCOM-BC2 were used to identify microbial features associated with lung cancer and host characteristics.
RESULTS: Lung cancer cases showed significantly reduced genus richness compared to controls. Beta-diversity (Aitchison distance) differed by case-control status, sex, age, and smoking history. ANCOM-BC2 identified Lactobacillus as differentially enriched in cases. However, this enrichment did not pass the pseudo-count test among never-smokers. Further sex-stratified analysis revealed that the Lactobacillus enrichment was driven primarily by male cases. Conversely, [Eubacterium] nodatum group, Mogibacterium, and Campylobacter emerged as robust inverse signatures for lung cancer, with their depletion consistently supported across stratified and unstratified differential abundance analyses, random forest modeling, and Wilcoxon rank-sum tests. However, these findings may still be subjected to residual confounding by exogenous factors, such as medication use, which could not be adequately adjusted for between case-control groups.
CONCLUSION: This pilot case-control study, conducted in a multiethnic Southeast Asian population, identified distinct respiratory microbiota signatures associated with lung cancer using robust differential abundance and machine-learning methods, providing preliminary evidence for a potential role of the respiratory microbiome to lung carcinogenesis, warranting validation in larger, longitudinal studies.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13402-026-01193-7.
Additional Links: PMID-41961381
PubMed:
Citation:
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@article {pmid41961381,
year = {2026},
author = {Low, A and Juang, YR and Ivan, FX and Ang, L and Ooi, LHS and Chan, SWJ and Mac Aogain, M and Jaggi, TK and Chotirmall, SH and Boucher, YF and Yii, ACA and Koh, MS and Lim, DWT and Lee, JWJ and Seow, WJ},
title = {Bacterial taxa associated with lung cancer cases in Southeast Asians: a pilot case-control study.},
journal = {Cellular oncology (Dordrecht, Netherlands)},
volume = {49},
number = {2},
pages = {},
pmid = {41961381},
issn = {2211-3436},
abstract = {PURPOSE: Lung cancer is the leading cause of cancer-related mortality worldwide, yet its underlying mechanisms remain unclear. Disruptions in the respiratory microbiome may promote inflammation and carcinogenesis. This study aimed to comprehensively compare genus-level sputum microbiota between lung cancer patients and healthy controls in a multiethnic Southeast Asian population.
METHODS: Sputum samples were collected from lung cancer patients across three Singapore hospitals. Socio-demographic data were obtained via questionnaire. We analyzed 16S rRNA amplicon sequences from 70 lung cancer patients and 47 healthy controls from a separate local cohort, using identical sequencing protocols to minimize batch effects. Alpha- and beta-diversity metrics, random forest models, and ANCOM-BC2 were used to identify microbial features associated with lung cancer and host characteristics.
RESULTS: Lung cancer cases showed significantly reduced genus richness compared to controls. Beta-diversity (Aitchison distance) differed by case-control status, sex, age, and smoking history. ANCOM-BC2 identified Lactobacillus as differentially enriched in cases. However, this enrichment did not pass the pseudo-count test among never-smokers. Further sex-stratified analysis revealed that the Lactobacillus enrichment was driven primarily by male cases. Conversely, [Eubacterium] nodatum group, Mogibacterium, and Campylobacter emerged as robust inverse signatures for lung cancer, with their depletion consistently supported across stratified and unstratified differential abundance analyses, random forest modeling, and Wilcoxon rank-sum tests. However, these findings may still be subjected to residual confounding by exogenous factors, such as medication use, which could not be adequately adjusted for between case-control groups.
CONCLUSION: This pilot case-control study, conducted in a multiethnic Southeast Asian population, identified distinct respiratory microbiota signatures associated with lung cancer using robust differential abundance and machine-learning methods, providing preliminary evidence for a potential role of the respiratory microbiome to lung carcinogenesis, warranting validation in larger, longitudinal studies.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13402-026-01193-7.},
}
RevDate: 2026-04-13
CmpDate: 2026-04-10
Spermidine Attenuates Neuroimmune Dysfunction in Gulf War Illness via Modulation of the Gut- Brain Axis.
Molecular neurobiology, 63(1):.
Gulf War illness (GWI) affects nearly one-third of US veterans deployed during the 1990-1991 Gulf War (GW) and is characterized by chronic fatigue, neuroinflammation, and gut dysbiosis. Through comprehensive fecal metabolomics sequencing, our lab previously reported the depletion of beneficial metabolites including spermidine in the preclinical GWI mouse model. Spermidine is an endogenously synthesized polyamine known for its anti-inflammatory and mucosal barrier protective effects in various pathological diseases. Given its established role in mitigating intestinal inflammation and maintaining homeostasis, this study investigated the therapeutic potential of spermidine in a persistent (22 weeks) GWI mouse model, with a specific focus on gut-brain axis regulation. Our results demonstrated that spermidine effectively restored both microbial richness and diversity by selectively enriching beneficial bacterial taxa and suppressing growth of opportunistic pathogens, which are otherwise dysregulated following exposure to GW chemicals. Spermidine treatment also improved gut epithelial barrier integrity and reduced epithelial release of high-mobility group box 1 (HMGB1) into systemic circulation. Recent studies on GWI have implicated a critical role of gut-derived damage-associated molecular patterns (DAMPs), particularly HMGB1 in mediating neuroinflammation. Our findings indicate that systemic levels of HMGB1 critically influence the extent of blood-brain barrier (BBB) disruption and subsequent microglial activation. Mechanistically, spermidine activated intestinal aryl hydrocarbon receptor (AhR)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling, which played a role in limiting intestinal HMGB1 release and suppressing downstream receptor for advanced glycation end-product (RAGE)-mediated microglial activation in the brain. In vitro results indicate spermidine promoted AhR/Nrf2 nuclear translocation which reduced LPS-induced HMGB1 release from primary intestinal epithelial cells (IECs), effects abrogated by AhR inhibition. Additionally, we observed that HMGB1 directly induces microglial activation via RAGE receptors in immortalized microglial (IMG) cell lines in a dose-dependent manner. These results demonstrate that spermidine decreases neuroinflammation by modulating gut-brain axis pathophysiology associated with GWI. Together, this study demonstrates the therapeutic role of spermidine in ameliorating systemic and neurological disturbances in GWI.
Additional Links: PMID-41961384
PubMed:
Citation:
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@article {pmid41961384,
year = {2026},
author = {Trivedi, A and Roy, S and More, M and Bose, D and Saha, P and Kumar, R and Sarkar, S and Skupsky, J and Tuteja, A and Sullivan, K and Klimas, N and Chatterjee, S},
title = {Spermidine Attenuates Neuroimmune Dysfunction in Gulf War Illness via Modulation of the Gut- Brain Axis.},
journal = {Molecular neurobiology},
volume = {63},
number = {1},
pages = {},
pmid = {41961384},
issn = {1559-1182},
mesh = {Animals ; *Spermidine/pharmacology/therapeutic use ; *Persian Gulf Syndrome/drug therapy/immunology/microbiology/metabolism ; *Brain/drug effects/metabolism ; *Gastrointestinal Microbiome/drug effects ; Mice ; Mice, Inbred C57BL ; Male ; Receptors, Aryl Hydrocarbon/metabolism ; HMGB1 Protein/metabolism ; Receptor for Advanced Glycation End Products/metabolism ; *Brain-Gut Axis/drug effects ; },
abstract = {Gulf War illness (GWI) affects nearly one-third of US veterans deployed during the 1990-1991 Gulf War (GW) and is characterized by chronic fatigue, neuroinflammation, and gut dysbiosis. Through comprehensive fecal metabolomics sequencing, our lab previously reported the depletion of beneficial metabolites including spermidine in the preclinical GWI mouse model. Spermidine is an endogenously synthesized polyamine known for its anti-inflammatory and mucosal barrier protective effects in various pathological diseases. Given its established role in mitigating intestinal inflammation and maintaining homeostasis, this study investigated the therapeutic potential of spermidine in a persistent (22 weeks) GWI mouse model, with a specific focus on gut-brain axis regulation. Our results demonstrated that spermidine effectively restored both microbial richness and diversity by selectively enriching beneficial bacterial taxa and suppressing growth of opportunistic pathogens, which are otherwise dysregulated following exposure to GW chemicals. Spermidine treatment also improved gut epithelial barrier integrity and reduced epithelial release of high-mobility group box 1 (HMGB1) into systemic circulation. Recent studies on GWI have implicated a critical role of gut-derived damage-associated molecular patterns (DAMPs), particularly HMGB1 in mediating neuroinflammation. Our findings indicate that systemic levels of HMGB1 critically influence the extent of blood-brain barrier (BBB) disruption and subsequent microglial activation. Mechanistically, spermidine activated intestinal aryl hydrocarbon receptor (AhR)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling, which played a role in limiting intestinal HMGB1 release and suppressing downstream receptor for advanced glycation end-product (RAGE)-mediated microglial activation in the brain. In vitro results indicate spermidine promoted AhR/Nrf2 nuclear translocation which reduced LPS-induced HMGB1 release from primary intestinal epithelial cells (IECs), effects abrogated by AhR inhibition. Additionally, we observed that HMGB1 directly induces microglial activation via RAGE receptors in immortalized microglial (IMG) cell lines in a dose-dependent manner. These results demonstrate that spermidine decreases neuroinflammation by modulating gut-brain axis pathophysiology associated with GWI. Together, this study demonstrates the therapeutic role of spermidine in ameliorating systemic and neurological disturbances in GWI.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Spermidine/pharmacology/therapeutic use
*Persian Gulf Syndrome/drug therapy/immunology/microbiology/metabolism
*Brain/drug effects/metabolism
*Gastrointestinal Microbiome/drug effects
Mice
Mice, Inbred C57BL
Male
Receptors, Aryl Hydrocarbon/metabolism
HMGB1 Protein/metabolism
Receptor for Advanced Glycation End Products/metabolism
*Brain-Gut Axis/drug effects
RevDate: 2026-04-10
The gut microbiota of hepato-pancreatico-biliary and gastric cancer patients is altered in composition and functionality.
Irish journal of medical science [Epub ahead of print].
Additional Links: PMID-41961453
PubMed:
Citation:
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@article {pmid41961453,
year = {2026},
author = {Daly, L and Sullivan, ES and Fouhy, F and Watkins, C and Linaries, D and Power, D and O'Suilleabhain, C and O'Sullivan, A and O'Toole, P and Ross, P and Stanton, C and Ryan, A},
title = {The gut microbiota of hepato-pancreatico-biliary and gastric cancer patients is altered in composition and functionality.},
journal = {Irish journal of medical science},
volume = {},
number = {},
pages = {},
pmid = {41961453},
issn = {1863-4362},
support = {SFI/12/RC/2273/SFI_/Science Foundation Ireland/Ireland ; },
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
The gut-brain axis and inflammatory mediators in suicide and mental disorders with high suicide rates: a review of current evidence.
Dialogues in clinical neuroscience, 28(1):145-156.
The interplay between gastrointestinal microbiota and mental disorders has recently been spotlighted. This review investigated discrete evidence suggesting associations between the gastrointestinal microbiome and inflammation with suicide. Fusicatenibavter, Hungatella, Veillonella, and Megasphaera have positive associations, but Clostridium, Butyricicoccus, Desulfovibrio piger, and Parabacteroides merdae have negative associations with suicidality. Additionally, lower species uniformity index, higher intestinal fatty acid binding protein secretion, lower zonulin secretion, higher interleukin-6 in cerebrospinal fluid, and laxative abuse are associated with suicidality. As nearly 90% of suicides occur in patients with mental disorders, the interaction between the gut microbiota and inflammation with these disorders together was also documented. Regarding this, major depressive disorder, psychosis and schizophrenia, generalised anxiety disorder, and substance use disorder were investigated. Bacteroidetes and Firmicutes show prominent changes in most cases. In addition, gut bacterial and non-bacterial microbiome alterations and subsequent dysbiosis may contribute to inflammation, in which cytokines affect microglial activity. Meanwhile, impaired intestinal homeostasis may influence these disorders through the vagus nerve, the hypothalamus-pituitary-adrenal axis, and the kynurenine pathway. Beyond these, direct effects of the gut microbiome on immunity are being hypothesised. In conclusion, the gut microbiota imbalance may influence the nervous system environment from non-inflammatory to inflammatory caused by pro-inflammatory cytokine influx into the brain. Consequently, microbiota imbalances may be associated with mental disorders. Specifically, limited evidence indicated possible links between microbiome alterations and suicide, highlighting the need for further research clarifying these associations and underpinning mechanisms. Other factors, including genetic vulnerability, environmental influences, and neurochemical pathways, should also be considered.
Additional Links: PMID-41961543
Publisher:
PubMed:
Citation:
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hide bibtex listing
@article {pmid41961543,
year = {2026},
author = {Shamabadi, A and Arabzadeh Bahri, R and Arab Bafrani, M and Karimi, H and Asadigandomani, H and Vahidi, H and Akhondzadeh, S},
title = {The gut-brain axis and inflammatory mediators in suicide and mental disorders with high suicide rates: a review of current evidence.},
journal = {Dialogues in clinical neuroscience},
volume = {28},
number = {1},
pages = {145-156},
doi = {10.1080/19585969.2026.2636468},
pmid = {41961543},
issn = {1958-5969},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Mental Disorders/metabolism/immunology/microbiology/psychology ; *Suicide/psychology ; *Brain/metabolism/immunology ; *Brain-Gut Axis/physiology ; *Inflammation Mediators/metabolism ; *Inflammation/metabolism ; Animals ; },
abstract = {The interplay between gastrointestinal microbiota and mental disorders has recently been spotlighted. This review investigated discrete evidence suggesting associations between the gastrointestinal microbiome and inflammation with suicide. Fusicatenibavter, Hungatella, Veillonella, and Megasphaera have positive associations, but Clostridium, Butyricicoccus, Desulfovibrio piger, and Parabacteroides merdae have negative associations with suicidality. Additionally, lower species uniformity index, higher intestinal fatty acid binding protein secretion, lower zonulin secretion, higher interleukin-6 in cerebrospinal fluid, and laxative abuse are associated with suicidality. As nearly 90% of suicides occur in patients with mental disorders, the interaction between the gut microbiota and inflammation with these disorders together was also documented. Regarding this, major depressive disorder, psychosis and schizophrenia, generalised anxiety disorder, and substance use disorder were investigated. Bacteroidetes and Firmicutes show prominent changes in most cases. In addition, gut bacterial and non-bacterial microbiome alterations and subsequent dysbiosis may contribute to inflammation, in which cytokines affect microglial activity. Meanwhile, impaired intestinal homeostasis may influence these disorders through the vagus nerve, the hypothalamus-pituitary-adrenal axis, and the kynurenine pathway. Beyond these, direct effects of the gut microbiome on immunity are being hypothesised. In conclusion, the gut microbiota imbalance may influence the nervous system environment from non-inflammatory to inflammatory caused by pro-inflammatory cytokine influx into the brain. Consequently, microbiota imbalances may be associated with mental disorders. Specifically, limited evidence indicated possible links between microbiome alterations and suicide, highlighting the need for further research clarifying these associations and underpinning mechanisms. Other factors, including genetic vulnerability, environmental influences, and neurochemical pathways, should also be considered.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology
*Mental Disorders/metabolism/immunology/microbiology/psychology
*Suicide/psychology
*Brain/metabolism/immunology
*Brain-Gut Axis/physiology
*Inflammation Mediators/metabolism
*Inflammation/metabolism
Animals
RevDate: 2026-04-10
CmpDate: 2026-04-10
Causal relationship between gut microbiome, plasma metabolites, inflammation, and aortic stenosis: A multi-omics Mendelian randomization analysis.
Medicine, 105(15):e48238.
As life expectancy increases and the population ages, aortic stenosis (AS) is the most common heart valve disease. Despite rapid improvements in interventional treatment options in recent years, morbidity and mortality from asymptomatic AS remain high. To date, there is no pharmacological therapy to prevent AS. In this study, we used multi-omics to systematically investigate potential causal association between the gut microbiome, human blood metabolites, inflammation and risk of AS, and search for potential biomarker for AS. Single-nucleotide polymorphisms associated with 207 gut microbiota, 1091 blood metabolites and the ratios of 309 metabolites, 731 immune cell phenotypes, 91 circulating inflammatory proteins, as exposures all were selected from recent large genome-wide association study and explored their causal association with AS using Mendelian randomization methods. We used the inverse variance weighted estimation method as the main method and other methods as supplementary methods. Mendelian randomization analysis has shown that 7 gut microbiota, 80 metabolites, 29 immune cells phenotypes, and 6 circulating inflammatory proteins are causally associated with AS. Co-localization analysis showed a significant correlation between 1-stearoyl-2-acryloyl-GPE levels and AS, with a P-value of .981 for posterior probability for hypothesis 4. In addition, metabolic pathway analysis revealed that the valine, leucine, and isoleucine biosynthesis (P = .0312) pathways were associated with AS. Four omics, including 207 gut microbiota, 1091 blood metabolites and the ratios of 309 metabolites, 731 immune cells, and 91 inflammatory proteins were used in this study to explain the causal relationship between multi-omics and AS.
Additional Links: PMID-41961656
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@article {pmid41961656,
year = {2026},
author = {Zhang, Y and Zhang, G},
title = {Causal relationship between gut microbiome, plasma metabolites, inflammation, and aortic stenosis: A multi-omics Mendelian randomization analysis.},
journal = {Medicine},
volume = {105},
number = {15},
pages = {e48238},
doi = {10.1097/MD.0000000000048238},
pmid = {41961656},
issn = {1536-5964},
mesh = {Humans ; Mendelian Randomization Analysis ; *Gastrointestinal Microbiome/genetics ; *Aortic Valve Stenosis/genetics/blood/microbiology ; *Inflammation/blood/genetics ; Polymorphism, Single Nucleotide ; Genome-Wide Association Study ; Biomarkers/blood ; Metabolomics ; Multiomics ; },
abstract = {As life expectancy increases and the population ages, aortic stenosis (AS) is the most common heart valve disease. Despite rapid improvements in interventional treatment options in recent years, morbidity and mortality from asymptomatic AS remain high. To date, there is no pharmacological therapy to prevent AS. In this study, we used multi-omics to systematically investigate potential causal association between the gut microbiome, human blood metabolites, inflammation and risk of AS, and search for potential biomarker for AS. Single-nucleotide polymorphisms associated with 207 gut microbiota, 1091 blood metabolites and the ratios of 309 metabolites, 731 immune cell phenotypes, 91 circulating inflammatory proteins, as exposures all were selected from recent large genome-wide association study and explored their causal association with AS using Mendelian randomization methods. We used the inverse variance weighted estimation method as the main method and other methods as supplementary methods. Mendelian randomization analysis has shown that 7 gut microbiota, 80 metabolites, 29 immune cells phenotypes, and 6 circulating inflammatory proteins are causally associated with AS. Co-localization analysis showed a significant correlation between 1-stearoyl-2-acryloyl-GPE levels and AS, with a P-value of .981 for posterior probability for hypothesis 4. In addition, metabolic pathway analysis revealed that the valine, leucine, and isoleucine biosynthesis (P = .0312) pathways were associated with AS. Four omics, including 207 gut microbiota, 1091 blood metabolites and the ratios of 309 metabolites, 731 immune cells, and 91 inflammatory proteins were used in this study to explain the causal relationship between multi-omics and AS.},
}
MeSH Terms:
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hide MeSH Terms
Humans
Mendelian Randomization Analysis
*Gastrointestinal Microbiome/genetics
*Aortic Valve Stenosis/genetics/blood/microbiology
*Inflammation/blood/genetics
Polymorphism, Single Nucleotide
Genome-Wide Association Study
Biomarkers/blood
Metabolomics
Multiomics
RevDate: 2026-04-10
CmpDate: 2026-04-10
Use of a cytochrome P450 humanized mouse model to refine schistosomiasis drug discovery.
Proceedings of the National Academy of Sciences of the United States of America, 123(15):e2600197123.
Control of schistosomiasis, a neglected tropical disease caused by infection with Schistosoma spp., remains reliant on a single chemotherapy, praziquantel (PZQ). This strategy presents a risk to global health should PZQ-resistant schistosomes establish in endemic areas and justifies the search for new drugs. However, species-specific metabolic differences between humans and preclinical models hinder the optimization of next-generation anti-schistosomal therapeutics. Here, to bypass these species-specific limitations, we exploited a humanized mouse model, 8HUM, engineered to express the principal human Phase I cytochrome P450 enzymes (CYP1A1/2, CYP2C9, CYP2D6, CYP3A4/7) as well as the transcription factors constitutive androstane receptor and pregnane X receptor in place of 35 murine orthologs. We characterized Schistosoma mansoni development, immunopathology, hepatic transcriptomic responses, intestinal microbiome changes, and PZQ metabolism as well as PZQ efficacy in 8HUM vs. wild-type (WT) mice. 8HUM mice supported normal S. mansoni maturation, infection-associated microbiome dysbiosis, Th2-dominant immune responses, and characteristic hepatic pathology. PZQ intrinsic clearance in 8HUM hepatic microsomes mirrored human levels and was >10-fold lower than that found for WT microsomes. Oral dosing revealed human-like PZQ exposures of (R)-PZQ and 4OH-PZQ in 8HUM mice at 25 mg/kg bodyweight and >90% reductions in worm burdens at 100 mg/kg bodyweight (equivalent to that seen in WT mice administered PZQ at 400 mg/kg bodyweight). Our results revealed that 8HUM mice recapitulate key features of murine schistosomiasis while exhibiting human-relevant drug metabolism. These findings establish 8HUM as a refined translational platform for anti-schistosomal drug development, improving predictive accuracy and accelerating therapeutic discovery.
Additional Links: PMID-41961851
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@article {pmid41961851,
year = {2026},
author = {Davey, SD and Forde-Thomas, JE and Hulme, BJ and Lees, K and Costain, AH and Evans, M and Rinaldi, G and Frame, L and Stojanovski, L and Simeons, FRC and Tavendale, A and MacLeod, AK and Pichon, R and Lee, YH and Polak, O and Chalmers, IW and Dankwa, B and Odhiambo, BK and Guimaraes, VH and Hegarty, M and Swain, MT and Aubrey, W and Caldwell, N and MacDonald, AS and Gilbert, IH and Baragaña, B and Read, KD and Hoffmann, KF},
title = {Use of a cytochrome P450 humanized mouse model to refine schistosomiasis drug discovery.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {15},
pages = {e2600197123},
doi = {10.1073/pnas.2600197123},
pmid = {41961851},
issn = {1091-6490},
support = {222153/Z/20/Z//Wellcome/ ; MR/W013568/1//UK Research and Innovation (UKRI)/ ; },
mesh = {Animals ; Mice ; *Cytochrome P-450 Enzyme System/metabolism/genetics ; Humans ; Disease Models, Animal ; Schistosoma mansoni/drug effects ; Praziquantel/pharmacology/therapeutic use ; *Drug Discovery/methods ; *Schistosomiasis mansoni/drug therapy/parasitology ; *Schistosomiasis/drug therapy/parasitology ; Anthelmintics/pharmacology ; Female ; Mice, Transgenic ; *Schistosomicides/pharmacology ; },
abstract = {Control of schistosomiasis, a neglected tropical disease caused by infection with Schistosoma spp., remains reliant on a single chemotherapy, praziquantel (PZQ). This strategy presents a risk to global health should PZQ-resistant schistosomes establish in endemic areas and justifies the search for new drugs. However, species-specific metabolic differences between humans and preclinical models hinder the optimization of next-generation anti-schistosomal therapeutics. Here, to bypass these species-specific limitations, we exploited a humanized mouse model, 8HUM, engineered to express the principal human Phase I cytochrome P450 enzymes (CYP1A1/2, CYP2C9, CYP2D6, CYP3A4/7) as well as the transcription factors constitutive androstane receptor and pregnane X receptor in place of 35 murine orthologs. We characterized Schistosoma mansoni development, immunopathology, hepatic transcriptomic responses, intestinal microbiome changes, and PZQ metabolism as well as PZQ efficacy in 8HUM vs. wild-type (WT) mice. 8HUM mice supported normal S. mansoni maturation, infection-associated microbiome dysbiosis, Th2-dominant immune responses, and characteristic hepatic pathology. PZQ intrinsic clearance in 8HUM hepatic microsomes mirrored human levels and was >10-fold lower than that found for WT microsomes. Oral dosing revealed human-like PZQ exposures of (R)-PZQ and 4OH-PZQ in 8HUM mice at 25 mg/kg bodyweight and >90% reductions in worm burdens at 100 mg/kg bodyweight (equivalent to that seen in WT mice administered PZQ at 400 mg/kg bodyweight). Our results revealed that 8HUM mice recapitulate key features of murine schistosomiasis while exhibiting human-relevant drug metabolism. These findings establish 8HUM as a refined translational platform for anti-schistosomal drug development, improving predictive accuracy and accelerating therapeutic discovery.},
}
MeSH Terms:
show MeSH Terms
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Animals
Mice
*Cytochrome P-450 Enzyme System/metabolism/genetics
Humans
Disease Models, Animal
Schistosoma mansoni/drug effects
Praziquantel/pharmacology/therapeutic use
*Drug Discovery/methods
*Schistosomiasis mansoni/drug therapy/parasitology
*Schistosomiasis/drug therapy/parasitology
Anthelmintics/pharmacology
Female
Mice, Transgenic
*Schistosomicides/pharmacology
RevDate: 2026-04-12
CmpDate: 2026-04-10
Genomic dissection of methane emission traits in cattle: A meta-GWAS and heritability analysis across populations.
PloS one, 21(4):e0344752.
Enteric methane emissions from ruminants represent a significant contributor to agricultural greenhouse gases, necessitating precise genetic tools to guide mitigation strategies. This study aimed to identify genomic regions and estimate heritability parameters associated with methane-related traits in cattle through an integrated meta-analytical framework. The meta-analysis of the genome-wide association studies (meta-GWAS) was carried out with the METAL software, combining SNP level data extracted from published studies. Simultaneously, a distinct random effects meta-analysis of genomic and pedigree-based heritability estimates was performed using Comprehensive Meta-Analysis software. Functional analysis of the post-GWAS, including: Gene Ontology, KEGG, and network-based enrichment analysis, was also performed to describe the biological context of significant genes. The meta-GWAS identified 74 significant SNPs that were significant for the traits of methane, which are related to 113 candidate genes. Functional enrichment analyses revealed pathways related to metabolism, immune response, ion transport, and host-microbiome interactions. The KEGG metabolic pathway emerged as a highly enriched term, encompassing key genes such as: ALDH7A1, CYP51A1, P4HA2, and SHPK, which are involved in amino acid catabolism, lipid processing, and redox regulation functions critical to energy balance and digestive efficiency. Network analysis with Cytoscape has revealed TRPV3, TRPV1, ANK3, PKD2 and SHPK as network hub genes. Heritability meta-analysis indicated that methane production exhibited the moderate genomic (h2 = 0.296) and pedigree-based (h2 = 0.299) heritability estimations, and methane yield was also found to have moderate and high heritability. The findings highlight the potential for methane-related traits as viable targets for genetic selection. This research demonstrates the value of integrating functional genomics and quantitative genetic approaches to enhance understanding of the biological and heritable components of methane emissions, providing a robust foundation for an environmentally sustainable livestock breeding program.
Additional Links: PMID-41961873
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@article {pmid41961873,
year = {2026},
author = {Golpasand, S and Ghavi Hossein-Zadeh, N and Ghovvati, S},
title = {Genomic dissection of methane emission traits in cattle: A meta-GWAS and heritability analysis across populations.},
journal = {PloS one},
volume = {21},
number = {4},
pages = {e0344752},
pmid = {41961873},
issn = {1932-6203},
mesh = {Animals ; Cattle/genetics ; *Methane/metabolism ; *Genome-Wide Association Study ; Polymorphism, Single Nucleotide ; *Quantitative Trait, Heritable ; Genomics ; Quantitative Trait Loci ; },
abstract = {Enteric methane emissions from ruminants represent a significant contributor to agricultural greenhouse gases, necessitating precise genetic tools to guide mitigation strategies. This study aimed to identify genomic regions and estimate heritability parameters associated with methane-related traits in cattle through an integrated meta-analytical framework. The meta-analysis of the genome-wide association studies (meta-GWAS) was carried out with the METAL software, combining SNP level data extracted from published studies. Simultaneously, a distinct random effects meta-analysis of genomic and pedigree-based heritability estimates was performed using Comprehensive Meta-Analysis software. Functional analysis of the post-GWAS, including: Gene Ontology, KEGG, and network-based enrichment analysis, was also performed to describe the biological context of significant genes. The meta-GWAS identified 74 significant SNPs that were significant for the traits of methane, which are related to 113 candidate genes. Functional enrichment analyses revealed pathways related to metabolism, immune response, ion transport, and host-microbiome interactions. The KEGG metabolic pathway emerged as a highly enriched term, encompassing key genes such as: ALDH7A1, CYP51A1, P4HA2, and SHPK, which are involved in amino acid catabolism, lipid processing, and redox regulation functions critical to energy balance and digestive efficiency. Network analysis with Cytoscape has revealed TRPV3, TRPV1, ANK3, PKD2 and SHPK as network hub genes. Heritability meta-analysis indicated that methane production exhibited the moderate genomic (h2 = 0.296) and pedigree-based (h2 = 0.299) heritability estimations, and methane yield was also found to have moderate and high heritability. The findings highlight the potential for methane-related traits as viable targets for genetic selection. This research demonstrates the value of integrating functional genomics and quantitative genetic approaches to enhance understanding of the biological and heritable components of methane emissions, providing a robust foundation for an environmentally sustainable livestock breeding program.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Cattle/genetics
*Methane/metabolism
*Genome-Wide Association Study
Polymorphism, Single Nucleotide
*Quantitative Trait, Heritable
Genomics
Quantitative Trait Loci
RevDate: 2026-04-13
CmpDate: 2026-04-10
Predicted meta-omics: A potential solution to multi-omics data scarcity in microbiome studies.
PloS one, 21(4):e0345919.
Imbalances in the gut microbiome have been linked to conditions such as inflammatory bowel disease, diabetes, and cancer. While metagenomics and amplicon sequencing are commonly used to study the microbiome, they do not capture all layers of microbial functions. Other meta-omics data can provide more insights, but these are more costly and laborious to procure. The growing availability of paired meta-omics data offers an opportunity to develop machine learning models that can infer connections between metagenomics data and other forms of meta-omics data, enabling the prediction of these other forms of meta-omics data from metagenomics. We evaluated several machine learning models for predicting meta-omics features from various meta-omics inputs. Simpler architectures such as elastic net regression and random forests generated reliable predictions of transcript and metabolite abundances, with correlations of up to 0.77 and 0.74, respectively, but predicting protein profiles was more challenging. We also identified a core set of well-predicted features for each meta-omics output type, and showed that multi-output regression neural networks performed similarly when trained using fewer output features. Lastly, our experiments demonstrated that predicted features can be used for the downstream task of inflammatory bowel disease classification, with performance comparable to that of experimental data.
Additional Links: PMID-41961886
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@article {pmid41961886,
year = {2026},
author = {Cosma, BM and Pillay, S and Calderón-Franco, D and Abeel, T},
title = {Predicted meta-omics: A potential solution to multi-omics data scarcity in microbiome studies.},
journal = {PloS one},
volume = {21},
number = {4},
pages = {e0345919},
pmid = {41961886},
issn = {1932-6203},
mesh = {Humans ; *Metagenomics/methods ; Machine Learning ; *Gastrointestinal Microbiome/genetics ; *Microbiota ; Inflammatory Bowel Diseases/microbiology ; Neural Networks, Computer ; Multiomics ; },
abstract = {Imbalances in the gut microbiome have been linked to conditions such as inflammatory bowel disease, diabetes, and cancer. While metagenomics and amplicon sequencing are commonly used to study the microbiome, they do not capture all layers of microbial functions. Other meta-omics data can provide more insights, but these are more costly and laborious to procure. The growing availability of paired meta-omics data offers an opportunity to develop machine learning models that can infer connections between metagenomics data and other forms of meta-omics data, enabling the prediction of these other forms of meta-omics data from metagenomics. We evaluated several machine learning models for predicting meta-omics features from various meta-omics inputs. Simpler architectures such as elastic net regression and random forests generated reliable predictions of transcript and metabolite abundances, with correlations of up to 0.77 and 0.74, respectively, but predicting protein profiles was more challenging. We also identified a core set of well-predicted features for each meta-omics output type, and showed that multi-output regression neural networks performed similarly when trained using fewer output features. Lastly, our experiments demonstrated that predicted features can be used for the downstream task of inflammatory bowel disease classification, with performance comparable to that of experimental data.},
}
MeSH Terms:
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Humans
*Metagenomics/methods
Machine Learning
*Gastrointestinal Microbiome/genetics
*Microbiota
Inflammatory Bowel Diseases/microbiology
Neural Networks, Computer
Multiomics
RevDate: 2026-04-10
Exposure to Environmental Microbes Alters Responsiveness of Tadpole Gut Microbiome to Dietary Tannins.
Integrative zoology [Epub ahead of print].
Amphibian larvae consume variable diets in the wild, which can include tannin-rich plant material. Tannins are secondary metabolites that, when consumed, could have complex effects on herbivorous amphibian larvae, including altering their microbiome. Previous studies on the effects of dietary tannic acid on tadpoles were performed using laboratory water, largely devoid of natural microbes. Given that tadpoles acquire much of their gut microbiota from the aquatic environment, we sought to understand the effect of dietary tannins on tadpole size and the gut microbiome when animals were raised in natural pond water, supplying a diverse repertoire of microbes. We raised Green Frog (Lithobates clamitans) tadpoles in autoclaved (microbially depleted) or natural (microbially rich) pond water treatments for 4 weeks. Tadpoles were fed a control diet or a diet containing 2% tannic acid. Tadpoles raised in natural pond water had a greater body mass and length than those raised in autoclaved pond water, but dietary tannins had no effect on body size. Gut bacterial diversity was profiled using 16S rRNA sequencing. The gut microbiome from tadpoles raised in natural pond water was more diverse than that of tadpoles raised in autoclaved pond water. In general, dietary tannins caused a decrease in bacterial diversity and a net reduction in the relative abundance of potentially pathogenic bacterial genera in tadpoles raised in natural pond water but not autoclaved pond water. This study highlights the importance of replicating natural microbial contexts in captive experiments to better investigate biological interactions, such as plant-herbivore and host-microbe interactions.
Additional Links: PMID-41962053
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PubMed:
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@article {pmid41962053,
year = {2026},
author = {Westcott, RG and Rudzki, EN and Emerson, KJ and Woodley, SK and Kohl, KD},
title = {Exposure to Environmental Microbes Alters Responsiveness of Tadpole Gut Microbiome to Dietary Tannins.},
journal = {Integrative zoology},
volume = {},
number = {},
pages = {},
doi = {10.1111/1749-4877.70102},
pmid = {41962053},
issn = {1749-4877},
support = {1945956//National Science Foundation/ ; 2139321//National Science Foundation/ ; },
abstract = {Amphibian larvae consume variable diets in the wild, which can include tannin-rich plant material. Tannins are secondary metabolites that, when consumed, could have complex effects on herbivorous amphibian larvae, including altering their microbiome. Previous studies on the effects of dietary tannic acid on tadpoles were performed using laboratory water, largely devoid of natural microbes. Given that tadpoles acquire much of their gut microbiota from the aquatic environment, we sought to understand the effect of dietary tannins on tadpole size and the gut microbiome when animals were raised in natural pond water, supplying a diverse repertoire of microbes. We raised Green Frog (Lithobates clamitans) tadpoles in autoclaved (microbially depleted) or natural (microbially rich) pond water treatments for 4 weeks. Tadpoles were fed a control diet or a diet containing 2% tannic acid. Tadpoles raised in natural pond water had a greater body mass and length than those raised in autoclaved pond water, but dietary tannins had no effect on body size. Gut bacterial diversity was profiled using 16S rRNA sequencing. The gut microbiome from tadpoles raised in natural pond water was more diverse than that of tadpoles raised in autoclaved pond water. In general, dietary tannins caused a decrease in bacterial diversity and a net reduction in the relative abundance of potentially pathogenic bacterial genera in tadpoles raised in natural pond water but not autoclaved pond water. This study highlights the importance of replicating natural microbial contexts in captive experiments to better investigate biological interactions, such as plant-herbivore and host-microbe interactions.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
The gut-brain axis and its role in obesity-induced homeostatic dysregulation.
Wiadomosci lekarskie (Warsaw, Poland : 1960), 79(3):597-604.
OBJECTIVE: Aim: The gut-brain axis (GBA) plays a crucial role in maintaining systemic homeostasis through bidirectional communication between the central nervous system and the gastrointestinal tract. This review aims to summarize current evidence regarding the impact of obesity on GBA function and to discuss potential therapeutic strategies targeting this pathway.
PATIENTS AND METHODS: Materials and Methods: A narrative literature review was conducted using scientific publications indexed in databases including PubMed, ScienceDirect, and the European Journal of Endocrinology. Studies addressing obesity-related alterations in neural signaling, gut microbiota composition, and peptide hormone regulation (e.g., cholecystokinin, peptide YY, ghrelin) were analyzed. Particular attention was given to mechanisms involving dopaminergic reward circuits and emerging therapeutic targets such as ghrelin antagonists, gamma-aminobutyric acid modulators, and melanocortin-4 receptor agonists. Evidence indicates that obesity is associated with significant alterations in gut microbiota composition, vagal signaling, and neuroendocrine regulation of appetite and reward pathways. These changes contribute to dysregulation of nutrient absorption, inflammatory responses, and metabolic homeostasis. Both invasive and non-invasive interventions - including dietary modification, microbiome-targeted therapies, pharmacological agents, and neurostimulation techniques - show potential to modulate GBA signaling and restore physiological balance.
CONCLUSION: Conclusions: Understanding the complex relationship between obesity and the gut-brain axis may provide novel therapeutic targets for improving metabolic regulation and reducing obesity-related complications. Further clinical and translational studies are required to confirm the long-term effectiveness of GBAoriented interventions.
Additional Links: PMID-41962103
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PubMed:
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@article {pmid41962103,
year = {2026},
author = {Paczwa, J and Wu, C and Mulica, J and Siwasan, K and Fuentes, K and Razowska, D},
title = {The gut-brain axis and its role in obesity-induced homeostatic dysregulation.},
journal = {Wiadomosci lekarskie (Warsaw, Poland : 1960)},
volume = {79},
number = {3},
pages = {597-604},
doi = {10.36740/WLek/218289},
pmid = {41962103},
issn = {0043-5147},
mesh = {Humans ; *Obesity/physiopathology/metabolism ; *Homeostasis ; *Gastrointestinal Microbiome/physiology ; *Brain/physiopathology/metabolism ; *Gastrointestinal Tract/physiopathology/metabolism ; *Brain-Gut Axis/physiology ; },
abstract = {OBJECTIVE: Aim: The gut-brain axis (GBA) plays a crucial role in maintaining systemic homeostasis through bidirectional communication between the central nervous system and the gastrointestinal tract. This review aims to summarize current evidence regarding the impact of obesity on GBA function and to discuss potential therapeutic strategies targeting this pathway.
PATIENTS AND METHODS: Materials and Methods: A narrative literature review was conducted using scientific publications indexed in databases including PubMed, ScienceDirect, and the European Journal of Endocrinology. Studies addressing obesity-related alterations in neural signaling, gut microbiota composition, and peptide hormone regulation (e.g., cholecystokinin, peptide YY, ghrelin) were analyzed. Particular attention was given to mechanisms involving dopaminergic reward circuits and emerging therapeutic targets such as ghrelin antagonists, gamma-aminobutyric acid modulators, and melanocortin-4 receptor agonists. Evidence indicates that obesity is associated with significant alterations in gut microbiota composition, vagal signaling, and neuroendocrine regulation of appetite and reward pathways. These changes contribute to dysregulation of nutrient absorption, inflammatory responses, and metabolic homeostasis. Both invasive and non-invasive interventions - including dietary modification, microbiome-targeted therapies, pharmacological agents, and neurostimulation techniques - show potential to modulate GBA signaling and restore physiological balance.
CONCLUSION: Conclusions: Understanding the complex relationship between obesity and the gut-brain axis may provide novel therapeutic targets for improving metabolic regulation and reducing obesity-related complications. Further clinical and translational studies are required to confirm the long-term effectiveness of GBAoriented interventions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Obesity/physiopathology/metabolism
*Homeostasis
*Gastrointestinal Microbiome/physiology
*Brain/physiopathology/metabolism
*Gastrointestinal Tract/physiopathology/metabolism
*Brain-Gut Axis/physiology
RevDate: 2026-04-10
CmpDate: 2026-04-10
Periodontitis as a systemic inflammatory disorder - implications for cardiovascular and neurodegenerative diseases.
Wiadomosci lekarskie (Warsaw, Poland : 1960), 79(3):646-650.
OBJECTIVE: Aim: Periodontitis is a chronic inflammatory condition associated with oral microbiome dysbiosis and the dominance of Gram-negative bacteria such as Porphyromonas gingivalis. It is characterized by progressive destruction of the supporting tissues of the tooth, leading to loss of connective tissue attachment, resorption of the alveolar bone, and, consequently to tooth loosening and loss. If left untreated, it leads to recurrent bacteremia and persistent systemic inflammation. The aim of this study is to discuss the mechanisms linking periodontitis to cardiovascular and neurodegenerative diseases.
PATIENTS AND METHODS: Materials and Methods: A comprehensive literature review was conducted examining clinical studies, systematic reviews, and meta-analyses assessing the impact of periodontal disease on the development of cardiovascular and neurodegenerative diseases.
CONCLUSION: Conclusions: Chronic activation of the immune response, oxidative stress, and lipid metabolism disorders promote endothelial dysfunction and the progression of atherosclerosis, increasing the risk of cardiovascular events. At the same time, systemic inflammation can affect the permeability of the blood-brain barrier and exacerbate neuroinflammatory processes, promoting β-amyloid accumulation and the progression of Alzheimer's disease. Analysis of the literature indicates the significant, albeit complex, nature of these relationships, emphasizing the importance of prevention and treatment of periodontal disease as part of comprehensive patient care. The key in the approach to periodontal patients is an interdisciplinary perspective, integrating dentistry, cardiology, neurology, and geriatrics.
Additional Links: PMID-41962111
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PubMed:
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@article {pmid41962111,
year = {2026},
author = {Sobiech, L and Wójcik, L and Jankowska, N and Turżańska, K},
title = {Periodontitis as a systemic inflammatory disorder - implications for cardiovascular and neurodegenerative diseases.},
journal = {Wiadomosci lekarskie (Warsaw, Poland : 1960)},
volume = {79},
number = {3},
pages = {646-650},
doi = {10.36740/WLek/218274},
pmid = {41962111},
issn = {0043-5147},
mesh = {Humans ; *Cardiovascular Diseases/etiology ; *Neurodegenerative Diseases/etiology ; *Periodontitis/complications/microbiology ; *Inflammation/complications ; },
abstract = {OBJECTIVE: Aim: Periodontitis is a chronic inflammatory condition associated with oral microbiome dysbiosis and the dominance of Gram-negative bacteria such as Porphyromonas gingivalis. It is characterized by progressive destruction of the supporting tissues of the tooth, leading to loss of connective tissue attachment, resorption of the alveolar bone, and, consequently to tooth loosening and loss. If left untreated, it leads to recurrent bacteremia and persistent systemic inflammation. The aim of this study is to discuss the mechanisms linking periodontitis to cardiovascular and neurodegenerative diseases.
PATIENTS AND METHODS: Materials and Methods: A comprehensive literature review was conducted examining clinical studies, systematic reviews, and meta-analyses assessing the impact of periodontal disease on the development of cardiovascular and neurodegenerative diseases.
CONCLUSION: Conclusions: Chronic activation of the immune response, oxidative stress, and lipid metabolism disorders promote endothelial dysfunction and the progression of atherosclerosis, increasing the risk of cardiovascular events. At the same time, systemic inflammation can affect the permeability of the blood-brain barrier and exacerbate neuroinflammatory processes, promoting β-amyloid accumulation and the progression of Alzheimer's disease. Analysis of the literature indicates the significant, albeit complex, nature of these relationships, emphasizing the importance of prevention and treatment of periodontal disease as part of comprehensive patient care. The key in the approach to periodontal patients is an interdisciplinary perspective, integrating dentistry, cardiology, neurology, and geriatrics.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Cardiovascular Diseases/etiology
*Neurodegenerative Diseases/etiology
*Periodontitis/complications/microbiology
*Inflammation/complications
RevDate: 2026-04-10
Host proteins and symbiotic bacteria mediate the thermal response differences of the two color phenotypes of Porites lutea to extreme marine heatwaves in Weizhou Island.
Marine pollution bulletin, 229:119723 pii:S0025-326X(26)00510-2 [Epub ahead of print].
Extreme marine heatwaves driven by global warming are the major threat to coral reefs, causing mass coral bleaching and mortality. Color polymorphism is a key coral phenotypic trait, but the mechanisms underlying thermal adaptability differences among color phenotypes remain unclear. This study investigated two Porites lutea phenotypes (green and brown) from Weizhou Island, integrating field surveys, proteomics, and symbiotic microbial community analyses to explore their thermal response differences and molecular mechanisms. Field monitoring during the 2020 marine heatwave revealed a 46% bleaching rate in brown P. lutea, whereas green P. lutea exhibited no bleaching, demonstrating the latter's superior thermal tolerance. Proteomics revealed that green coral hosts maintained thermal adaptability by regulating proteins related to heat shock response, antioxidant defense, and green fluorescent protein (GFP), with GFP expression significantly upregulated by 7.2-fold compared to the brown phenotype. Additionally, the two phenotypes differed in symbiotic bacterial relative abundance: the green P. lutea was dominated by Proteobacteria and Chloroflexi (aiding nitrogen fixation and photosynthesis), while the brown P. lutea was enriched with Thermus and Prosthecochloris (enhancing antioxidant capacity and thermal resistance). No significant differences were found in the community structure or density of Symbiodiniaceae. In conclusion, differential host protein expression and functional complementarity of symbiotic bacteria jointly mediate thermal adaptation differentiation between the two P. lutea phenotypes. This study reveals color phenotypic differentiation as an effective coral survival strategy against environmental stresses, enhancing adaptive potential under future climate change and providing theoretical and technical support for coral reef ecological early warning and restoration under global warming.
Additional Links: PMID-41962296
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@article {pmid41962296,
year = {2026},
author = {Wang, Y and Yu, K and Meng, L and Gong, S and Yu, X and Huang, X and Huang, W},
title = {Host proteins and symbiotic bacteria mediate the thermal response differences of the two color phenotypes of Porites lutea to extreme marine heatwaves in Weizhou Island.},
journal = {Marine pollution bulletin},
volume = {229},
number = {},
pages = {119723},
doi = {10.1016/j.marpolbul.2026.119723},
pmid = {41962296},
issn = {1879-3363},
abstract = {Extreme marine heatwaves driven by global warming are the major threat to coral reefs, causing mass coral bleaching and mortality. Color polymorphism is a key coral phenotypic trait, but the mechanisms underlying thermal adaptability differences among color phenotypes remain unclear. This study investigated two Porites lutea phenotypes (green and brown) from Weizhou Island, integrating field surveys, proteomics, and symbiotic microbial community analyses to explore their thermal response differences and molecular mechanisms. Field monitoring during the 2020 marine heatwave revealed a 46% bleaching rate in brown P. lutea, whereas green P. lutea exhibited no bleaching, demonstrating the latter's superior thermal tolerance. Proteomics revealed that green coral hosts maintained thermal adaptability by regulating proteins related to heat shock response, antioxidant defense, and green fluorescent protein (GFP), with GFP expression significantly upregulated by 7.2-fold compared to the brown phenotype. Additionally, the two phenotypes differed in symbiotic bacterial relative abundance: the green P. lutea was dominated by Proteobacteria and Chloroflexi (aiding nitrogen fixation and photosynthesis), while the brown P. lutea was enriched with Thermus and Prosthecochloris (enhancing antioxidant capacity and thermal resistance). No significant differences were found in the community structure or density of Symbiodiniaceae. In conclusion, differential host protein expression and functional complementarity of symbiotic bacteria jointly mediate thermal adaptation differentiation between the two P. lutea phenotypes. This study reveals color phenotypic differentiation as an effective coral survival strategy against environmental stresses, enhancing adaptive potential under future climate change and providing theoretical and technical support for coral reef ecological early warning and restoration under global warming.},
}
RevDate: 2026-04-10
Effect of TU-100 on Colorectal Liver Metastasis in Mouse Model of MASH.
The Journal of surgical research, 322:10-16 pii:S0022-4804(26)00184-8 [Epub ahead of print].
INTRODUCTION: The incidence of metabolic dysfunction-associated steatohepatitis (MASH) is rapidly increasing, and colorectal liver metastasis (CLM) has been reported to be enhanced in MASH. We previously reported that the herbal medicine Daikenchuto (TU-100) regulates the intestinal microbiome and MASH in a mouse model. This study was performed to examine the effect of TU-100 on CLM using a Western diet (WD)-fed mouse model.
METHODS: Six-week-old male C57BL/6J mice were used. Mice in the WD group were fed a WD, and TU-100 was administered to mice in the WD+TU-100 group. Splenic injection of MC38 colon cancer cells was performed at 16 wk, and mice were sacrificed 2 wk after splenic injection to assess steatosis, fibrosis, and hepatic mRNA expression.
RESULTS: The degree of steatosis was significantly reduced in the WD+TU-100 group compared with the WD group (P < 0.05). The maximum tumor diameter was significantly smaller in the WD+TU-100 group than in the WD group (P < 0.05). Hepatic mRNA expression of serum amyloid A1 and tissue inhibitor of matrix metalloproteinases 1 was significantly suppressed in the WD+TU-100 group compared with the WD group (P < 0.05).
CONCLUSIONS: TU-100 improved hepatic steatosis in an MASH mouse model and suppressed CLM. Suppression of hepatic serum amyloid A1 and tissue inhibitor of matrix metalloproteinases 1 expression may contribute to these effects.
Additional Links: PMID-41962521
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@article {pmid41962521,
year = {2026},
author = {Yamada, S and Morine, Y and Ikemoto, T and Saito, Y and Teraoku, H and Miyazaki, K and Shimada, M},
title = {Effect of TU-100 on Colorectal Liver Metastasis in Mouse Model of MASH.},
journal = {The Journal of surgical research},
volume = {322},
number = {},
pages = {10-16},
doi = {10.1016/j.jss.2026.03.073},
pmid = {41962521},
issn = {1095-8673},
abstract = {INTRODUCTION: The incidence of metabolic dysfunction-associated steatohepatitis (MASH) is rapidly increasing, and colorectal liver metastasis (CLM) has been reported to be enhanced in MASH. We previously reported that the herbal medicine Daikenchuto (TU-100) regulates the intestinal microbiome and MASH in a mouse model. This study was performed to examine the effect of TU-100 on CLM using a Western diet (WD)-fed mouse model.
METHODS: Six-week-old male C57BL/6J mice were used. Mice in the WD group were fed a WD, and TU-100 was administered to mice in the WD+TU-100 group. Splenic injection of MC38 colon cancer cells was performed at 16 wk, and mice were sacrificed 2 wk after splenic injection to assess steatosis, fibrosis, and hepatic mRNA expression.
RESULTS: The degree of steatosis was significantly reduced in the WD+TU-100 group compared with the WD group (P < 0.05). The maximum tumor diameter was significantly smaller in the WD+TU-100 group than in the WD group (P < 0.05). Hepatic mRNA expression of serum amyloid A1 and tissue inhibitor of matrix metalloproteinases 1 was significantly suppressed in the WD+TU-100 group compared with the WD group (P < 0.05).
CONCLUSIONS: TU-100 improved hepatic steatosis in an MASH mouse model and suppressed CLM. Suppression of hepatic serum amyloid A1 and tissue inhibitor of matrix metalloproteinases 1 expression may contribute to these effects.},
}
RevDate: 2026-04-10
Exposure to a High-Fat Diet Compromises Gut Health, Behavior, and HPA Axis Function, with Partial Reversal When Limited to Adolescence.
Brain research bulletin pii:S0361-9230(26)00169-3 [Epub ahead of print].
High-fat diet (HFD) consumption contributes to obesity, yet its impact on females of (pre)reproductive age and the effects of dietary modification after adolescence remain underexplored. This study examined how continuous HFD exposure or an adolescent switch from HFD to a standard diet (SD) shapes the gut microbiome, behavior, neurochemistry, metabolism, and key components of the hypothalamic-pituitary-adrenal (HPA) axis in female rats. Because HPA-axis alterations can occur across generations after HFD exposure, we examined reproductive-tissue HPA-axis components as potential mechanisms of transmission. Females received SD, HFD, or HFD followed by SD after majority of adolescence (postnatal day 60). HFD exposure impaired HPA-axis regulation and switching to SD during adolescence did not prevent persistent dysfunction into adulthood. However, reproductive HPA-axis components remained unaltered. Diet also strongly influenced the microbiome: while HFD disrupted microbial composition in adolescence, switching to SD partially restored it by adulthood. Behavioral and metabolic effects, including increased adiposity and anxiety-like behavior, emerged only with prolonged HFD exposure. Brain neurotransmitter concentrations remained largely unaffected. Overall, dietary history across adolescence and early adulthood shaped long-term HPA-axis function, microbiome composition, and behavioral outcomes. The absence of reproductive HPA-axis alterations suggests it is not a major mediator of maternal HFD-induced intergenerational effects. Persistent HPA-axis dysfunction despite dietary switching indicates limited reversibility, whereas the microbiome showed the greatest adaptive capacity. In contrast, lasting behavioral and metabolic consequences of HFD require continued exposure to adulthood.
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@article {pmid41962594,
year = {2026},
author = {Ott, A and Gül, AZ and Löber, U and Birkner, T and Popova, E and Winter, C and Hadar, R},
title = {Exposure to a High-Fat Diet Compromises Gut Health, Behavior, and HPA Axis Function, with Partial Reversal When Limited to Adolescence.},
journal = {Brain research bulletin},
volume = {},
number = {},
pages = {111883},
doi = {10.1016/j.brainresbull.2026.111883},
pmid = {41962594},
issn = {1873-2747},
abstract = {High-fat diet (HFD) consumption contributes to obesity, yet its impact on females of (pre)reproductive age and the effects of dietary modification after adolescence remain underexplored. This study examined how continuous HFD exposure or an adolescent switch from HFD to a standard diet (SD) shapes the gut microbiome, behavior, neurochemistry, metabolism, and key components of the hypothalamic-pituitary-adrenal (HPA) axis in female rats. Because HPA-axis alterations can occur across generations after HFD exposure, we examined reproductive-tissue HPA-axis components as potential mechanisms of transmission. Females received SD, HFD, or HFD followed by SD after majority of adolescence (postnatal day 60). HFD exposure impaired HPA-axis regulation and switching to SD during adolescence did not prevent persistent dysfunction into adulthood. However, reproductive HPA-axis components remained unaltered. Diet also strongly influenced the microbiome: while HFD disrupted microbial composition in adolescence, switching to SD partially restored it by adulthood. Behavioral and metabolic effects, including increased adiposity and anxiety-like behavior, emerged only with prolonged HFD exposure. Brain neurotransmitter concentrations remained largely unaffected. Overall, dietary history across adolescence and early adulthood shaped long-term HPA-axis function, microbiome composition, and behavioral outcomes. The absence of reproductive HPA-axis alterations suggests it is not a major mediator of maternal HFD-induced intergenerational effects. Persistent HPA-axis dysfunction despite dietary switching indicates limited reversibility, whereas the microbiome showed the greatest adaptive capacity. In contrast, lasting behavioral and metabolic consequences of HFD require continued exposure to adulthood.},
}
RevDate: 2026-04-10
Epigenetic Modulation of the Gut-Muscle Axis in Pompe Disease: Microbiota Fingerprints to Cellular and Molecular Pathomechanisms.
Molecular metabolism pii:S2212-8778(26)00048-7 [Epub ahead of print].
Inter-organ cross-talk is increasingly recognised as a fundamental determinant in the pathogenesis of neurodegenerative and neuromuscular disorders, modulating neuroinflammation, protein misfolding, and cellular dysfunction through systemic mediators such as cytokines, adipokines, and growth factors. In neuromuscular diseases, particularly Pompe disease, muscle degeneration is tightly linked to impaired autophagy and chronic inflammation. Recent evidence highlights the gut microbiota as a key regulator of innate and adaptive immune responses, exerting direct effects on skeletal muscle and supporting the existence of a gut-muscle axis. Dysbiosis has been proposed to influence myopathy progression, suggesting that modulation of the intestinal ecosystem may hold therapeutic relevance. Consequently, interventions employing probiotics, prebiotics, and targeted nutritional compounds have emerged as promising strategies to modulate immune activity, attenuate inflammation, and enhance autophagic efficiency, thereby contributing to the restoration of intestinal eubiosis and complementing enzyme replacement therapy.In parallel, epigenetic mechanisms are gaining prominence as additional modulators of pathogenic pathways, with the potential to influence microbiome composition and function. Collectively, these insights position the gut-muscle axis as a central regulatory node in Pompe disease and a compelling target for personalised nutritional and nutraceutical approaches. This review aims to provide a comprehensive examination of the gut-muscle axis and its implications in Pompe disease. Understanding how nutrient-induced changes in microbial gene expression may be harnessed to develop novel, synergistic therapeutic strategies could ultimately improve clinical outcomes and enhance the quality of life of affected individuals.
Additional Links: PMID-41962630
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@article {pmid41962630,
year = {2026},
author = {Venezia, M and Russo, M and Colomba, P and Zizzo, C and Vinci, M and Marsana, EM and D'Errico, A and Giacalone, I and Duro, G and Moschetti, M},
title = {Epigenetic Modulation of the Gut-Muscle Axis in Pompe Disease: Microbiota Fingerprints to Cellular and Molecular Pathomechanisms.},
journal = {Molecular metabolism},
volume = {},
number = {},
pages = {102364},
doi = {10.1016/j.molmet.2026.102364},
pmid = {41962630},
issn = {2212-8778},
abstract = {Inter-organ cross-talk is increasingly recognised as a fundamental determinant in the pathogenesis of neurodegenerative and neuromuscular disorders, modulating neuroinflammation, protein misfolding, and cellular dysfunction through systemic mediators such as cytokines, adipokines, and growth factors. In neuromuscular diseases, particularly Pompe disease, muscle degeneration is tightly linked to impaired autophagy and chronic inflammation. Recent evidence highlights the gut microbiota as a key regulator of innate and adaptive immune responses, exerting direct effects on skeletal muscle and supporting the existence of a gut-muscle axis. Dysbiosis has been proposed to influence myopathy progression, suggesting that modulation of the intestinal ecosystem may hold therapeutic relevance. Consequently, interventions employing probiotics, prebiotics, and targeted nutritional compounds have emerged as promising strategies to modulate immune activity, attenuate inflammation, and enhance autophagic efficiency, thereby contributing to the restoration of intestinal eubiosis and complementing enzyme replacement therapy.In parallel, epigenetic mechanisms are gaining prominence as additional modulators of pathogenic pathways, with the potential to influence microbiome composition and function. Collectively, these insights position the gut-muscle axis as a central regulatory node in Pompe disease and a compelling target for personalised nutritional and nutraceutical approaches. This review aims to provide a comprehensive examination of the gut-muscle axis and its implications in Pompe disease. Understanding how nutrient-induced changes in microbial gene expression may be harnessed to develop novel, synergistic therapeutic strategies could ultimately improve clinical outcomes and enhance the quality of life of affected individuals.},
}
RevDate: 2026-04-12
Bisphenol A-mediated root exudates of ryegrass as potential activators of functional succession in the rhizosphere microorganisms: Mechanistic insights into microbial community assembly and biodegradation.
Environmental research, 300:124466 pii:S0013-9351(26)00797-8 [Epub ahead of print].
The toxic threat of bisphenol A (BPA) pollution to plant growth has drawn increasing attention. Although the plant's inherent repair mechanisms and the regulation of rhizosphere microecological processes hold promise as green remediation strategies, the specific mechanisms by which plants actively modulate rhizosphere metabolites at this critical interface to directionally enhance microbial remediation capacity under BPA stress remain to be further elucidated. Here, during the reclamation process of ryegrass exposed to a BPA concentration of 50 mg kg[-1], the contents of key rhizosphere metabolites (abscisic acid, xanthine, trehalose) in the rhizosphere soil solution significantly increased from 95 ± 12.4 to 201.7 ± 19.1 mg L[-1]. Multi-omics analysis revealed that BPA stress induced the phased accumulation of three key metabolites. From days 0-30, abscisic acid peaked (114.6 ± 11.1 mg L[-1]), coinciding with the upregulation of microbial genes related to cell membrane biosynthesis (slp, lolC) by 1.3-3.8 folds. During days 30-60, xanthine peaked (201.7 ± 19.1 mg L[-1]), corresponding to the highest BPA degradation percentages (62.5 ± 4.2%) and upregulation of TCA cycle-related genes (CS, aco, mdh) by 2.2-4.6 folds. From days 60-90, trehalose accumulation peaked (159.4 ± 19.5 mg L[-1]), alongside stabilized BPA degradation and upregulation of glycolytic pathway genes (ATH1, NTH1, HK) by 2.2-4.6 folds. A structural equation model further demonstrated that these metabolites directly and indirectly influence microbial community function, with abscisic acid, xanthine, trehalose strongly affecting microbial structure and functional gene. This study provides inspiration for the development of technologies related to phytoremediation and root exudates to reduce pollutant in agriculture.
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@article {pmid41962883,
year = {2026},
author = {Li, D and Du, H and Xu, J and Zhang, C and Hou, N},
title = {Bisphenol A-mediated root exudates of ryegrass as potential activators of functional succession in the rhizosphere microorganisms: Mechanistic insights into microbial community assembly and biodegradation.},
journal = {Environmental research},
volume = {300},
number = {},
pages = {124466},
doi = {10.1016/j.envres.2026.124466},
pmid = {41962883},
issn = {1096-0953},
abstract = {The toxic threat of bisphenol A (BPA) pollution to plant growth has drawn increasing attention. Although the plant's inherent repair mechanisms and the regulation of rhizosphere microecological processes hold promise as green remediation strategies, the specific mechanisms by which plants actively modulate rhizosphere metabolites at this critical interface to directionally enhance microbial remediation capacity under BPA stress remain to be further elucidated. Here, during the reclamation process of ryegrass exposed to a BPA concentration of 50 mg kg[-1], the contents of key rhizosphere metabolites (abscisic acid, xanthine, trehalose) in the rhizosphere soil solution significantly increased from 95 ± 12.4 to 201.7 ± 19.1 mg L[-1]. Multi-omics analysis revealed that BPA stress induced the phased accumulation of three key metabolites. From days 0-30, abscisic acid peaked (114.6 ± 11.1 mg L[-1]), coinciding with the upregulation of microbial genes related to cell membrane biosynthesis (slp, lolC) by 1.3-3.8 folds. During days 30-60, xanthine peaked (201.7 ± 19.1 mg L[-1]), corresponding to the highest BPA degradation percentages (62.5 ± 4.2%) and upregulation of TCA cycle-related genes (CS, aco, mdh) by 2.2-4.6 folds. From days 60-90, trehalose accumulation peaked (159.4 ± 19.5 mg L[-1]), alongside stabilized BPA degradation and upregulation of glycolytic pathway genes (ATH1, NTH1, HK) by 2.2-4.6 folds. A structural equation model further demonstrated that these metabolites directly and indirectly influence microbial community function, with abscisic acid, xanthine, trehalose strongly affecting microbial structure and functional gene. This study provides inspiration for the development of technologies related to phytoremediation and root exudates to reduce pollutant in agriculture.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
Antibiotic resistance genes (ARGs) in rice: Source attribution and putative mobility patterns.
Food microbiology, 138:105055.
Rice grains can harbor antibiotic resistance genes (ARGs), yet the relative roles of seed-associated and environmental reservoirs remain unclear. We used shotgun metagenomics on rice tissues (grain, seed, leaf, stem, root) and surrounding matrices (bulk/rhizosphere soil, irrigation water, rainwater, PM10). In total, 1019 ARG subtypes were detected; grains contained 395, the largely overlapping with seeds (290) and environmental samples (322). FEAST source tracking revealed contrasting attribution patterns: seed sources explained nearly half of the grain microbiome (average contribution 49.49%) versus 8.45% from environmental sources, whereas environmental sources contributed more strongly to the grain resistome (20.68%). 747 metagenome-assembled genomes (MAGs) were reconstructed, including 275 ARG-carrying MAGs. Phylogenetic screening identified 39 near-identical (≥99%) ARG linkages across samples, operationally classified by host consistency (same vs different predicted hosts) into 11 putative VGT-like and 28 putative HGT-like patterns. For example, blaGOB-50 in grains and seeds shared near-identical sequences within Elizabethkingia anopheles (VGT-like), while APH(9)-Ic in grains (Burkholderia) matched PM10 (Comamonas), consistent with an HGT-like linkage. In selected cases, ARG-MGE co-localization (e.g., umuC, cca) further supported mobility interpretations. Together, these results indicate seedborne signatures in the grain microbiome but comparatively stronger environmental association for the grain resistome, informing efforts to trace ARG reservoirs in rice systems.
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@article {pmid41963036,
year = {2026},
author = {Hou, J and Li, Y and Liu, M and Li, L and Chen, H and An, Y and Xu, H and Yao, Y},
title = {Antibiotic resistance genes (ARGs) in rice: Source attribution and putative mobility patterns.},
journal = {Food microbiology},
volume = {138},
number = {},
pages = {105055},
doi = {10.1016/j.fm.2026.105055},
pmid = {41963036},
issn = {1095-9998},
mesh = {*Oryza/microbiology/genetics ; *Bacteria/genetics/drug effects/classification/isolation & purification ; Phylogeny ; Metagenomics ; Anti-Bacterial Agents/pharmacology ; Soil Microbiology ; Seeds/microbiology ; Microbiota ; Metagenome ; *Genes, Bacterial ; *Drug Resistance, Microbial/genetics ; },
abstract = {Rice grains can harbor antibiotic resistance genes (ARGs), yet the relative roles of seed-associated and environmental reservoirs remain unclear. We used shotgun metagenomics on rice tissues (grain, seed, leaf, stem, root) and surrounding matrices (bulk/rhizosphere soil, irrigation water, rainwater, PM10). In total, 1019 ARG subtypes were detected; grains contained 395, the largely overlapping with seeds (290) and environmental samples (322). FEAST source tracking revealed contrasting attribution patterns: seed sources explained nearly half of the grain microbiome (average contribution 49.49%) versus 8.45% from environmental sources, whereas environmental sources contributed more strongly to the grain resistome (20.68%). 747 metagenome-assembled genomes (MAGs) were reconstructed, including 275 ARG-carrying MAGs. Phylogenetic screening identified 39 near-identical (≥99%) ARG linkages across samples, operationally classified by host consistency (same vs different predicted hosts) into 11 putative VGT-like and 28 putative HGT-like patterns. For example, blaGOB-50 in grains and seeds shared near-identical sequences within Elizabethkingia anopheles (VGT-like), while APH(9)-Ic in grains (Burkholderia) matched PM10 (Comamonas), consistent with an HGT-like linkage. In selected cases, ARG-MGE co-localization (e.g., umuC, cca) further supported mobility interpretations. Together, these results indicate seedborne signatures in the grain microbiome but comparatively stronger environmental association for the grain resistome, informing efforts to trace ARG reservoirs in rice systems.},
}
MeSH Terms:
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*Oryza/microbiology/genetics
*Bacteria/genetics/drug effects/classification/isolation & purification
Phylogeny
Metagenomics
Anti-Bacterial Agents/pharmacology
Soil Microbiology
Seeds/microbiology
Microbiota
Metagenome
*Genes, Bacterial
*Drug Resistance, Microbial/genetics
RevDate: 2026-04-10
CmpDate: 2026-04-10
Microbial community succession and functional potential during processing and storage of cooked ham assessed by shotgun metagenomics.
Food microbiology, 138:105075.
Wet-cured ham is a ready-to-eat meat product in which microbial communities contribute to desired product characteristics related to product quality, while also presenting as a spoilage risk. Microorganisms are introduced early during the live brining of raw meat, with the brine representing a long-standing, complex and active culture that influences nitrate generation, preservation, and flavour development. To support quality control and identify early indicators of spoilage, this study investigated taxonomic and functional microbiome changes across production stages, from brining and cooking to cold storage, slicing, and packaging under modified atmosphere. Using metagenomics, we characterised microbial community composition and functional profiles across 67 samples from raw ingredients, intermediate production steps, and final products. Microbial communities differed significantly between stages, despite sharing a related taxonomic structure. Brining markedly reduced diversity, and cooking further decreased richness and evenness. A set of 28 taxa was consistently detected across stages, though their relative abundance varied. Latilactobacillus curvatus was abundant prior to cooking but declined sharply afterwards, while Arthrobacter rhombi, initially rare, became dominant in the cooked product. During chilled storage, microbial succession continued, with some taxa re-emerging after being nearly eliminated by cooking. Functional gene profiling revealed distinct metabolic pathway shifts across stages, particularly involving respiration, amino acid metabolism, and fermentation. These findings provide a detailed baseline of microbial and functional dynamics in the production and storage of wet-cured ham. The results offer a foundation for spoilage risk assessment and contribute to the development of microbiological monitoring strategies to support product safety and shelf-life management.
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@article {pmid41963048,
year = {2026},
author = {Diaz, M and Wilson, N and Ponsero, AJ and Seecharran, T and Som, N and Al-Khanaq, H and Gutiérrez, AV and Gilmour, M},
title = {Microbial community succession and functional potential during processing and storage of cooked ham assessed by shotgun metagenomics.},
journal = {Food microbiology},
volume = {138},
number = {},
pages = {105075},
doi = {10.1016/j.fm.2026.105075},
pmid = {41963048},
issn = {1095-9998},
mesh = {Metagenomics ; *Bacteria/classification/genetics/isolation & purification/metabolism ; Animals ; Swine ; Food Storage ; *Meat Products/microbiology/analysis ; Cooking ; *Microbiota ; Food Microbiology ; Food Handling ; },
abstract = {Wet-cured ham is a ready-to-eat meat product in which microbial communities contribute to desired product characteristics related to product quality, while also presenting as a spoilage risk. Microorganisms are introduced early during the live brining of raw meat, with the brine representing a long-standing, complex and active culture that influences nitrate generation, preservation, and flavour development. To support quality control and identify early indicators of spoilage, this study investigated taxonomic and functional microbiome changes across production stages, from brining and cooking to cold storage, slicing, and packaging under modified atmosphere. Using metagenomics, we characterised microbial community composition and functional profiles across 67 samples from raw ingredients, intermediate production steps, and final products. Microbial communities differed significantly between stages, despite sharing a related taxonomic structure. Brining markedly reduced diversity, and cooking further decreased richness and evenness. A set of 28 taxa was consistently detected across stages, though their relative abundance varied. Latilactobacillus curvatus was abundant prior to cooking but declined sharply afterwards, while Arthrobacter rhombi, initially rare, became dominant in the cooked product. During chilled storage, microbial succession continued, with some taxa re-emerging after being nearly eliminated by cooking. Functional gene profiling revealed distinct metabolic pathway shifts across stages, particularly involving respiration, amino acid metabolism, and fermentation. These findings provide a detailed baseline of microbial and functional dynamics in the production and storage of wet-cured ham. The results offer a foundation for spoilage risk assessment and contribute to the development of microbiological monitoring strategies to support product safety and shelf-life management.},
}
MeSH Terms:
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Metagenomics
*Bacteria/classification/genetics/isolation & purification/metabolism
Animals
Swine
Food Storage
*Meat Products/microbiology/analysis
Cooking
*Microbiota
Food Microbiology
Food Handling
RevDate: 2026-04-10
CmpDate: 2026-04-10
Psychrotolerant spoilage bacteria enhanced Campylobacter jejuni culturability on refrigerated chicken meat.
Food microbiology, 138:105051.
Campylobacter jejuni is a leading cause of bacterial foodborne illness, with poultry as a major transmission vehicle. The bacterium can enter a viable but non-culturable (VBNC) state, which complicates detection using culture-based methods. While cold and oxidative stress are known VBNC inducers, the role of poultry-associated microbiota in influencing C. jejuni culturability and viability during refrigeration is poorly understood. This study characterized the effect of retail chicken microbiota on C. jejuni over 10 days of cold storage in aerobic and vacuum conditions. We profiled microbiota from chicken breasts in aerobic, modified atmosphere, and vacuum packaging, and from whole chicken under aerobic packaging conditions. Microbiota composition varied with packaging, with Pseudomonas, Brochothrix, and Acinetobacter dominating in aerobic, and Lactococcus and Leuconostoc in vacuum conditions. These genera were isolated and assessed for growth and biofilm formation at 4 °C. Psychrotolerant isolates were whole genome sequenced and used to evaluate their effect on C. jejuni viability and culturability on chicken breast. Three microbiome treatments, including T1 (Pseudomonas, Brochothrix, Acinetobacter), T2 (Lactococcus, Leuconostoc), and T3 (T1 + T2), were co-inoculated with C. jejuni and stored at 4 °C. Viability was assessed by viability qPCR and culturability by plating on Campy Cefex and mCCDA agars. Campy Cefex recovered significantly more (0.74 log10) C. jejuni than mCCDA on day 10 but underestimated viable cell concentration by 2.87 log10. All microbiome treatments improved culturability by > 1 log under aerobic conditions, but not vacuum, highlighting the need to further explore the interactions between non-pathogens and Campylobacter in meat stored aerobically. Microbiome effects on viability were modest and variable. Overall, culture-based methods underestimated C. jejuni viability, underscoring the need for complementary molecular quantification in food safety assessments.
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@article {pmid41963066,
year = {2026},
author = {Yan, R and Watson, SC and Wei, X and Kovac, J},
title = {Psychrotolerant spoilage bacteria enhanced Campylobacter jejuni culturability on refrigerated chicken meat.},
journal = {Food microbiology},
volume = {138},
number = {},
pages = {105051},
doi = {10.1016/j.fm.2026.105051},
pmid = {41963066},
issn = {1095-9998},
mesh = {Animals ; *Campylobacter jejuni/growth & development/genetics/isolation & purification/physiology ; Chickens/microbiology ; *Meat/microbiology ; Refrigeration ; Microbial Viability ; Microbiota ; Food Packaging ; Food Microbiology ; *Bacteria/isolation & purification/genetics/classification/growth & development ; Food Storage ; },
abstract = {Campylobacter jejuni is a leading cause of bacterial foodborne illness, with poultry as a major transmission vehicle. The bacterium can enter a viable but non-culturable (VBNC) state, which complicates detection using culture-based methods. While cold and oxidative stress are known VBNC inducers, the role of poultry-associated microbiota in influencing C. jejuni culturability and viability during refrigeration is poorly understood. This study characterized the effect of retail chicken microbiota on C. jejuni over 10 days of cold storage in aerobic and vacuum conditions. We profiled microbiota from chicken breasts in aerobic, modified atmosphere, and vacuum packaging, and from whole chicken under aerobic packaging conditions. Microbiota composition varied with packaging, with Pseudomonas, Brochothrix, and Acinetobacter dominating in aerobic, and Lactococcus and Leuconostoc in vacuum conditions. These genera were isolated and assessed for growth and biofilm formation at 4 °C. Psychrotolerant isolates were whole genome sequenced and used to evaluate their effect on C. jejuni viability and culturability on chicken breast. Three microbiome treatments, including T1 (Pseudomonas, Brochothrix, Acinetobacter), T2 (Lactococcus, Leuconostoc), and T3 (T1 + T2), were co-inoculated with C. jejuni and stored at 4 °C. Viability was assessed by viability qPCR and culturability by plating on Campy Cefex and mCCDA agars. Campy Cefex recovered significantly more (0.74 log10) C. jejuni than mCCDA on day 10 but underestimated viable cell concentration by 2.87 log10. All microbiome treatments improved culturability by > 1 log under aerobic conditions, but not vacuum, highlighting the need to further explore the interactions between non-pathogens and Campylobacter in meat stored aerobically. Microbiome effects on viability were modest and variable. Overall, culture-based methods underestimated C. jejuni viability, underscoring the need for complementary molecular quantification in food safety assessments.},
}
MeSH Terms:
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Animals
*Campylobacter jejuni/growth & development/genetics/isolation & purification/physiology
Chickens/microbiology
*Meat/microbiology
Refrigeration
Microbial Viability
Microbiota
Food Packaging
Food Microbiology
*Bacteria/isolation & purification/genetics/classification/growth & development
Food Storage
RevDate: 2026-04-10
Biological protection of grapevine pruning wounds: Training system design and mycobiome dynamics.
Pest management science [Epub ahead of print].
BACKGROUND: Grapevine trunk diseases (GTD) lead to progressive vine decline and are a major threat to viticulture sustainability worldwide. GTD can involve multiple fungal species, with Phaeomoniella chlamydospora being one of the most prevalent pathogens. Pruning wounds are the primary entry point for wood-inhabiting fungi. This study assesses the effectiveness of the biological control agent (BCA) Trichoderma atroviride strain SC1 in preventing natural GTD pathogen infections across three vineyard training systems.
RESULTS: Trichoderma recovery was significantly lowest (48.1%) in the double-cordon training system (V3) and consistently higher (71.9%) in the head/spur system (V1). The treatment reduced GTD infection by 3.75%, and disease control declined markedly 1 year after application (61.1%) compared with ≤90 days post-treatment (92.6%). The controlled assay including culture-dependent and culture-independent approaches (high-throughput sequencing and quantitative polymerase chain reaction) revealed distinct detection patterns: culture methods favoured fast-growing fungi such as Trichoderma, whereas molecular tools enabled the detection of slower-growing taxa like P. chlamydospora. T. atroviride colonised wood up to 1-2 cm from the application point, whereas P. chlamydospora spread up to 5 cm. Overall, the pathogen had a stronger impact on wood mycobiome than the BCA, supporting the compatibility of Trichoderma with the resident grapevine microbiome.
CONCLUSION: These findings provide new insights into the integration of BCAs within vineyard GTD management strategies and contribute to the broader transition towards sustainable viticulture and integrated pest management. © 2026 Society of Chemical Industry.
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@article {pmid41963103,
year = {2026},
author = {García-García, B and de Oro, LM and Dorado-Rico, MJ and Martín, L},
title = {Biological protection of grapevine pruning wounds: Training system design and mycobiome dynamics.},
journal = {Pest management science},
volume = {},
number = {},
pages = {},
doi = {10.1002/ps.70804},
pmid = {41963103},
issn = {1526-4998},
support = {//Junta de Extremadura/ ; //European Regional Development Fund/ ; //Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria/ ; //Agencia Estatal de Investigación/ ; },
abstract = {BACKGROUND: Grapevine trunk diseases (GTD) lead to progressive vine decline and are a major threat to viticulture sustainability worldwide. GTD can involve multiple fungal species, with Phaeomoniella chlamydospora being one of the most prevalent pathogens. Pruning wounds are the primary entry point for wood-inhabiting fungi. This study assesses the effectiveness of the biological control agent (BCA) Trichoderma atroviride strain SC1 in preventing natural GTD pathogen infections across three vineyard training systems.
RESULTS: Trichoderma recovery was significantly lowest (48.1%) in the double-cordon training system (V3) and consistently higher (71.9%) in the head/spur system (V1). The treatment reduced GTD infection by 3.75%, and disease control declined markedly 1 year after application (61.1%) compared with ≤90 days post-treatment (92.6%). The controlled assay including culture-dependent and culture-independent approaches (high-throughput sequencing and quantitative polymerase chain reaction) revealed distinct detection patterns: culture methods favoured fast-growing fungi such as Trichoderma, whereas molecular tools enabled the detection of slower-growing taxa like P. chlamydospora. T. atroviride colonised wood up to 1-2 cm from the application point, whereas P. chlamydospora spread up to 5 cm. Overall, the pathogen had a stronger impact on wood mycobiome than the BCA, supporting the compatibility of Trichoderma with the resident grapevine microbiome.
CONCLUSION: These findings provide new insights into the integration of BCAs within vineyard GTD management strategies and contribute to the broader transition towards sustainable viticulture and integrated pest management. © 2026 Society of Chemical Industry.},
}
RevDate: 2026-04-10
Metabolic and functional pathways of gut microbiota in patients with gastric cancer.
Scientific reports pii:10.1038/s41598-026-47830-x [Epub ahead of print].
We analysed the differences in bacterial composition between 475 Japanese patients with advanced gastric cancer (median age, 70 years; median BMI 20.0) and 106 healthy individuals using a comprehensive metagenome shotgun analysis. Among the patients with advanced gastric cancer, 71% were male, 37% had relapsed, and 55.5% previously underwent gastrectomy. Bifidobacterium, Anaerostipes, and Parabacteroides were predominant in healthy individuals, whereas Streptococcus, Lactobacillus, and Odoribacter were predominant in patients with advanced gastric cancer. Additionally, Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that butanoate and pyruvate metabolism was enriched in healthy individuals, whereas factors, such as ABC transporters and ribosomes, were enriched in patients with advanced gastric cancer. Cluster analysis broadly classified patients with advanced gastric cancer and healthy individuals into two clusters; however, clustering using pathway data more clearly classified patients with advanced gastric cancer and healthy individuals than clustering using flora analysis. Moreover, healthy individuals showed higher bacterial flora diversity than those with advanced gastric cancer. Although the dataset we used was limited and may be difficult to generalise, we identified some molecular characteristics and functional pathways of the microbial genera within the intestines of patients with advanced gastric cancer.
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@article {pmid41963512,
year = {2026},
author = {Matoba, R and Iijima, H and Sakamoto, Y and Kawabata, R and Ishiguro, A and Akamaru, Y and Kito, Y and Aizawa, M and Matsuyama, J and Takahashi, M and Makiyama, A and Suzuki, T and Tsuda, M and Yasui, H and Hihara, J and Okuda, H and Kawada, J and Yoshioka, T and Kawakami, H and Eguchi Nakajima, T and Muro, K and Ichikawa, W and Fujii, M and Sunakawa, Y},
title = {Metabolic and functional pathways of gut microbiota in patients with gastric cancer.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-47830-x},
pmid = {41963512},
issn = {2045-2322},
abstract = {We analysed the differences in bacterial composition between 475 Japanese patients with advanced gastric cancer (median age, 70 years; median BMI 20.0) and 106 healthy individuals using a comprehensive metagenome shotgun analysis. Among the patients with advanced gastric cancer, 71% were male, 37% had relapsed, and 55.5% previously underwent gastrectomy. Bifidobacterium, Anaerostipes, and Parabacteroides were predominant in healthy individuals, whereas Streptococcus, Lactobacillus, and Odoribacter were predominant in patients with advanced gastric cancer. Additionally, Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that butanoate and pyruvate metabolism was enriched in healthy individuals, whereas factors, such as ABC transporters and ribosomes, were enriched in patients with advanced gastric cancer. Cluster analysis broadly classified patients with advanced gastric cancer and healthy individuals into two clusters; however, clustering using pathway data more clearly classified patients with advanced gastric cancer and healthy individuals than clustering using flora analysis. Moreover, healthy individuals showed higher bacterial flora diversity than those with advanced gastric cancer. Although the dataset we used was limited and may be difficult to generalise, we identified some molecular characteristics and functional pathways of the microbial genera within the intestines of patients with advanced gastric cancer.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
Full-length 16S rRNA nanopore sequencing enables species resolution of Fusobacterium associated with colorectal cancer.
Gut microbes, 18(1):2656004.
Recent studies have revealed that the long-recognized link between the historically defined Fusobacterium nucleatum group and colorectal cancer is largely driven by Fusobacterium animalis. This species, along with two others (Fusobacterium polymorphum and Fusobacterium vincentii), was recently reclassified as distinct from F. nucleatum, highlighting functional divergence within this group. Due to their close genetic relatedness, traditional partial 16S rRNA gene sequencing lacks the resolution to reliably distinguish these species. Nevertheless, accurate species-level identification remains essential in cancer-associated microbiome research. Here, we demonstrate that full-length 16S rRNA sequencing using Oxford Nanopore Technology, combined with a novel custom demultiplexing software, enables robust species-level discrimination within the Fusobacterium genus. Our approach accurately classified clinically relevant Fusobacterium species and recovered their expected proportions from whole cells, DNA mixtures, and clinical CRC specimens. This method provides high-resolution profiling to elucidate species-specific roles of Fusobacterium in colorectal cancer.
Additional Links: PMID-41963777
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@article {pmid41963777,
year = {2026},
author = {Rosenbaum, W and Rubio Garcia, M and Löfgren-Burström, A and Larsson, P and Edin, S and Bronnec, V and Palmqvist, R},
title = {Full-length 16S rRNA nanopore sequencing enables species resolution of Fusobacterium associated with colorectal cancer.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2656004},
doi = {10.1080/19490976.2026.2656004},
pmid = {41963777},
issn = {1949-0984},
mesh = {*Colorectal Neoplasms/microbiology ; Humans ; *RNA, Ribosomal, 16S/genetics ; *Fusobacterium/genetics/classification/isolation & purification ; *Nanopore Sequencing/methods ; *Fusobacterium Infections/microbiology ; DNA, Bacterial/genetics ; Phylogeny ; Sequence Analysis, DNA/methods ; Gastrointestinal Microbiome ; },
abstract = {Recent studies have revealed that the long-recognized link between the historically defined Fusobacterium nucleatum group and colorectal cancer is largely driven by Fusobacterium animalis. This species, along with two others (Fusobacterium polymorphum and Fusobacterium vincentii), was recently reclassified as distinct from F. nucleatum, highlighting functional divergence within this group. Due to their close genetic relatedness, traditional partial 16S rRNA gene sequencing lacks the resolution to reliably distinguish these species. Nevertheless, accurate species-level identification remains essential in cancer-associated microbiome research. Here, we demonstrate that full-length 16S rRNA sequencing using Oxford Nanopore Technology, combined with a novel custom demultiplexing software, enables robust species-level discrimination within the Fusobacterium genus. Our approach accurately classified clinically relevant Fusobacterium species and recovered their expected proportions from whole cells, DNA mixtures, and clinical CRC specimens. This method provides high-resolution profiling to elucidate species-specific roles of Fusobacterium in colorectal cancer.},
}
MeSH Terms:
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*Colorectal Neoplasms/microbiology
Humans
*RNA, Ribosomal, 16S/genetics
*Fusobacterium/genetics/classification/isolation & purification
*Nanopore Sequencing/methods
*Fusobacterium Infections/microbiology
DNA, Bacterial/genetics
Phylogeny
Sequence Analysis, DNA/methods
Gastrointestinal Microbiome
RevDate: 2026-04-10
Unraveling the relationship between the vaginal microbiome and return to estrus in post-weaning sows.
BMC veterinary research pii:10.1186/s12917-026-05467-y [Epub ahead of print].
BACKGROUND: Return to estrus in post-weaning sows has a significant impact on reproduction performance. Changes in sex hormone levels influence the composition of the vaginal microbiota in sows. However, the relationship between return to estrus and the vaginal microbiota in post-weaning sows remains poorly understood.
RESULTS: In this study, we characterized the vaginal microbiota of 74 Landrace × Yorkshire post-weaning sows including 40 normal-return and 34 non-return sows by sequencing the V3-V4 region of the 16 S rRNA gene. The results revealed significant differences in both the composition and predicted functional capacities of the vaginal microbiota between normal-return and non-return sows. Non-return sows were characterized by reduced abundances of Clostridium sensu stricto 1, Lactobacillus, and Christensenellaceae R-7 group, and increased abundances of Facklamia and Weissella. Furthermore, the predicted functional pathways of Clostridium acetobutylicum acidogenic fermentation and pyruvate fermentation to butanoate were significantly enriched in normal-return sows. Significant differences were also observed in the co-occurrence networks of the vaginal microbiota between normal and non-return sows, revealing distinct microbial interaction patterns between normal return and non-return sows. A random forest analysis identified several vaginal bacterial taxa that showed high discriminatory capacity between normal and non-return sows (AUC = 0.907), including Rikenellaceae RC9 gut group and Christensenellaceae R-7 group that were strongly associated with return to estrus in post-weaning sows.
CONCLUSIONS: We observed significant differences in the composition and predicted functional capacities of the vaginal microbiota between normal-return and non-return sows, and identified several bacterial taxa associated with return to estrus of weaned sows. These findings enhance our understanding of the relationship between the vaginal microbiota and return to estrus in post-weaning sows and provide a foundation for future mechanistic and interventional studies.
Additional Links: PMID-41963929
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@article {pmid41963929,
year = {2026},
author = {Liu, M and Zhou, M and Zhang, J and Chen, C},
title = {Unraveling the relationship between the vaginal microbiome and return to estrus in post-weaning sows.},
journal = {BMC veterinary research},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12917-026-05467-y},
pmid = {41963929},
issn = {1746-6148},
support = {2022YFA1304204//National Key R&D Program of China/ ; },
abstract = {BACKGROUND: Return to estrus in post-weaning sows has a significant impact on reproduction performance. Changes in sex hormone levels influence the composition of the vaginal microbiota in sows. However, the relationship between return to estrus and the vaginal microbiota in post-weaning sows remains poorly understood.
RESULTS: In this study, we characterized the vaginal microbiota of 74 Landrace × Yorkshire post-weaning sows including 40 normal-return and 34 non-return sows by sequencing the V3-V4 region of the 16 S rRNA gene. The results revealed significant differences in both the composition and predicted functional capacities of the vaginal microbiota between normal-return and non-return sows. Non-return sows were characterized by reduced abundances of Clostridium sensu stricto 1, Lactobacillus, and Christensenellaceae R-7 group, and increased abundances of Facklamia and Weissella. Furthermore, the predicted functional pathways of Clostridium acetobutylicum acidogenic fermentation and pyruvate fermentation to butanoate were significantly enriched in normal-return sows. Significant differences were also observed in the co-occurrence networks of the vaginal microbiota between normal and non-return sows, revealing distinct microbial interaction patterns between normal return and non-return sows. A random forest analysis identified several vaginal bacterial taxa that showed high discriminatory capacity between normal and non-return sows (AUC = 0.907), including Rikenellaceae RC9 gut group and Christensenellaceae R-7 group that were strongly associated with return to estrus in post-weaning sows.
CONCLUSIONS: We observed significant differences in the composition and predicted functional capacities of the vaginal microbiota between normal-return and non-return sows, and identified several bacterial taxa associated with return to estrus of weaned sows. These findings enhance our understanding of the relationship between the vaginal microbiota and return to estrus in post-weaning sows and provide a foundation for future mechanistic and interventional studies.},
}
RevDate: 2026-04-10
Interpretable multi-omics machine learning reveals drought-driven shifts in plant-microbe interactions.
Environmental microbiome pii:10.1186/s40793-026-00883-x [Epub ahead of print].
BACKGROUND: Plant-microbe interactions in the rhizosphere are central to plant growth, nutrient acquisition, and stress resilience. Although multi-omics approaches enable comprehensive profiling of different biological layers, integrating these data to understand the mechanisms underlying plant-microbe symbiosis, particularly under drought stress, remains a challenge.
RESULTS: Genomic, metabolomic, and microbiome data from 198 soybean accessions grown under both control and drought conditions were integrated to identify environment-specific predictive features of the plant phenotypes. We compared best linear unbiased prediction (BLUP), genome-wide association study (GWAS), and a nonlinear machine learning model to evaluate their ability to detect informative features. The machine learning models provided flexible variable selection and outperformed linear models in capturing nonlinear dependencies. Model interpretation using SHapley Additive exPlanations (SHAP) indicated that the isoflavone derivative, daidzin, and the drought-tolerant Candidatus Nitrosocosmicus, were major contributors to phenotypic variation, specifically under drought stress. SHAP-based interaction networks indicated cross-omics links, including connections between daidzin, gamma-aminobutyric acid (GABA), and Paenibacillus.
CONCLUSION: The proposed interpretable machine learning approach for plant phenotype prediction identified multi-omics biomarkers and interactions, providing insights into plant adaptation to drought stress through environment-dependent rhizosphere networks and symbiotic associations.
Additional Links: PMID-41964025
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@article {pmid41964025,
year = {2026},
author = {Yoshioka, H and Debeljak, P and Prado, S and Fuji, Y and Ichihashi, Y and Iwata, H},
title = {Interpretable multi-omics machine learning reveals drought-driven shifts in plant-microbe interactions.},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-026-00883-x},
pmid = {41964025},
issn = {2524-6372},
support = {JP23KJ0506//Japan Society for the Promotion of Science/ ; JPMJCR16O2//Japan Science and Technology Agency/ ; },
abstract = {BACKGROUND: Plant-microbe interactions in the rhizosphere are central to plant growth, nutrient acquisition, and stress resilience. Although multi-omics approaches enable comprehensive profiling of different biological layers, integrating these data to understand the mechanisms underlying plant-microbe symbiosis, particularly under drought stress, remains a challenge.
RESULTS: Genomic, metabolomic, and microbiome data from 198 soybean accessions grown under both control and drought conditions were integrated to identify environment-specific predictive features of the plant phenotypes. We compared best linear unbiased prediction (BLUP), genome-wide association study (GWAS), and a nonlinear machine learning model to evaluate their ability to detect informative features. The machine learning models provided flexible variable selection and outperformed linear models in capturing nonlinear dependencies. Model interpretation using SHapley Additive exPlanations (SHAP) indicated that the isoflavone derivative, daidzin, and the drought-tolerant Candidatus Nitrosocosmicus, were major contributors to phenotypic variation, specifically under drought stress. SHAP-based interaction networks indicated cross-omics links, including connections between daidzin, gamma-aminobutyric acid (GABA), and Paenibacillus.
CONCLUSION: The proposed interpretable machine learning approach for plant phenotype prediction identified multi-omics biomarkers and interactions, providing insights into plant adaptation to drought stress through environment-dependent rhizosphere networks and symbiotic associations.},
}
RevDate: 2026-04-11
Bacteria-dependent modulation of immune responses in the bovine udder.
Veterinary research pii:10.1186/s13567-026-01754-6 [Epub ahead of print].
Subclinical mastitis remains difficult to characterize due to the complex interplay between pathogens, local microbiota, and host immune responses. The aim of this study was to investigate how different bacterial species detected in the hindmilk influenced bovine udder immune response and its regulation. Quarter-level hind milk samples were collected from 24 healthy Norwegian Red cows before drying off and through a next full lactation period. Somatic cell populations, cytokines and host-proteome were assessed and combined with the presence of different pathogens. Quarters harboring Staphylococcus aureus and Streptococcus spp. showed significantly elevated somatic cell counts and inflammation associated patterns of somatic cell populations, while those with minor pathogens exhibited lower counts, particularly fewer granulocytes. Cytokines profiling revealed suppressed levels of IFN-γ, IL-10 and TNF-α in the presence of Staphylococcus chromogenes in contrast to the intensive inflammatory activity associated with S. aureus. Weighted gene co-expression network analysis of the host proteome identified two modules of proteins that were negatively correlated with increasing somatic cells count and several modules with strong positive correlation with the SCC. At protein level, we detected 67 proteins differentially expressed based on the pathogen present in the hindmilk. Of these, 19 were linked to immune system functions such as TLR2 and lactoferrin. Our study provides insights into host response in bovine mastitis and reveals a notable lack of interaction between S. chromogenes and the host body compared to an intense immune response in the presence of other pathogens such as S. aureus.
Additional Links: PMID-41964088
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@article {pmid41964088,
year = {2026},
author = {Krysmann, A and Woolsey, I and da Silva Duarte, V and Kranjec, C and Porcellato, D and Boysen, P},
title = {Bacteria-dependent modulation of immune responses in the bovine udder.},
journal = {Veterinary research},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13567-026-01754-6},
pmid = {41964088},
issn = {1297-9716},
support = {314733//Norges Forskningsråd/ ; },
abstract = {Subclinical mastitis remains difficult to characterize due to the complex interplay between pathogens, local microbiota, and host immune responses. The aim of this study was to investigate how different bacterial species detected in the hindmilk influenced bovine udder immune response and its regulation. Quarter-level hind milk samples were collected from 24 healthy Norwegian Red cows before drying off and through a next full lactation period. Somatic cell populations, cytokines and host-proteome were assessed and combined with the presence of different pathogens. Quarters harboring Staphylococcus aureus and Streptococcus spp. showed significantly elevated somatic cell counts and inflammation associated patterns of somatic cell populations, while those with minor pathogens exhibited lower counts, particularly fewer granulocytes. Cytokines profiling revealed suppressed levels of IFN-γ, IL-10 and TNF-α in the presence of Staphylococcus chromogenes in contrast to the intensive inflammatory activity associated with S. aureus. Weighted gene co-expression network analysis of the host proteome identified two modules of proteins that were negatively correlated with increasing somatic cells count and several modules with strong positive correlation with the SCC. At protein level, we detected 67 proteins differentially expressed based on the pathogen present in the hindmilk. Of these, 19 were linked to immune system functions such as TLR2 and lactoferrin. Our study provides insights into host response in bovine mastitis and reveals a notable lack of interaction between S. chromogenes and the host body compared to an intense immune response in the presence of other pathogens such as S. aureus.},
}
RevDate: 2026-04-11
Phytosterols improve feed efficiency in yaks by enriching rumen Succiniclasticum.
Animal microbiome pii:10.1186/s42523-026-00562-9 [Epub ahead of print].
BACKGROUND: Yaks are important livestock species on the Qinghai-Tibet Plateau (QTP), but their productivity is constrained by the harsh alpine environment and the seasonal scarcity of forage resources. Improving feed efficiency has become the key to the sustainable development of Plateau Yak breeding industry. Phytosterols have shown a good application prospect in ruminant feed efficiency improvement, but the impact on yaks is not clear. This study explored the effects of dietary phytosterols supplementation on growth performance, nutrient digestibility, rumen microbial community structure and metabolic function of yaks fed in a barn.
RESULTS: Twenty-eight 1.5-year-old male yaks (137.10 ± 8.70 kg) were randomly divided into two groups after 28 days of pre feeding period: the control group (Con, n = 14) was fed with basic diet, and the experimental group (PS, n = 14) was added with 200 mg/kg phytosterols in concentrate. The formal test period was 60 days. Compared with Con group, PS group significantly increased average daily gain (P = 0.001), apparent digestibility of crude protein (P = 0.036) and neutral detergent fiber (P = 0.006), and reduced feed conversion rate (P = 0.002). The rumen fermentation mode of PS group changed, the proportion of propionate increased significantly (P = 0.001), while the proportion of acetate (P = 0.006), acetate to propionate ratio (P = 0.001) and lactate (P = 0.035) concentration decreased significantly. Phytosterols significantly changed the structure of rumen microbial community and significantly increased the copy number of rumen bacteria (P < 0.05). Metatranscriptomic analysis showed that PS group significantly increased the relative abundance of key bacteria, including Succiniclasticum, Faecalibacterium, Ruminococcus, Butyrivibrio, and Alistipes (P < 0.05). Microbial co-occurrence network analysis revealed that the number of edges, average degree and modular index of microbial community structure network in PS group increased. Rumen function analysis showed that glycolysis / gluconeogenesis and propionate metabolism were significantly enhanced in PS group (P < 0.05), and the expression of key enzymes such as hexokinase and fumarate hydratase were significantly enhanced (P < 0.05). Metabolomic analysis revealed that phosphoenolpyruvic acid, fumarate and methylmalonyl-CoA were significantly accumulated in the rumen of PS group (P < 0.05). Pathway analysis showed that the pathway impact value of propionate metabolism and glycolysis / gluconeogenesis was greater than 0.1.
CONCLUSIONS: Phytosterols (200 mg/kg of concentrate) can effectively improve the feed efficiency of yaks by regulating the structure and function of rumen microorganisms and altering the fermentation patterns.
Additional Links: PMID-41964093
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PubMed:
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@article {pmid41964093,
year = {2026},
author = {Wang, Q and Duan, C and Dai, H and Lv, D and Shi, Z and Joshi, N and Gierus, M and Zhu, W and Hao, L and Cheng, Y},
title = {Phytosterols improve feed efficiency in yaks by enriching rumen Succiniclasticum.},
journal = {Animal microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s42523-026-00562-9},
pmid = {41964093},
issn = {2524-4671},
support = {2024-ZJ-905//Qinghai Provincial Natural Science Fund for Distinguished Young Scholars/ ; 2022YFD1302103//National Key Research and Development Program of China/ ; 2025KTST04//Qinghai University Research Ability Enhancement Project/ ; 2025, L.Z.H.//Qinghai University Graduate Supervisor Innovation Team/ ; QHKLYC-GDCXCY-2024-071//Leading talent of "Kunlun Talents High-level Innovation and Entrepreneurial Talents" in Qinghai Province/ ; },
abstract = {BACKGROUND: Yaks are important livestock species on the Qinghai-Tibet Plateau (QTP), but their productivity is constrained by the harsh alpine environment and the seasonal scarcity of forage resources. Improving feed efficiency has become the key to the sustainable development of Plateau Yak breeding industry. Phytosterols have shown a good application prospect in ruminant feed efficiency improvement, but the impact on yaks is not clear. This study explored the effects of dietary phytosterols supplementation on growth performance, nutrient digestibility, rumen microbial community structure and metabolic function of yaks fed in a barn.
RESULTS: Twenty-eight 1.5-year-old male yaks (137.10 ± 8.70 kg) were randomly divided into two groups after 28 days of pre feeding period: the control group (Con, n = 14) was fed with basic diet, and the experimental group (PS, n = 14) was added with 200 mg/kg phytosterols in concentrate. The formal test period was 60 days. Compared with Con group, PS group significantly increased average daily gain (P = 0.001), apparent digestibility of crude protein (P = 0.036) and neutral detergent fiber (P = 0.006), and reduced feed conversion rate (P = 0.002). The rumen fermentation mode of PS group changed, the proportion of propionate increased significantly (P = 0.001), while the proportion of acetate (P = 0.006), acetate to propionate ratio (P = 0.001) and lactate (P = 0.035) concentration decreased significantly. Phytosterols significantly changed the structure of rumen microbial community and significantly increased the copy number of rumen bacteria (P < 0.05). Metatranscriptomic analysis showed that PS group significantly increased the relative abundance of key bacteria, including Succiniclasticum, Faecalibacterium, Ruminococcus, Butyrivibrio, and Alistipes (P < 0.05). Microbial co-occurrence network analysis revealed that the number of edges, average degree and modular index of microbial community structure network in PS group increased. Rumen function analysis showed that glycolysis / gluconeogenesis and propionate metabolism were significantly enhanced in PS group (P < 0.05), and the expression of key enzymes such as hexokinase and fumarate hydratase were significantly enhanced (P < 0.05). Metabolomic analysis revealed that phosphoenolpyruvic acid, fumarate and methylmalonyl-CoA were significantly accumulated in the rumen of PS group (P < 0.05). Pathway analysis showed that the pathway impact value of propionate metabolism and glycolysis / gluconeogenesis was greater than 0.1.
CONCLUSIONS: Phytosterols (200 mg/kg of concentrate) can effectively improve the feed efficiency of yaks by regulating the structure and function of rumen microorganisms and altering the fermentation patterns.},
}
RevDate: 2026-04-11
Loss of salivary agglutinin induces changes in the salivary microbiome and accelerates development of oral cancer.
Microbiome pii:10.1186/s40168-026-02337-5 [Epub ahead of print].
BACKGROUND: Salivary agglutinin, also known as deleted in malignant brain tumors 1 (DMBT1), is an anti-microbial protein. DMBT1 is low in saliva from patients with oral squamous cell carcinoma (OSCC) and dramatically increases after treatment, with accompanying microbial changes. While this suggests an association between DMBT1 suppression and changes in the oral microbiota, causation has not been established. DMBT1 is also a tumor suppressor protein; its loss promotes OSCC progression, but its role in OSCC development is unknown. In this study, OSCC development was investigated in a murine carcinogen model that simulates human OSCC. Microbiota were standardized between Dmbt1 knockout (Dmbt1[-/-]) and wild-type (Dmbt1[+/+]) mice via interbreeding and co-housing. Saliva was collected at baseline and at 4, 8, 12, 16, and 22 weeks post-carcinogen initiation (stopped at 16 weeks). Tongues were harvested at week 22 for histopathology, and the salivary microbiome was profiled by 16S rRNA sequencing. Microbial diversity metrics and conditional dependence networks assessed community structure, while longitudinal patterns were analyzed using a locally sparse varying coefficient mixed model and functional principal component analysis (fPCA).
RESULTS: Despite microbiota standardization, Dmbt1[-/-] and Dmbt1[+/+] displayed differences in microbiome composition based on β-diversity metrics. At endpoint, carcinogen-treated Dmbt1[-/-] showed higher OSCC prevalence and more aggressive invasion than Dmbt1[+/+]. Several OTUs, including those from Lachnospiraceae, Sphingomonas, Carnobacteriaceae, and Candidatus Saccharibacteria families, demonstrated differential abundance patterns over time, either genotype-specific, diagnosis-specific, or both. Notably, Sphingomonas and Lachnospiraceae exhibited time-dependent abundance differences in mice that developed OSCC. fPCA identified taxa with abundance trajectories that were different between OSCC and precancer and genotype specific.
CONCLUSIONS: Thus, DMBT1 shapes salivary microbiota composition and protects against OSCC development. Dynamic, genotype-specific microbial shifts during carcinogenesis underscore the complex interplay between the oral microbiota and cancer progression. Video Abstract.
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@article {pmid41964098,
year = {2026},
author = {de Medeiros, MC and Fontaine, S and Danella, E and Hillman, E and Schmidt, TM and Furgal, A and Wellik, DM and Inohara, N and Núñez, G and Li, G and Chen, GY and D'Silva, NJ},
title = {Loss of salivary agglutinin induces changes in the salivary microbiome and accelerates development of oral cancer.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02337-5},
pmid = {41964098},
issn = {2049-2618},
support = {CA250214/CA/NCI NIH HHS/United States ; },
abstract = {BACKGROUND: Salivary agglutinin, also known as deleted in malignant brain tumors 1 (DMBT1), is an anti-microbial protein. DMBT1 is low in saliva from patients with oral squamous cell carcinoma (OSCC) and dramatically increases after treatment, with accompanying microbial changes. While this suggests an association between DMBT1 suppression and changes in the oral microbiota, causation has not been established. DMBT1 is also a tumor suppressor protein; its loss promotes OSCC progression, but its role in OSCC development is unknown. In this study, OSCC development was investigated in a murine carcinogen model that simulates human OSCC. Microbiota were standardized between Dmbt1 knockout (Dmbt1[-/-]) and wild-type (Dmbt1[+/+]) mice via interbreeding and co-housing. Saliva was collected at baseline and at 4, 8, 12, 16, and 22 weeks post-carcinogen initiation (stopped at 16 weeks). Tongues were harvested at week 22 for histopathology, and the salivary microbiome was profiled by 16S rRNA sequencing. Microbial diversity metrics and conditional dependence networks assessed community structure, while longitudinal patterns were analyzed using a locally sparse varying coefficient mixed model and functional principal component analysis (fPCA).
RESULTS: Despite microbiota standardization, Dmbt1[-/-] and Dmbt1[+/+] displayed differences in microbiome composition based on β-diversity metrics. At endpoint, carcinogen-treated Dmbt1[-/-] showed higher OSCC prevalence and more aggressive invasion than Dmbt1[+/+]. Several OTUs, including those from Lachnospiraceae, Sphingomonas, Carnobacteriaceae, and Candidatus Saccharibacteria families, demonstrated differential abundance patterns over time, either genotype-specific, diagnosis-specific, or both. Notably, Sphingomonas and Lachnospiraceae exhibited time-dependent abundance differences in mice that developed OSCC. fPCA identified taxa with abundance trajectories that were different between OSCC and precancer and genotype specific.
CONCLUSIONS: Thus, DMBT1 shapes salivary microbiota composition and protects against OSCC development. Dynamic, genotype-specific microbial shifts during carcinogenesis underscore the complex interplay between the oral microbiota and cancer progression. Video Abstract.},
}
RevDate: 2026-04-11
Gepotidacin for the Treatment of Uncomplicated Urogenital Gonorrhea.
The Annals of pharmacotherapy [Epub ahead of print].
OBJECTIVE: To review the efficacy and safety of gepotidacin for the treatment of uncomplicated urogenital gonorrhea (uUGG).
DATA SOURCES: A literature search of PubMed and Google Scholar (January 2010 to January 2026) was conducted using the terms gepotidacin and GSK2140944. Additional sources included conference abstracts, the manufacturer's website, and prescribing information.
Relevant English-language studies evaluating the efficacy and safety of gepotidacin for uUGG were included.
DATA SYNTHESIS: Gepotidacin is a first-in-class triazaacenaphthylene antibiotic with a novel mechanism of action and potent activity against Neisseria gonorrhoeae. In the phase 3 EAGLE-1 trial, gepotidacin demonstrated noninferiority to ceftriaxone plus azithromycin for uUGG treatment. It was generally well tolerated, with gastrointestinal adverse effects most commonly reported. Gepotidacin is administered as 3000 mg orally every 12 hours for 2 doses and is approved for adults and pediatric patients aged ≥12 years weighing ≥45 kg with limited or no alternative treatment options. Administration with food is recommended to reduce gastrointestinal adverse effects.Relevance to Patient Care and Clinical Practice in Comparison to Existing Drugs:Gepotidacin provides a new 2-dose oral option for uUGG treatment. Compared with ceftriaxone, the current drug of choice, oral administration may improve convenience and access. Similar to cefixime and zoliflodacin, its oral formulation may facilitate treatment while potentially reducing microbiome disruption compared with ceftriaxone.
CONCLUSIONS: Gepotidacin is a promising oral antibiotic with a novel mechanism of action and demonstrated efficacy for uUGG treatment.
Additional Links: PMID-41964141
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PubMed:
Citation:
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@article {pmid41964141,
year = {2026},
author = {Durham, SH and McAllister, AK and Chahine, EB},
title = {Gepotidacin for the Treatment of Uncomplicated Urogenital Gonorrhea.},
journal = {The Annals of pharmacotherapy},
volume = {},
number = {},
pages = {10600280261435593},
doi = {10.1177/10600280261435593},
pmid = {41964141},
issn = {1542-6270},
abstract = {OBJECTIVE: To review the efficacy and safety of gepotidacin for the treatment of uncomplicated urogenital gonorrhea (uUGG).
DATA SOURCES: A literature search of PubMed and Google Scholar (January 2010 to January 2026) was conducted using the terms gepotidacin and GSK2140944. Additional sources included conference abstracts, the manufacturer's website, and prescribing information.
Relevant English-language studies evaluating the efficacy and safety of gepotidacin for uUGG were included.
DATA SYNTHESIS: Gepotidacin is a first-in-class triazaacenaphthylene antibiotic with a novel mechanism of action and potent activity against Neisseria gonorrhoeae. In the phase 3 EAGLE-1 trial, gepotidacin demonstrated noninferiority to ceftriaxone plus azithromycin for uUGG treatment. It was generally well tolerated, with gastrointestinal adverse effects most commonly reported. Gepotidacin is administered as 3000 mg orally every 12 hours for 2 doses and is approved for adults and pediatric patients aged ≥12 years weighing ≥45 kg with limited or no alternative treatment options. Administration with food is recommended to reduce gastrointestinal adverse effects.Relevance to Patient Care and Clinical Practice in Comparison to Existing Drugs:Gepotidacin provides a new 2-dose oral option for uUGG treatment. Compared with ceftriaxone, the current drug of choice, oral administration may improve convenience and access. Similar to cefixime and zoliflodacin, its oral formulation may facilitate treatment while potentially reducing microbiome disruption compared with ceftriaxone.
CONCLUSIONS: Gepotidacin is a promising oral antibiotic with a novel mechanism of action and demonstrated efficacy for uUGG treatment.},
}
RevDate: 2026-04-11
Commentary on oral microbiota analysis in HPV-infected individuals: considerations for future research.
Future microbiology [Epub ahead of print].
Additional Links: PMID-41964374
Publisher:
PubMed:
Citation:
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@article {pmid41964374,
year = {2026},
author = {Mustafa, AM},
title = {Commentary on oral microbiota analysis in HPV-infected individuals: considerations for future research.},
journal = {Future microbiology},
volume = {},
number = {},
pages = {1-2},
doi = {10.1080/17460913.2026.2656108},
pmid = {41964374},
issn = {1746-0921},
}
RevDate: 2026-04-11
Decoding the genetic mechanism of heterosis in rice: insights from multi-omics and systems approaches.
Annals of botany pii:8643988 [Epub ahead of print].
Heterosis, or hybrid vigour, describes the superior growth, yield and adaptability of F1 hybrids from genetically diverse parents and is vital for global food security. Although widely applied for over a century, its molecular basis remains unresolved. Classical hypotheses, including dominance, overdominance and epistasis, serve as theoretical frameworks to explain this complex phenomenon. Recent progress in genomics and multi-omics technologies has deepened our understanding, but genome-level insights alone are insufficient to fully account for hybrid performance. This review synthesizes current advances in elucidating the genetic architecture and regulatory mechanisms underlying heterosis in rice. It emphasizes key genetic loci, the integration of high-throughput omics data, and insights gained from structural variation and plant-microbiome interactions. By integrating diverse omics layers through classical genetic frameworks, the field is moving towards a more comprehensive model of heterosis. These advances offer new strategies for molecular design breeding in rice and point to future directions for enhancing the utilization of heterosis in crop improvement.
Additional Links: PMID-41964509
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PubMed:
Citation:
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@article {pmid41964509,
year = {2026},
author = {Chen, Z and Zhu, P and Kong, D and Luo, L and Yu, X and Liu, G},
title = {Decoding the genetic mechanism of heterosis in rice: insights from multi-omics and systems approaches.},
journal = {Annals of botany},
volume = {},
number = {},
pages = {},
doi = {10.1093/aob/mcag010},
pmid = {41964509},
issn = {1095-8290},
support = {23015821200//Project for Demonstration and Industrialization of Water-Saving and Drought-Resistant Rice in Hainan/ ; //Qinghe Program/ ; //Shanghai Agrobiological Gene Center/ ; },
abstract = {Heterosis, or hybrid vigour, describes the superior growth, yield and adaptability of F1 hybrids from genetically diverse parents and is vital for global food security. Although widely applied for over a century, its molecular basis remains unresolved. Classical hypotheses, including dominance, overdominance and epistasis, serve as theoretical frameworks to explain this complex phenomenon. Recent progress in genomics and multi-omics technologies has deepened our understanding, but genome-level insights alone are insufficient to fully account for hybrid performance. This review synthesizes current advances in elucidating the genetic architecture and regulatory mechanisms underlying heterosis in rice. It emphasizes key genetic loci, the integration of high-throughput omics data, and insights gained from structural variation and plant-microbiome interactions. By integrating diverse omics layers through classical genetic frameworks, the field is moving towards a more comprehensive model of heterosis. These advances offer new strategies for molecular design breeding in rice and point to future directions for enhancing the utilization of heterosis in crop improvement.},
}
RevDate: 2026-04-11
CmpDate: 2026-04-11
A systematic assessment of the short- and long-term effects of commonly used breast cancer chemotherapeutics on the gut microbiome‒blood‒brain axis of female mice.
Gut microbes, 18(1):2655149.
Chemotherapy affects over 300,000 U.S. breast cancer patients, which disrupts the gut microbiome and induces gut inflammation-an effect hypothesized to drive gastrointestinal side effects (e.g., diarrhea, vomiting) experienced by 50%-80% of patients. Preclinical studies have found causal links amongst chemotherapy-induced gut microbiome disruption, systemic inflammation, and brain-mediated side effects. Therefore, the gut microbiome represents a therapeutic target to attenuate chemotherapy side effects. Because clinical populations are administered multiple chemotherapeutics in combination, a comprehensive understanding of which treatments disrupt the gut microbiome‒blood‒brain axis is lacking. Here, translationally-relevant regimens of four commonly used breast cancer chemotherapies (paclitaxel, cyclophosphamide, cisplatin, and doxorubicin) were given to adult female C57BL/6 mice, and inflammatory, metabolomics and/or bacteriome outcomes were measured in the gut, gut contents, blood, and brain tissues, along with a fatigue and anxiety-like behavioral assessment. Many inter-chemotherapy differences were observed but notable findings include prolonged circulation and central proinflammatory signals by paclitaxel and sustained disruption of the gut microbiome by cisplatin. In contrast, cyclophosphamide and doxorubicin modestly disrupted the gut microbiome‒blood‒brain axis. Taken together, this study systematically identified that paclitaxel and cisplatin most robustly disrupted the gut microbiome‒blood‒brain axis, suggesting that those treated with these drugs may benefit the most from gut-targeted interventions for associated side effects.
Additional Links: PMID-41964565
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PubMed:
Citation:
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@article {pmid41964565,
year = {2026},
author = {Valentine, YA and Duff, AF and Bailey, MT and Pyter, LM},
title = {A systematic assessment of the short- and long-term effects of commonly used breast cancer chemotherapeutics on the gut microbiome‒blood‒brain axis of female mice.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2655149},
doi = {10.1080/19490976.2026.2655149},
pmid = {41964565},
issn = {1949-0984},
mesh = {Animals ; Female ; *Gastrointestinal Microbiome/drug effects ; Mice ; Mice, Inbred C57BL ; *Breast Neoplasms/drug therapy/microbiology ; Cyclophosphamide/adverse effects ; *Antineoplastic Agents/adverse effects/therapeutic use ; Cisplatin/adverse effects ; *Brain/drug effects/metabolism ; Doxorubicin/adverse effects ; Paclitaxel/adverse effects ; Bacteria/classification/genetics/drug effects/isolation & purification ; },
abstract = {Chemotherapy affects over 300,000 U.S. breast cancer patients, which disrupts the gut microbiome and induces gut inflammation-an effect hypothesized to drive gastrointestinal side effects (e.g., diarrhea, vomiting) experienced by 50%-80% of patients. Preclinical studies have found causal links amongst chemotherapy-induced gut microbiome disruption, systemic inflammation, and brain-mediated side effects. Therefore, the gut microbiome represents a therapeutic target to attenuate chemotherapy side effects. Because clinical populations are administered multiple chemotherapeutics in combination, a comprehensive understanding of which treatments disrupt the gut microbiome‒blood‒brain axis is lacking. Here, translationally-relevant regimens of four commonly used breast cancer chemotherapies (paclitaxel, cyclophosphamide, cisplatin, and doxorubicin) were given to adult female C57BL/6 mice, and inflammatory, metabolomics and/or bacteriome outcomes were measured in the gut, gut contents, blood, and brain tissues, along with a fatigue and anxiety-like behavioral assessment. Many inter-chemotherapy differences were observed but notable findings include prolonged circulation and central proinflammatory signals by paclitaxel and sustained disruption of the gut microbiome by cisplatin. In contrast, cyclophosphamide and doxorubicin modestly disrupted the gut microbiome‒blood‒brain axis. Taken together, this study systematically identified that paclitaxel and cisplatin most robustly disrupted the gut microbiome‒blood‒brain axis, suggesting that those treated with these drugs may benefit the most from gut-targeted interventions for associated side effects.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Female
*Gastrointestinal Microbiome/drug effects
Mice
Mice, Inbred C57BL
*Breast Neoplasms/drug therapy/microbiology
Cyclophosphamide/adverse effects
*Antineoplastic Agents/adverse effects/therapeutic use
Cisplatin/adverse effects
*Brain/drug effects/metabolism
Doxorubicin/adverse effects
Paclitaxel/adverse effects
Bacteria/classification/genetics/drug effects/isolation & purification
RevDate: 2026-04-11
Difficile to treat: advanced management strategies in difficult to treat clostridioides difficile infections.
Expert review of anti-infective therapy [Epub ahead of print].
INTRODUCTION: Clostridioides difficile infection (CDI) remains a leading cause of healthcare-associated infectious diarrhea, with a major burden driven by recurrences and severe or even fulminant disease in vulnerable hosts. The therapeutic landscape has shifted toward fidaxomicin-based antibiotic regimens, and microbiota restoration strategies including standardized microbiota-based products.
AREAS COVERED: Recent international guidelines, outcome studies and pivotal trials focused on difficult-to-treat phenotypes: refractory or fulminant CDI, multiply recurrent CDI, and CDI in high-risk populations (immunocompromised, inflammatory bowel disease, critical illness) were reviewed. A PubMed search was supplemented by hand-searching additional references, guideline and regulatory documents. Evidence is summarized for optimized antibiotic regimens, bezlotoxumab, conventional fecal microbiota transplantation (FMT), FDA-approved microbiota-based products, and salvage strategies including intracolonic therapy and surgery.
EXPERT OPINION: Advanced CDI management is moving from repeated antibiotic cycling toward individualized recurrence prevention and microbiota restoration strategies. Implementation requires diagnostic stewardship, earlier recognition of recurrences, clear pathways for microbiota-based therapy access, and multidisciplinary care for fulminant infection. Over the next five years, standardized microbiota therapeutics and better risk tools should shift care toward earlier, more durable recurrence prevention.
Additional Links: PMID-41964647
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PubMed:
Citation:
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@article {pmid41964647,
year = {2026},
author = {Khanna, S and Bloom, PP},
title = {Difficile to treat: advanced management strategies in difficult to treat clostridioides difficile infections.},
journal = {Expert review of anti-infective therapy},
volume = {},
number = {},
pages = {},
doi = {10.1080/14787210.2026.2659725},
pmid = {41964647},
issn = {1744-8336},
abstract = {INTRODUCTION: Clostridioides difficile infection (CDI) remains a leading cause of healthcare-associated infectious diarrhea, with a major burden driven by recurrences and severe or even fulminant disease in vulnerable hosts. The therapeutic landscape has shifted toward fidaxomicin-based antibiotic regimens, and microbiota restoration strategies including standardized microbiota-based products.
AREAS COVERED: Recent international guidelines, outcome studies and pivotal trials focused on difficult-to-treat phenotypes: refractory or fulminant CDI, multiply recurrent CDI, and CDI in high-risk populations (immunocompromised, inflammatory bowel disease, critical illness) were reviewed. A PubMed search was supplemented by hand-searching additional references, guideline and regulatory documents. Evidence is summarized for optimized antibiotic regimens, bezlotoxumab, conventional fecal microbiota transplantation (FMT), FDA-approved microbiota-based products, and salvage strategies including intracolonic therapy and surgery.
EXPERT OPINION: Advanced CDI management is moving from repeated antibiotic cycling toward individualized recurrence prevention and microbiota restoration strategies. Implementation requires diagnostic stewardship, earlier recognition of recurrences, clear pathways for microbiota-based therapy access, and multidisciplinary care for fulminant infection. Over the next five years, standardized microbiota therapeutics and better risk tools should shift care toward earlier, more durable recurrence prevention.},
}
RevDate: 2026-04-11
A novel Azospirillum vistecanum strain from methane digestate promotes plant growth via indole-3-acetic acid biosynthesis.
Applied microbiology and biotechnology pii:10.1007/s00253-026-13808-y [Epub ahead of print].
The urgent need for sustainable agricultural inputs has accelerated the search for microbial alternatives to synthetic agrochemicals. In this study, we report the isolation and comprehensive characterization of a novel strain, Azospirillum vistecanum VT-I1, obtained from a methane-enriched digestate system. This strain demonstrated exceptional plant growth-promoting potential through the biosynthesis of indole-3-acetic acid (IAA), a key phytohormone. Genome sequencing and annotation revealed the presence of genes associated with the indole-3-pyruvate (IPyA) pathway, aro9, ipdC, and aldA, with no detectable IAA-degrading gene clusters, supporting a high net auxin yield. Under optimized culture conditions, VT-I1 produced up to 1.206 mM of IAA, significantly surpassing the levels observed in A. brasilense. Functional assays confirmed the bioactivity of this microbial IAA, which enhanced root development in Exacum affine and improved seed germination in Andrographis paniculata. Collectively, these results establish A. vistecanum VT-I1 as a promising candidate for next-generation biofertilizers, offering a scalable, eco-friendly alternative to chemically synthesized auxins. This work expands our understanding of auxin biosynthesis in rhizobacteria and provides a strong foundation for future field applications and microbiome-based crop enhancement strategies. KEY POINTS: • A novel Azospirillum vistecanum was isolated from methane digestate. • The strain produces high levels of indole-3 acetic acid via the IPyA pathway. • Microbial IAA enhances root growth and seed germination in model plants.
Additional Links: PMID-41964677
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PubMed:
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@article {pmid41964677,
year = {2026},
author = {Moomthong, S and Woraruthai, T and Tirapanampai, C and Rungjroenchaiwat, S and Kruasuwan, W and Uthaipaisanwong, P and Kusonmano, K and Jenjaroenpun, P and Wongsurawat, T and Wongnate, T},
title = {A novel Azospirillum vistecanum strain from methane digestate promotes plant growth via indole-3-acetic acid biosynthesis.},
journal = {Applied microbiology and biotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00253-026-13808-y},
pmid = {41964677},
issn = {1432-0614},
abstract = {The urgent need for sustainable agricultural inputs has accelerated the search for microbial alternatives to synthetic agrochemicals. In this study, we report the isolation and comprehensive characterization of a novel strain, Azospirillum vistecanum VT-I1, obtained from a methane-enriched digestate system. This strain demonstrated exceptional plant growth-promoting potential through the biosynthesis of indole-3-acetic acid (IAA), a key phytohormone. Genome sequencing and annotation revealed the presence of genes associated with the indole-3-pyruvate (IPyA) pathway, aro9, ipdC, and aldA, with no detectable IAA-degrading gene clusters, supporting a high net auxin yield. Under optimized culture conditions, VT-I1 produced up to 1.206 mM of IAA, significantly surpassing the levels observed in A. brasilense. Functional assays confirmed the bioactivity of this microbial IAA, which enhanced root development in Exacum affine and improved seed germination in Andrographis paniculata. Collectively, these results establish A. vistecanum VT-I1 as a promising candidate for next-generation biofertilizers, offering a scalable, eco-friendly alternative to chemically synthesized auxins. This work expands our understanding of auxin biosynthesis in rhizobacteria and provides a strong foundation for future field applications and microbiome-based crop enhancement strategies. KEY POINTS: • A novel Azospirillum vistecanum was isolated from methane digestate. • The strain produces high levels of indole-3 acetic acid via the IPyA pathway. • Microbial IAA enhances root growth and seed germination in model plants.},
}
RevDate: 2026-04-11
CmpDate: 2026-04-11
Morphological plasticity of endophytic Chitinophaga pinensis.
Antonie van Leeuwenhoek, 119(5):.
Environmental changes, whether due to climate change or human influences, compromise the resilience of plants to biotic and abiotic stresses, such as pathogens, drought and heat. Plant microbiota are known to promote plant resilience. To be able to harness the power of the plant microbiome we need to identify microbiota with health-promoting properties. Recent studies have demonstrated that the bacterium Chitinophaga pinensis enhances plant health and increases resistance to fungal infections. Here, we show that C. pinensis exhibits an unusually high morphological plasticity, switching between a filamentous and a spherical cell state, each of which is characterized by a distinct transcriptional profile. Despite these transcriptional differences, spherical cells remained metabolically active and replicating, while lacking structural characteristics typically associated with dormant states. Furthermore, the spherical cell morphology of C. pinensis facilitates hitchhiking behaviour and motility via surfactin cheating, potentially influencing its dispersal and interactions within the plant microbiome. To investigate the structural dynamics and transcriptional adaptation of this plant endophyte, we applied a combination of microscopy and culture-based techniques. Taken together, our study provides new insights into the morphological flexibility and transcriptional regulation of the plant-beneficial C. pinensis.
Additional Links: PMID-41964722
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Citation:
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@article {pmid41964722,
year = {2026},
author = {Liedtke, J and Rodenburg, F and Du, C and Zhang, L and Raaijmakers, JM and van Wezel, GP and Briegel, A},
title = {Morphological plasticity of endophytic Chitinophaga pinensis.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {5},
pages = {},
pmid = {41964722},
issn = {1572-9699},
mesh = {*Endophytes/genetics/cytology/physiology ; Microbiota ; },
abstract = {Environmental changes, whether due to climate change or human influences, compromise the resilience of plants to biotic and abiotic stresses, such as pathogens, drought and heat. Plant microbiota are known to promote plant resilience. To be able to harness the power of the plant microbiome we need to identify microbiota with health-promoting properties. Recent studies have demonstrated that the bacterium Chitinophaga pinensis enhances plant health and increases resistance to fungal infections. Here, we show that C. pinensis exhibits an unusually high morphological plasticity, switching between a filamentous and a spherical cell state, each of which is characterized by a distinct transcriptional profile. Despite these transcriptional differences, spherical cells remained metabolically active and replicating, while lacking structural characteristics typically associated with dormant states. Furthermore, the spherical cell morphology of C. pinensis facilitates hitchhiking behaviour and motility via surfactin cheating, potentially influencing its dispersal and interactions within the plant microbiome. To investigate the structural dynamics and transcriptional adaptation of this plant endophyte, we applied a combination of microscopy and culture-based techniques. Taken together, our study provides new insights into the morphological flexibility and transcriptional regulation of the plant-beneficial C. pinensis.},
}
MeSH Terms:
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hide MeSH Terms
*Endophytes/genetics/cytology/physiology
Microbiota
RevDate: 2026-04-11
CmpDate: 2026-04-11
Dysregulation of the Gut-Adipose Tissue-Liver Axis: a Possible Mechanism Behind the Relationship Between Metabolic Dysfunction-Associated Steatotic Liver Disease and Type 2 Diabetes.
Current diabetes reports, 26(1):.
PURPOSE OF REVIEW: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a hepatic manifestation of metabolic syndrome, frequently occurring alongside type 2 diabetes (T2D), and it can present in varied phenotypes. This review provides a critical analysis of gut-adipose tissue-liver axis (GALA) dysregulation in MASLD pathogenesis, contextualizing the discussion within both established and emerging paradigms. The review elucidates how GALA dysregulation shapes the interplay between MASLD and T2D, emphasizing inter-organ crosstalk among the gut, liver, and adipose tissue, and highlighting the role of microbial metabolites, notably bile acids. The review further summarizes recent advances in stratifying MASLD into distinct clusters, examining intricate associations with cardiometabolic comorbidities, and critically evaluates novel therapeutic approaches targeting GALA modulation.
RECENT FINDINGS: MASLD can show heterogeneous phenotypes. It significantly increases the risk of developing new-onset T2D, and both conditions often coexist due to their shared pathophysiological basis in insulin resistance. The gut microbiota influences immune function and modulates host metabolism by regulating glucose tolerance and insulin sensitivity through a specific crosstalk between the gut, liver, and adipose tissue. The dysregulation of the GALA may be a mechanism underlying the interplay between MASLD and T2D, influencing IR and metabolic syndrome. A thorough investigation of GALA's role in the physiopathogenesis of MASLD and T2D highlights its potential to distinguish specific MASLD clusters and to identify personalized therapeutic strategies.
Additional Links: PMID-41964817
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Citation:
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@article {pmid41964817,
year = {2026},
author = {Longo, S and Rinaldi, TG and Fernández-Real, JM and Federici, M},
title = {Dysregulation of the Gut-Adipose Tissue-Liver Axis: a Possible Mechanism Behind the Relationship Between Metabolic Dysfunction-Associated Steatotic Liver Disease and Type 2 Diabetes.},
journal = {Current diabetes reports},
volume = {26},
number = {1},
pages = {},
pmid = {41964817},
issn = {1539-0829},
mesh = {Humans ; *Diabetes Mellitus, Type 2/metabolism/complications ; *Adipose Tissue/metabolism ; *Liver/metabolism ; Gastrointestinal Microbiome/physiology ; *Metabolic Syndrome/metabolism/complications ; *Fatty Liver/metabolism ; Insulin Resistance ; Animals ; },
abstract = {PURPOSE OF REVIEW: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a hepatic manifestation of metabolic syndrome, frequently occurring alongside type 2 diabetes (T2D), and it can present in varied phenotypes. This review provides a critical analysis of gut-adipose tissue-liver axis (GALA) dysregulation in MASLD pathogenesis, contextualizing the discussion within both established and emerging paradigms. The review elucidates how GALA dysregulation shapes the interplay between MASLD and T2D, emphasizing inter-organ crosstalk among the gut, liver, and adipose tissue, and highlighting the role of microbial metabolites, notably bile acids. The review further summarizes recent advances in stratifying MASLD into distinct clusters, examining intricate associations with cardiometabolic comorbidities, and critically evaluates novel therapeutic approaches targeting GALA modulation.
RECENT FINDINGS: MASLD can show heterogeneous phenotypes. It significantly increases the risk of developing new-onset T2D, and both conditions often coexist due to their shared pathophysiological basis in insulin resistance. The gut microbiota influences immune function and modulates host metabolism by regulating glucose tolerance and insulin sensitivity through a specific crosstalk between the gut, liver, and adipose tissue. The dysregulation of the GALA may be a mechanism underlying the interplay between MASLD and T2D, influencing IR and metabolic syndrome. A thorough investigation of GALA's role in the physiopathogenesis of MASLD and T2D highlights its potential to distinguish specific MASLD clusters and to identify personalized therapeutic strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Diabetes Mellitus, Type 2/metabolism/complications
*Adipose Tissue/metabolism
*Liver/metabolism
Gastrointestinal Microbiome/physiology
*Metabolic Syndrome/metabolism/complications
*Fatty Liver/metabolism
Insulin Resistance
Animals
RevDate: 2026-04-11
Oral Microbiome Dysbiosis in Primary Sjögren's Syndrome: A Systematic Review and Meta-Analysis.
Rheumatology (Oxford, England) pii:8644331 [Epub ahead of print].
OBJECTIVES: Dry mouth symptoms in patients with primary Sjögren's syndrome (pSS) may be associated with oral microbiome dysbiosis, which plays a critical role in the pathogenesis of pSS and potentially contributes to disease progression. This study systematically reviews and meta-analyzes the latest research on the relationship between the oral microbiome and pSS to identify potential diagnostic biomarkers.
METHODS: A systematic search was conducted across nine international databases (PubMed, Cochrane Library, Embase, Web of Science, Scopus, VIP, CNKI, Wanfang, and SinoMed) up to October 1, 2024, using a combination of Medical Subject Headings (MeSH) and free-text terms: "oral microbiome" OR "oral flora" AND "Sjögren's Syndrome" OR "pSS." Only studies analyzing the oral microbiota of pSS patients were included. A random-effects meta-analysis was performed for quantitative synthesis. And use a funnel chart to assess the publication bias of the included articles. The conclusions are tempered by the moderate risk of bias in some included studies, substantial heterogeneity (partly attributed to methodological), and the limited number of studies for certain subgroup analyses, which may affect the precision of the pooled estimates.
RESULTS: A total of 833 studies were identified, 21 of which were included, with 16S rRNA sequencing being the most commonly used technique. QIIME (Quantitative Insights Into Microbial Ecology) is a mainstream bioinformatics analysis tool. Of the 21 studies (1094 participants) included, 19 provided data on α diversity. Overall, declines in the α diversity index were common in pSS (Chao1: SMD = -0.79, [95% CI = -1.381, -0.21], p<0.001; Shannon index: SMD = -0.16, [95%CI = -0.53, -0.21], p=0.400; Simpson index: SMD = -0.14, [95% CI = -0.79, -1.06]), p=0.770. Ten of these studies provided data on β diversity, suggesting a clear difference between the pSS group and the healthy control group. Firmicutes (mainly including Streptococcus spp., Velon spp., etc.) showed a significant enrichment trend in pSS patients, and the relative relative abundance of Proteobacteria (Haemophilus), Actinomycetes and Spiromycetes decreased in pSS patients.
CONCLUSION: pSS patients demonstrate reduced oral microbiome diversity compared to HCs(Healthy controls). Enrichment of Veillonella, Streptococcus, and Prevotella may correlate with pSS pathogenesis, whereas Haemophilus parainfluenzae might serve as a protective taxon. Oral dysbiosis appears to be a distinctive feature of pSS compared to systemic lupus erythematosus (SLE). Further mechanistic studies are needed to explore causal relationships and therapeutic targets.
Additional Links: PMID-41965068
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PubMed:
Citation:
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@article {pmid41965068,
year = {2026},
author = {Wu, H and Hu, L and Pu, J and Yang, L and Han, F and Wang, Y and Tu, A and Gao, R and Lin, K and Liang, Y and Wu, Z and Pan, S and Song, J and Tang, J and Wang, X},
title = {Oral Microbiome Dysbiosis in Primary Sjögren's Syndrome: A Systematic Review and Meta-Analysis.},
journal = {Rheumatology (Oxford, England)},
volume = {},
number = {},
pages = {},
doi = {10.1093/rheumatology/keag178},
pmid = {41965068},
issn = {1462-0332},
abstract = {OBJECTIVES: Dry mouth symptoms in patients with primary Sjögren's syndrome (pSS) may be associated with oral microbiome dysbiosis, which plays a critical role in the pathogenesis of pSS and potentially contributes to disease progression. This study systematically reviews and meta-analyzes the latest research on the relationship between the oral microbiome and pSS to identify potential diagnostic biomarkers.
METHODS: A systematic search was conducted across nine international databases (PubMed, Cochrane Library, Embase, Web of Science, Scopus, VIP, CNKI, Wanfang, and SinoMed) up to October 1, 2024, using a combination of Medical Subject Headings (MeSH) and free-text terms: "oral microbiome" OR "oral flora" AND "Sjögren's Syndrome" OR "pSS." Only studies analyzing the oral microbiota of pSS patients were included. A random-effects meta-analysis was performed for quantitative synthesis. And use a funnel chart to assess the publication bias of the included articles. The conclusions are tempered by the moderate risk of bias in some included studies, substantial heterogeneity (partly attributed to methodological), and the limited number of studies for certain subgroup analyses, which may affect the precision of the pooled estimates.
RESULTS: A total of 833 studies were identified, 21 of which were included, with 16S rRNA sequencing being the most commonly used technique. QIIME (Quantitative Insights Into Microbial Ecology) is a mainstream bioinformatics analysis tool. Of the 21 studies (1094 participants) included, 19 provided data on α diversity. Overall, declines in the α diversity index were common in pSS (Chao1: SMD = -0.79, [95% CI = -1.381, -0.21], p<0.001; Shannon index: SMD = -0.16, [95%CI = -0.53, -0.21], p=0.400; Simpson index: SMD = -0.14, [95% CI = -0.79, -1.06]), p=0.770. Ten of these studies provided data on β diversity, suggesting a clear difference between the pSS group and the healthy control group. Firmicutes (mainly including Streptococcus spp., Velon spp., etc.) showed a significant enrichment trend in pSS patients, and the relative relative abundance of Proteobacteria (Haemophilus), Actinomycetes and Spiromycetes decreased in pSS patients.
CONCLUSION: pSS patients demonstrate reduced oral microbiome diversity compared to HCs(Healthy controls). Enrichment of Veillonella, Streptococcus, and Prevotella may correlate with pSS pathogenesis, whereas Haemophilus parainfluenzae might serve as a protective taxon. Oral dysbiosis appears to be a distinctive feature of pSS compared to systemic lupus erythematosus (SLE). Further mechanistic studies are needed to explore causal relationships and therapeutic targets.},
}
RevDate: 2026-04-11
Microbiomic and immunogenic biomarkers of adjuvant chemotherapy efficacy in stage III colorectal cancer.
JNCI cancer spectrum pii:8649460 [Epub ahead of print].
BACKGROUND: The standard treatment for stage III colorectal cancer (CRC) is surgery, followed by adjuvant chemotherapy (AC). However, the efficacy of AC is limited and approximately 30% of patients experience recurrence. Therefore, easily assessable molecular biomarkers that can predict the response to AC are needed. Here, we aimed to identify predictive biomarkers of the response to AC using tumor transcriptomic data.
METHODS: Tumor specimens from 253 patients who underwent surgery for stage III CRC between 1997 and 2019 were analyzed using RNA sequencing. Transcriptional subtyping and analyses of gut microbiome, immune cell fractions, and T-cell receptors (TCRs) were performed to identify factors associated with recurrence-free survival (RFS) in patients treated with or without AC.
RESULTS: Among 253 patients, 118 (46.6%) received AC. Twenty phyla and 799 species were identified in the microbiomes, among which Fusobacteria were identified in 247 patients (97.6%). Multivariable Cox proportional hazards regression analysis of patients who received AC showed that intratumoral Fusobacterium abundance (hazard ratio [HR], 3.95; 95% confidence interval [CI], 1.05 to 14.8; P = 0.042) and TCR α and δ (TRAD) diversity (HR, 0.41; 95% CI, 0.20 to 0.87; P = 0.020) were independently associated with RFS.
CONCLUSION: Fusobacterium abundance and TRAD diversity were associated with the response to AC, suggesting that these factors could serve as biomarkers for personalized treatment in stage III CRC.
Additional Links: PMID-41965123
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PubMed:
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@article {pmid41965123,
year = {2026},
author = {Machida, E and Takamizawa, Y and Takayanagi, D and Cho, H and Shida, D and Yamada, M and Asami, Y and Ono, H and Takeuchi, M and Hamamoto, R and Rikiyama, T and Suzuki, K and Kanemitsu, Y and Kohno, T and Takashima, A and Sekine, S and Shiraishi, K},
title = {Microbiomic and immunogenic biomarkers of adjuvant chemotherapy efficacy in stage III colorectal cancer.},
journal = {JNCI cancer spectrum},
volume = {},
number = {},
pages = {},
doi = {10.1093/jncics/pkag036},
pmid = {41965123},
issn = {2515-5091},
abstract = {BACKGROUND: The standard treatment for stage III colorectal cancer (CRC) is surgery, followed by adjuvant chemotherapy (AC). However, the efficacy of AC is limited and approximately 30% of patients experience recurrence. Therefore, easily assessable molecular biomarkers that can predict the response to AC are needed. Here, we aimed to identify predictive biomarkers of the response to AC using tumor transcriptomic data.
METHODS: Tumor specimens from 253 patients who underwent surgery for stage III CRC between 1997 and 2019 were analyzed using RNA sequencing. Transcriptional subtyping and analyses of gut microbiome, immune cell fractions, and T-cell receptors (TCRs) were performed to identify factors associated with recurrence-free survival (RFS) in patients treated with or without AC.
RESULTS: Among 253 patients, 118 (46.6%) received AC. Twenty phyla and 799 species were identified in the microbiomes, among which Fusobacteria were identified in 247 patients (97.6%). Multivariable Cox proportional hazards regression analysis of patients who received AC showed that intratumoral Fusobacterium abundance (hazard ratio [HR], 3.95; 95% confidence interval [CI], 1.05 to 14.8; P = 0.042) and TCR α and δ (TRAD) diversity (HR, 0.41; 95% CI, 0.20 to 0.87; P = 0.020) were independently associated with RFS.
CONCLUSION: Fusobacterium abundance and TRAD diversity were associated with the response to AC, suggesting that these factors could serve as biomarkers for personalized treatment in stage III CRC.},
}
RevDate: 2026-04-11
Intestinal dysbiosis associates with silica-induced pulmonary fibrosis in mice via arginine and tryptophan pathways.
BMC microbiology pii:10.1186/s12866-026-05023-6 [Epub ahead of print].
BACKGROUND: Pulmonary fibrosis (PF) is a life-threatening interstitial lung disease with a lack of effective therapeutic approaches. Silicosis is a subtype of PF that is specifically caused by the inhalation of crystalline silica particles. In recent years, the gut-lung axis has been shown to be involved in the occurrence and progression of various respiratory diseases. However, the involvement and specific mechanism of action of the gut microbiome in silica-induced PF remain to be elucidated. Therefore, we established a silica-induced PF murine model using an inhalation exposure system, and combined gut metagenomic and untargeted metabolomics data to correlate microbial and metabolic changes with profibrotic cytokine levels.
RESULTS: In mice exposed to silica dust for 64 days and 128 days, Akkermansia muciniphila and Staphylococcus lentus were significantly enriched, whereas the abundance of Lactobacillus murinus was notably reduced. Relevant network analysis revealed that these gut microbiota changes were highly correlated with metabolic disorders of tryptophan and arginine. Moreover, changes in the gut microbiome composition corresponded with the fluctuations in the levels of profibrotic cytokines, including transforming growth factor-beta, tumor necrosis factor-alpha, fibroblast growth factor, and hydroxyproline.
CONCLUSION: We successfully established a murine model of PF induced by silica inhalation. Our results suggest that Lactobacillus murinus, Akkermansia muciniphila, and Staphylococcus lentus are key microorganisms involved in the development of silica-induced PF, while the arginine and tryptophan metabolic pathways serve as key regulatory pathways in the gut-lung axis contributing to disease development.
Additional Links: PMID-41965517
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PubMed:
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@article {pmid41965517,
year = {2026},
author = {Han, J and Zhou, X and Guo, M and Zhang, C and Liu, C and Cai, L and Zhao, H},
title = {Intestinal dysbiosis associates with silica-induced pulmonary fibrosis in mice via arginine and tryptophan pathways.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05023-6},
pmid = {41965517},
issn = {1471-2180},
support = {2025QN03136//Natural Science Foundation of Inner Mongolia/ ; 2025MS03093//Natural Science Foundation of Inner Mongolia/ ; 62231013//National Natural Science Foundation of China/ ; 62261043//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Pulmonary fibrosis (PF) is a life-threatening interstitial lung disease with a lack of effective therapeutic approaches. Silicosis is a subtype of PF that is specifically caused by the inhalation of crystalline silica particles. In recent years, the gut-lung axis has been shown to be involved in the occurrence and progression of various respiratory diseases. However, the involvement and specific mechanism of action of the gut microbiome in silica-induced PF remain to be elucidated. Therefore, we established a silica-induced PF murine model using an inhalation exposure system, and combined gut metagenomic and untargeted metabolomics data to correlate microbial and metabolic changes with profibrotic cytokine levels.
RESULTS: In mice exposed to silica dust for 64 days and 128 days, Akkermansia muciniphila and Staphylococcus lentus were significantly enriched, whereas the abundance of Lactobacillus murinus was notably reduced. Relevant network analysis revealed that these gut microbiota changes were highly correlated with metabolic disorders of tryptophan and arginine. Moreover, changes in the gut microbiome composition corresponded with the fluctuations in the levels of profibrotic cytokines, including transforming growth factor-beta, tumor necrosis factor-alpha, fibroblast growth factor, and hydroxyproline.
CONCLUSION: We successfully established a murine model of PF induced by silica inhalation. Our results suggest that Lactobacillus murinus, Akkermansia muciniphila, and Staphylococcus lentus are key microorganisms involved in the development of silica-induced PF, while the arginine and tryptophan metabolic pathways serve as key regulatory pathways in the gut-lung axis contributing to disease development.},
}
RevDate: 2026-04-11
Artificial intelligence in microbiology: implications for metagenomics, diagnostics, and AMR surveillance.
Biomedical engineering online pii:10.1186/s12938-026-01568-9 [Epub ahead of print].
Artificial intelligence (AI) is now a key player in modern microbiology, as it enables high-resolution analyses of genomic, metagenomic, and clinical data for the monitoring of infectious disease and antimicrobial resistance (AMR). Considerable advancements in deep learning, transformer-based sequence models, graph neural networks, and multimodal architectures have greatly improved microbial classification accuracy, antibiotic resistance gene (ARG) detection, and resistance prediction. Taking metagenomic sequencing into consideration, these advancements have contributed to the development of sensitive, scalable, and non-invasive methods to profile microbiomes, determine novel resistance, and monitor AMR trends at the population level. This review summarizes recent advances in AI-aided microbiology, with a particular emphasis on AMR surveillance. Specific topics include deep learning frameworks for ARG annotation, emerging approaches to identifying new resistance genes, and multimodal applications (genomic and clinical metadata) aimed at improving phenotype prediction. The role of metagenome-assembled genomes (MAGs) to enhance AMR surveillance efforts is noted, along with their noted limitations relative to isolate genomes. The discussion includes the examination of explainable AI (XAI) techniques including SHAP, attention mechanism approaches, and gradient-based attribution approaches, with the aim of increasing transparency and clinical explainability. We also cover potential applications including AI-enabled non-invasive fecal microbiome diagnostics, laboratory automation, and environmental surveillance. While there has been significant progress, unresolved issues exist relating to dataset variations, liability of models to datasets, interpretability, and regulatory approval. Overcoming these barriers, however, will require standardized frameworks for these workflows, privacy-preserving federated learning methods, and interpretable AI frameworks for clinical and public health tools. AI could fundamentally change AMR surveillance by allowing for earlier resistance detection, advanced risk assessment recommendation, and improved monitoring strategies globally.
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PubMed:
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@article {pmid41965741,
year = {2026},
author = {Khangarot, R and Kumari, V and Mishra, R and Singh, A},
title = {Artificial intelligence in microbiology: implications for metagenomics, diagnostics, and AMR surveillance.},
journal = {Biomedical engineering online},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12938-026-01568-9},
pmid = {41965741},
issn = {1475-925X},
abstract = {Artificial intelligence (AI) is now a key player in modern microbiology, as it enables high-resolution analyses of genomic, metagenomic, and clinical data for the monitoring of infectious disease and antimicrobial resistance (AMR). Considerable advancements in deep learning, transformer-based sequence models, graph neural networks, and multimodal architectures have greatly improved microbial classification accuracy, antibiotic resistance gene (ARG) detection, and resistance prediction. Taking metagenomic sequencing into consideration, these advancements have contributed to the development of sensitive, scalable, and non-invasive methods to profile microbiomes, determine novel resistance, and monitor AMR trends at the population level. This review summarizes recent advances in AI-aided microbiology, with a particular emphasis on AMR surveillance. Specific topics include deep learning frameworks for ARG annotation, emerging approaches to identifying new resistance genes, and multimodal applications (genomic and clinical metadata) aimed at improving phenotype prediction. The role of metagenome-assembled genomes (MAGs) to enhance AMR surveillance efforts is noted, along with their noted limitations relative to isolate genomes. The discussion includes the examination of explainable AI (XAI) techniques including SHAP, attention mechanism approaches, and gradient-based attribution approaches, with the aim of increasing transparency and clinical explainability. We also cover potential applications including AI-enabled non-invasive fecal microbiome diagnostics, laboratory automation, and environmental surveillance. While there has been significant progress, unresolved issues exist relating to dataset variations, liability of models to datasets, interpretability, and regulatory approval. Overcoming these barriers, however, will require standardized frameworks for these workflows, privacy-preserving federated learning methods, and interpretable AI frameworks for clinical and public health tools. AI could fundamentally change AMR surveillance by allowing for earlier resistance detection, advanced risk assessment recommendation, and improved monitoring strategies globally.},
}
RevDate: 2026-04-11
Microbiome/transforming growth factor-β axis as a diagnostic and therapeutic target for MASLD in Egyptian patients.
Gut pathogens pii:10.1186/s13099-026-00826-4 [Epub ahead of print].
Additional Links: PMID-41965779
Publisher:
PubMed:
Citation:
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@article {pmid41965779,
year = {2026},
author = {Marawan, AE and Elmetwally, OA and Abass, SA and Marwan, MM and El-Sokkary, MMA and Eissa, LA},
title = {Microbiome/transforming growth factor-β axis as a diagnostic and therapeutic target for MASLD in Egyptian patients.},
journal = {Gut pathogens},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13099-026-00826-4},
pmid = {41965779},
issn = {1757-4749},
}
RevDate: 2026-04-11
Lung microbiome predictors of epigenetic aging and potential associations with smoking and electronic cigarette use.
Clinical epigenetics pii:10.1186/s13148-026-02126-9 [Epub ahead of print].
BACKGROUND: The lungs harbor diverse microbial communities that may influence pulmonary health, potentially through lung aging. While accelerated lung aging can increase susceptibility to pulmonary diseases, no studies have yet linked the lung microbiome to biological aging in disease-free individuals.
MATERIALS AND METHODS: We assessed well-studied methylation-based biological aging (mAge) markers (Horvath, GrimAge, PhenoAge, and telomere-length) in the lungs of healthy smokers (SM), electronic cigarette (EC) users, and never-smokers (NS) (n = 26, 21-30 years). We used metatranscriptome profiling to detect live bacteria. Using XGBoost, we performed feature selection on 1016 bacterial species to predict faster or slower lung mAge, and the selected bacterial species were used as explanatory variables in a logistic regression model. Linear regression analyses examined the associations between identified bacterial species and urinary metabolites of exposure to smoking and EC use, including volatile organic compounds (VOCs) and polycyclic aromatic hydrocarbons (PAHs).
RESULTS: The logistic regression models identified bacterial species that classified individuals with faster or slower lung aging based on each mAge estimate (accuracy 77%-85%; AUC 0.78-0.91). Two species strongly predictive of GrimAge, Alistipes finegoldii and Arachidicoccus sp.BS20 were significantly less present in SM compared to NS. Arachidicoccus sp.BS20 was significantly associated with nicotine-intake-adjusted metabolites of several VOCs and PAHs in SM and EC users.
CONCLUSION: For the first time, our study suggests potential associations of the microbiome with biological aging in the lungs of healthy individuals. In addition, the findings indicate that exposure to smoking and EC may be linked to shifts in particular microbial profiles associated with biological aging of the lungs. These results support the need for larger studies to better understand the direction and possible mechanisms of these relationships, and to further explore the lung microbiome as a potential target for interventions aimed at mitigating pulmonary aging and disease risk.
Additional Links: PMID-41965787
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PubMed:
Citation:
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@article {pmid41965787,
year = {2026},
author = {Khan, A and Choi, B and Kang, S and Weng, DY and Ying, K and McElroy, JP and Kamel, S and Reisinger, SA and Wewers, MD and Shields, PG and Song, MA},
title = {Lung microbiome predictors of epigenetic aging and potential associations with smoking and electronic cigarette use.},
journal = {Clinical epigenetics},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13148-026-02126-9},
pmid = {41965787},
issn = {1868-7083},
support = {RS- 202300245056//Ministry of Education/ ; (P30 CA016058)//National Cancer Institute of the National Institutes of Health (NIH)/ ; (P50CA180908)//The Food and Drug Administration Center for Tobacco Products (CTP)/ ; (UM1TR004548)//The Clinical and Translational Science Award (CTSA)/ ; (UL1TR001070)//The National Center for Advancing Translational Sciences/ ; },
abstract = {BACKGROUND: The lungs harbor diverse microbial communities that may influence pulmonary health, potentially through lung aging. While accelerated lung aging can increase susceptibility to pulmonary diseases, no studies have yet linked the lung microbiome to biological aging in disease-free individuals.
MATERIALS AND METHODS: We assessed well-studied methylation-based biological aging (mAge) markers (Horvath, GrimAge, PhenoAge, and telomere-length) in the lungs of healthy smokers (SM), electronic cigarette (EC) users, and never-smokers (NS) (n = 26, 21-30 years). We used metatranscriptome profiling to detect live bacteria. Using XGBoost, we performed feature selection on 1016 bacterial species to predict faster or slower lung mAge, and the selected bacterial species were used as explanatory variables in a logistic regression model. Linear regression analyses examined the associations between identified bacterial species and urinary metabolites of exposure to smoking and EC use, including volatile organic compounds (VOCs) and polycyclic aromatic hydrocarbons (PAHs).
RESULTS: The logistic regression models identified bacterial species that classified individuals with faster or slower lung aging based on each mAge estimate (accuracy 77%-85%; AUC 0.78-0.91). Two species strongly predictive of GrimAge, Alistipes finegoldii and Arachidicoccus sp.BS20 were significantly less present in SM compared to NS. Arachidicoccus sp.BS20 was significantly associated with nicotine-intake-adjusted metabolites of several VOCs and PAHs in SM and EC users.
CONCLUSION: For the first time, our study suggests potential associations of the microbiome with biological aging in the lungs of healthy individuals. In addition, the findings indicate that exposure to smoking and EC may be linked to shifts in particular microbial profiles associated with biological aging of the lungs. These results support the need for larger studies to better understand the direction and possible mechanisms of these relationships, and to further explore the lung microbiome as a potential target for interventions aimed at mitigating pulmonary aging and disease risk.},
}
RevDate: 2026-04-11
Bacterial and fungal biomarkers in irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD): trans-kingdom interactions, Blastocystis carriage, and enterotype-succinotype stratification.
Gut pathogens pii:10.1186/s13099-026-00819-3 [Epub ahead of print].
Additional Links: PMID-41965848
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PubMed:
Citation:
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@article {pmid41965848,
year = {2026},
author = {El-Badry, AA and Al-Quorain, AA and Hosin, N and van der Giezen, M and Seyoum, Y},
title = {Bacterial and fungal biomarkers in irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD): trans-kingdom interactions, Blastocystis carriage, and enterotype-succinotype stratification.},
journal = {Gut pathogens},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13099-026-00819-3},
pmid = {41965848},
issn = {1757-4749},
}
RevDate: 2026-04-11
Dietary iron and metal-based growth differentially modulate growth and gut microbiome of weaned piglets.
Animal microbiome pii:10.1186/s42523-026-00561-w [Epub ahead of print].
Additional Links: PMID-41965860
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PubMed:
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@article {pmid41965860,
year = {2026},
author = {Navazesh, S and Ter Horst, A and Wen, W and Brown, CT and Ji, P},
title = {Dietary iron and metal-based growth differentially modulate growth and gut microbiome of weaned piglets.},
journal = {Animal microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s42523-026-00561-w},
pmid = {41965860},
issn = {2524-4671},
support = {NNFSA210073688//Novo Nordisk Fonden/ ; },
}
RevDate: 2026-04-11
CmpDate: 2026-04-11
Post-transport recovery trajectory of the canine gut microbiome and metabolome.
Journal of animal science and biotechnology, 17(1):.
BACKGROUND: Transportation induces a multisystem stress response in companion animals, yet the integrated recovery dynamics across physiological, microbial, and metabolic domains remain poorly characterized. This study comprehensively tracked the 7-day recovery trajectory in dogs following road transport by analyzing clinical parameters, fecal microbiome and metabolome.
RESULTS: Time-dependent changes were observed across domains, with differing temporal patterns. Fecal consistency improved rapidly, while behavioral scores exhibited a decrease followed by stabilization. Microbial alpha diversity initially decreased, with significant community restructuring persisting throughout recovery, culminating in a new stable state distinct from the arrival (D0) state. This shift was characterized by early enrichment of Fusobacterium and Clostridium sensu stricto 1, followed by late dominance of Erysipelatoclostridium, contrasting with the initial post-transport (D0) community dominated by Prevotella 9, Lactobacillus, Phascolarctobacterium, Anaerobiospirillum, Parabacteroides, and Prevotellaceae GA6A1 group. Metabolomic profiling confirmed a sustained metabolic shift, involving pathways in the biosynthesis of steroid and unsaturated fatty acids and the metabolism of butanoate and several amino acids. Strong cross-domain correlations linked specific microbial genera and metabolites with behavioral improvement, underscoring gut-brain axis involvement.
CONCLUSION: By D7, several measures remained distinct from the arrival (D0) state, indicating persistent multi-system differences during the first week after transport. These findings elucidate the complex, coordinated adaptation to transport stress, highlighting ongoing clinical, microbial, and metabolic differences by D7 and providing a framework for interventions aimed at enhancing welfare and resilience in transported companion animals.
Additional Links: PMID-41965866
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@article {pmid41965866,
year = {2026},
author = {Lyu, Y and Su, C and Sun, K and Wang, Y and Zhang, L and Pu, J and Wu, C and Thomas, D and Che, L},
title = {Post-transport recovery trajectory of the canine gut microbiome and metabolome.},
journal = {Journal of animal science and biotechnology},
volume = {17},
number = {1},
pages = {},
pmid = {41965866},
issn = {1674-9782},
abstract = {BACKGROUND: Transportation induces a multisystem stress response in companion animals, yet the integrated recovery dynamics across physiological, microbial, and metabolic domains remain poorly characterized. This study comprehensively tracked the 7-day recovery trajectory in dogs following road transport by analyzing clinical parameters, fecal microbiome and metabolome.
RESULTS: Time-dependent changes were observed across domains, with differing temporal patterns. Fecal consistency improved rapidly, while behavioral scores exhibited a decrease followed by stabilization. Microbial alpha diversity initially decreased, with significant community restructuring persisting throughout recovery, culminating in a new stable state distinct from the arrival (D0) state. This shift was characterized by early enrichment of Fusobacterium and Clostridium sensu stricto 1, followed by late dominance of Erysipelatoclostridium, contrasting with the initial post-transport (D0) community dominated by Prevotella 9, Lactobacillus, Phascolarctobacterium, Anaerobiospirillum, Parabacteroides, and Prevotellaceae GA6A1 group. Metabolomic profiling confirmed a sustained metabolic shift, involving pathways in the biosynthesis of steroid and unsaturated fatty acids and the metabolism of butanoate and several amino acids. Strong cross-domain correlations linked specific microbial genera and metabolites with behavioral improvement, underscoring gut-brain axis involvement.
CONCLUSION: By D7, several measures remained distinct from the arrival (D0) state, indicating persistent multi-system differences during the first week after transport. These findings elucidate the complex, coordinated adaptation to transport stress, highlighting ongoing clinical, microbial, and metabolic differences by D7 and providing a framework for interventions aimed at enhancing welfare and resilience in transported companion animals.},
}
RevDate: 2026-04-12
Integrating metagenomics into legume breeding: A breeder-centered roadmap from core microbiomes to precision inoculation.
Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases pii:S1567-1348(26)00065-1 [Epub ahead of print].
Metagenomics, culture-independent profiling of genetic material recovered from environmental samples, provides a powerful route to characterize microbial communities associated with legumes and to translate their functional potential into breeding targets that enhance resilience and productivity. Across analyses of rhizosphere, endosphere, and seed microbiomes, repeated studies consistently identify a conserved set of microbial functions linked to nutrient cycling, responses to abiotic and biotic stress, and biological control of pathogens, thereby offering mechanistic support that community-level functional capacities can shape host outcomes, including seedling vigor, nutrient-use efficiency, and stress tolerance. To move from descriptive discovery to actionable breeding, three complementary translational strategies have emerged: (i) synthetic microbial communities (SynComs) engineered to deliver targeted metabolic functions while enabling rigorous assessment of community stability and functional consistency; (ii) predictive model systems that integrate metagenomic features with phenotypic measurements to prioritize candidate taxa or functions for subsequent validation; and (iii) precision inoculation approaches that deploy validated microbes or consortia in agronomic settings to test whether metagenome-inferred functions confer robust performance under field-relevant conditions. A critical appraisal of metagenomic, multi-omics, and translational studies indicates that functional-phenotypic mappings are promising, yet substantial barriers continue to constrain reproducibility and scalability, including heterogeneity in sampling and experimental design, biases introduced by DNA extraction and sequencing, variability across bioinformatics workflows and reference databases, and overarching biosafety and regulatory constraints that can obscure true biological signals and weaken the reliability of functional inferences intended to guide selection decisions. To mainstream metagenomics in conventional legume breeding, we propose a breeders' roadmap centered on coordinated standardization and decision-ready analytics, encompassing standardized metagenomics-compatible sampling and sequencing platforms, harmonized computational frameworks and metabolic inference tools to ensure comparable functional calls, high-throughput phenotyping protocols aligned to microbiome-sensitive host traits, and selection frameworks that explicitly incorporate microbiome-oriented decision rules rather than treating microbial signals as ancillary. Finally, integrating machine learning with multi-omics datasets alongside precision delivery systems offers a practical route to generate actionable holobiont-level selection indices, and, when coupled with clearly defined translational pipelines and methodological standardization, metagenomics can broaden breeding gains beyond those achievable using host genomics alone, enabling more reliable, function-driven microbiome-assisted improvement of legume performance.
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@article {pmid41966291,
year = {2026},
author = {Ashango, ZA and Seyum, EG and Nwogha, JS},
title = {Integrating metagenomics into legume breeding: A breeder-centered roadmap from core microbiomes to precision inoculation.},
journal = {Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases},
volume = {},
number = {},
pages = {105941},
doi = {10.1016/j.meegid.2026.105941},
pmid = {41966291},
issn = {1567-7257},
abstract = {Metagenomics, culture-independent profiling of genetic material recovered from environmental samples, provides a powerful route to characterize microbial communities associated with legumes and to translate their functional potential into breeding targets that enhance resilience and productivity. Across analyses of rhizosphere, endosphere, and seed microbiomes, repeated studies consistently identify a conserved set of microbial functions linked to nutrient cycling, responses to abiotic and biotic stress, and biological control of pathogens, thereby offering mechanistic support that community-level functional capacities can shape host outcomes, including seedling vigor, nutrient-use efficiency, and stress tolerance. To move from descriptive discovery to actionable breeding, three complementary translational strategies have emerged: (i) synthetic microbial communities (SynComs) engineered to deliver targeted metabolic functions while enabling rigorous assessment of community stability and functional consistency; (ii) predictive model systems that integrate metagenomic features with phenotypic measurements to prioritize candidate taxa or functions for subsequent validation; and (iii) precision inoculation approaches that deploy validated microbes or consortia in agronomic settings to test whether metagenome-inferred functions confer robust performance under field-relevant conditions. A critical appraisal of metagenomic, multi-omics, and translational studies indicates that functional-phenotypic mappings are promising, yet substantial barriers continue to constrain reproducibility and scalability, including heterogeneity in sampling and experimental design, biases introduced by DNA extraction and sequencing, variability across bioinformatics workflows and reference databases, and overarching biosafety and regulatory constraints that can obscure true biological signals and weaken the reliability of functional inferences intended to guide selection decisions. To mainstream metagenomics in conventional legume breeding, we propose a breeders' roadmap centered on coordinated standardization and decision-ready analytics, encompassing standardized metagenomics-compatible sampling and sequencing platforms, harmonized computational frameworks and metabolic inference tools to ensure comparable functional calls, high-throughput phenotyping protocols aligned to microbiome-sensitive host traits, and selection frameworks that explicitly incorporate microbiome-oriented decision rules rather than treating microbial signals as ancillary. Finally, integrating machine learning with multi-omics datasets alongside precision delivery systems offers a practical route to generate actionable holobiont-level selection indices, and, when coupled with clearly defined translational pipelines and methodological standardization, metagenomics can broaden breeding gains beyond those achievable using host genomics alone, enabling more reliable, function-driven microbiome-assisted improvement of legume performance.},
}
RevDate: 2026-04-12
Machine Learning and Artificial Intelligence in Nutrition Research: Analytical Methods, Applications, and Key Considerations.
The Journal of nutrition pii:S0022-3166(26)00177-X [Epub ahead of print].
Nutrition research is increasingly utilizing artificial intelligence (AI) and machine learning to address analytical challenges posed by high-dimensional data and to enable personalized recommendations and health predictions. This review provides an overview of machine learning techniques and their application in nutrition research. The article is structured according to the steps of a typical analysis pipeline. First, we outline data quality control, preprocessing, and classical statistical tests for detecting group differences, assessing covariate associations, and prescreening input features. Next, dimension reduction and visualization methods such as principal component analysis (PCA), t-distributed stochastic neighbor embedding (t-SNE), and uniform manifold approximation and projection (UMAP) are presented to simplify high-dimensional data and reveal nutrition indicators. Supervised learning approaches that support classification and outcome prediction are then reviewed, followed by unsupervised learning methods for clustering unlabeled observations. Integrative tools combining approaches such as canonical correlation analysis (CCA) and supervised multiblock methods are discussed for their suitability in multi-omics and multimodal studies. A comparison of commonly used supervised approaches is presented, including random forest, gradient boosting regression, penalized regression methods, least absolute shrinkage and selection operator (LASSO), support vector machines (SVM), and k-nearest neighbors (k-NN). Deep learning techniques, including convolutional neural networks (CNNs), recurrent neural networks (RNNs), long short-term memory (LSTM) models, natural language processing (NLP), and large language models (LLMs), are highlighted for analyzing unstructured, sequential, and text-based data. To ensure the reproducibility and generalizability of findings, we discuss strategies for model validation, including cross-validation, external replication, and permutation testing. We also discuss practical considerations for implementing advanced analytic approaches in nutrition research, such as interpretability, sample size constraints, and overfitting, to guide responsible implementation. Collectively, this review provides a framework for understanding and thoughtfully applying machine learning approaches to nutrition research.
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@article {pmid41966331,
year = {2026},
author = {Southey, NL and Zhu, R and Holscher, HD},
title = {Machine Learning and Artificial Intelligence in Nutrition Research: Analytical Methods, Applications, and Key Considerations.},
journal = {The Journal of nutrition},
volume = {},
number = {},
pages = {101528},
doi = {10.1016/j.tjnut.2026.101528},
pmid = {41966331},
issn = {1541-6100},
abstract = {Nutrition research is increasingly utilizing artificial intelligence (AI) and machine learning to address analytical challenges posed by high-dimensional data and to enable personalized recommendations and health predictions. This review provides an overview of machine learning techniques and their application in nutrition research. The article is structured according to the steps of a typical analysis pipeline. First, we outline data quality control, preprocessing, and classical statistical tests for detecting group differences, assessing covariate associations, and prescreening input features. Next, dimension reduction and visualization methods such as principal component analysis (PCA), t-distributed stochastic neighbor embedding (t-SNE), and uniform manifold approximation and projection (UMAP) are presented to simplify high-dimensional data and reveal nutrition indicators. Supervised learning approaches that support classification and outcome prediction are then reviewed, followed by unsupervised learning methods for clustering unlabeled observations. Integrative tools combining approaches such as canonical correlation analysis (CCA) and supervised multiblock methods are discussed for their suitability in multi-omics and multimodal studies. A comparison of commonly used supervised approaches is presented, including random forest, gradient boosting regression, penalized regression methods, least absolute shrinkage and selection operator (LASSO), support vector machines (SVM), and k-nearest neighbors (k-NN). Deep learning techniques, including convolutional neural networks (CNNs), recurrent neural networks (RNNs), long short-term memory (LSTM) models, natural language processing (NLP), and large language models (LLMs), are highlighted for analyzing unstructured, sequential, and text-based data. To ensure the reproducibility and generalizability of findings, we discuss strategies for model validation, including cross-validation, external replication, and permutation testing. We also discuss practical considerations for implementing advanced analytic approaches in nutrition research, such as interpretability, sample size constraints, and overfitting, to guide responsible implementation. Collectively, this review provides a framework for understanding and thoughtfully applying machine learning approaches to nutrition research.},
}
RevDate: 2026-04-12
Interventions Targeting Gut Colonization by Multidrug-Resistant Organisms in Healthcare Settings: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.
The Journal of hospital infection pii:S0195-6701(26)00126-X [Epub ahead of print].
BACKGROUND: Gut colonization with multidrug-resistant organisms (MDRO) increases risks of infection, transmission and mortality in healthcare settings. Although decolonization strategies have been attempted to reduce the impact of gut MDRO, no consensus exists on their effectiveness. Our study evaluates the effectiveness of these strategies.
METHODS: We searched PubMed, EMBASE, CENTRAL, CINAHL and Web of Science for randomized controlled trials (RCTs) published from Jan 2005 to Dec 2024. Eligible studies included patients in healthcare settings, with baseline MDRO colonization confirmed by rectal swab or stool sample. The primary outcome was reduction in colonization rates in the short term (<28 days) and long term (≥28 days). Two reviewers independently screened studies, extracted data and assessed bias using the Cochrane RoB2 tool. A random-effects model was used for meta-analysis.
PROSPERO: CRD42025625291.
RESULTS: Of 900 studies screened, 14 RCTs were included. Interventions included probiotics (n=7), oral non-absorbable antibiotics (n=6), and fecal microbiota transplantation (FMT) with antibiotics (n=1). No significant effect was observed for short-term (RR=1.18; 95% CI 0.81-1.71; p=0.39) and long-term decolonization (RR=1.12; 95% CI 0.95-1.32; p=0.16). Post-hoc subgroup analyses showed no significant differences across immune status, target organisms, intervention types and timing of outcome assessment. Risk of bias was low in four studies, with seven having some concerns and three at high risk. Certainty of evidence was low.
CONCLUSION: Current evidence does not support routine use of interventions for gut MDRO decolonization. Well-powered RCTs focused on pathogen-specific interventions and clinically meaningful endpoints are needed to evaluate promising strategies for sustained decolonization (e.g. FMT) and emerging strategies (e.g. bacteriophages).
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@article {pmid41966334,
year = {2026},
author = {M, P and Rajendiran, U and Wahab, MT and Venkatachalam, I},
title = {Interventions Targeting Gut Colonization by Multidrug-Resistant Organisms in Healthcare Settings: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.},
journal = {The Journal of hospital infection},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jhin.2026.03.035},
pmid = {41966334},
issn = {1532-2939},
abstract = {BACKGROUND: Gut colonization with multidrug-resistant organisms (MDRO) increases risks of infection, transmission and mortality in healthcare settings. Although decolonization strategies have been attempted to reduce the impact of gut MDRO, no consensus exists on their effectiveness. Our study evaluates the effectiveness of these strategies.
METHODS: We searched PubMed, EMBASE, CENTRAL, CINAHL and Web of Science for randomized controlled trials (RCTs) published from Jan 2005 to Dec 2024. Eligible studies included patients in healthcare settings, with baseline MDRO colonization confirmed by rectal swab or stool sample. The primary outcome was reduction in colonization rates in the short term (<28 days) and long term (≥28 days). Two reviewers independently screened studies, extracted data and assessed bias using the Cochrane RoB2 tool. A random-effects model was used for meta-analysis.
PROSPERO: CRD42025625291.
RESULTS: Of 900 studies screened, 14 RCTs were included. Interventions included probiotics (n=7), oral non-absorbable antibiotics (n=6), and fecal microbiota transplantation (FMT) with antibiotics (n=1). No significant effect was observed for short-term (RR=1.18; 95% CI 0.81-1.71; p=0.39) and long-term decolonization (RR=1.12; 95% CI 0.95-1.32; p=0.16). Post-hoc subgroup analyses showed no significant differences across immune status, target organisms, intervention types and timing of outcome assessment. Risk of bias was low in four studies, with seven having some concerns and three at high risk. Certainty of evidence was low.
CONCLUSION: Current evidence does not support routine use of interventions for gut MDRO decolonization. Well-powered RCTs focused on pathogen-specific interventions and clinically meaningful endpoints are needed to evaluate promising strategies for sustained decolonization (e.g. FMT) and emerging strategies (e.g. bacteriophages).},
}
RevDate: 2026-04-12
Phytogenic feed additives mitigate in vitro methanogenesis and alter microbial community and functional pathways in the dairy cow rumen.
Anaerobe, 98:103046 pii:S1075-9964(26)00026-0 [Epub ahead of print].
OBJECTIVES: Using phytogenic feed additives (PFA) could be a promising strategy for mitigating enteric methane (CH4) emissions from ruminants. This study aimed to evaluate the efficacy of specific phytogenic additives on rumen fermentation, methanogenesis, microbial community, and functional pathways.
METHODS: This 2 x 4 x 3 factorial study was conducted using an in vitro rumen fermentation system for a period of 72 h. Treatments included two silage-to-concentrate ratios (60:40 and 40:60), four PFA (great burnet leaves, GBL; oregano leaves, OL; cumin seeds, CS; and garlic bulbs, GB), and three inclusion levels (0, 10, and 20 g kg[-1] DM) for each PFA.
RESULTS: The GB addition proved the most potent anti-methanogenic additive, reducing CH4 by up to 32.8% at 20 g kg[-1] DM, followed by GBL with a 28.5% reduction at 10 g kg[-1] DM, without impairing total volatile fatty acid production. Methane suppression was associated with a lower acetate-to-propionate ratio, decreased abundance of methanogenic archaea (particularly Methanobrevibacter), and reduced expression of the key methanogenesis gene mcrA and fmdB. While GB exhibited a strong anti-protozoal effect, OL effectively reduced ruminal ammonia concentrations. Additionally, metagenomic analysis identified Porcincola was among the core and most abundant genera in our bovine rumen dataset.
CONCLUSION: Optimising the inclusion of specific phytogenic additives can selectively manipulate the rumen microbiome, concurrently reduce methane production and influence nitrogen metabolism. Further research is warranted to evaluate potential synergistic interactions among these additives to enhance fermentation efficiency of ruminant diets.
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@article {pmid41966472,
year = {2026},
author = {Merkhan, K and Chaudhry, AS},
title = {Phytogenic feed additives mitigate in vitro methanogenesis and alter microbial community and functional pathways in the dairy cow rumen.},
journal = {Anaerobe},
volume = {98},
number = {},
pages = {103046},
doi = {10.1016/j.anaerobe.2026.103046},
pmid = {41966472},
issn = {1095-8274},
abstract = {OBJECTIVES: Using phytogenic feed additives (PFA) could be a promising strategy for mitigating enteric methane (CH4) emissions from ruminants. This study aimed to evaluate the efficacy of specific phytogenic additives on rumen fermentation, methanogenesis, microbial community, and functional pathways.
METHODS: This 2 x 4 x 3 factorial study was conducted using an in vitro rumen fermentation system for a period of 72 h. Treatments included two silage-to-concentrate ratios (60:40 and 40:60), four PFA (great burnet leaves, GBL; oregano leaves, OL; cumin seeds, CS; and garlic bulbs, GB), and three inclusion levels (0, 10, and 20 g kg[-1] DM) for each PFA.
RESULTS: The GB addition proved the most potent anti-methanogenic additive, reducing CH4 by up to 32.8% at 20 g kg[-1] DM, followed by GBL with a 28.5% reduction at 10 g kg[-1] DM, without impairing total volatile fatty acid production. Methane suppression was associated with a lower acetate-to-propionate ratio, decreased abundance of methanogenic archaea (particularly Methanobrevibacter), and reduced expression of the key methanogenesis gene mcrA and fmdB. While GB exhibited a strong anti-protozoal effect, OL effectively reduced ruminal ammonia concentrations. Additionally, metagenomic analysis identified Porcincola was among the core and most abundant genera in our bovine rumen dataset.
CONCLUSION: Optimising the inclusion of specific phytogenic additives can selectively manipulate the rumen microbiome, concurrently reduce methane production and influence nitrogen metabolism. Further research is warranted to evaluate potential synergistic interactions among these additives to enhance fermentation efficiency of ruminant diets.},
}
RevDate: 2026-04-12
Plant exosomes as multifunctional platforms for metabolic targeting and drug delivery in cancer therapy.
Biochemical pharmacology pii:S0006-2952(26)00289-3 [Epub ahead of print].
Plant-based extracellular vesicles (Ph-EXs) represent an innovative new approach for targeting cancer, as they combine natural anti-cancer activity with an advanced ability to deliver drugs. Ph-EXs have direct killing activity against cancer cells through different mechanisms, including the initiation of apoptotic pathways, inhibition of cell growth signals, alteration of the metabolism of cancer cells, and overcoming the effects of drug resistance. Ph-EXs have the ability to alter immune cells' programming, modify cancer-associated fibroblasts, and change the composition of the microbiome, impacting the tumor microenvironment as well as contributing to tumor formation. Additionally, Ph-EXs can cross biological barriers (specifically across the blood-brain barrier) and, due to their lower costs in comparison with other anti-cancer drug delivery methods, present a feasible alternative to synthetics. Ph-EXs have been developed with many engineering efforts, including novel ways to load therapeutic agents onto exosomes as well as surface functionalization. There are several challenges associated with translating Ph-EXs into the clinical setting; these include: potential variability in effect depending on the botanicals they were extracted from, standardization of extraction and characterization methods, and regulatory obstacles for clinical implementation. This review identifies critical knowledge gaps and proposes priority research directions to advance Ph-EX-based platforms toward clinical use.
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@article {pmid41966488,
year = {2026},
author = {Sucheta, and Basha, NS and Yadav, K and Khan, L and Siddiqui, AA and Dubey, A and Pradhan, M and Minz, S and Sahu, KK},
title = {Plant exosomes as multifunctional platforms for metabolic targeting and drug delivery in cancer therapy.},
journal = {Biochemical pharmacology},
volume = {},
number = {},
pages = {117956},
doi = {10.1016/j.bcp.2026.117956},
pmid = {41966488},
issn = {1873-2968},
abstract = {Plant-based extracellular vesicles (Ph-EXs) represent an innovative new approach for targeting cancer, as they combine natural anti-cancer activity with an advanced ability to deliver drugs. Ph-EXs have direct killing activity against cancer cells through different mechanisms, including the initiation of apoptotic pathways, inhibition of cell growth signals, alteration of the metabolism of cancer cells, and overcoming the effects of drug resistance. Ph-EXs have the ability to alter immune cells' programming, modify cancer-associated fibroblasts, and change the composition of the microbiome, impacting the tumor microenvironment as well as contributing to tumor formation. Additionally, Ph-EXs can cross biological barriers (specifically across the blood-brain barrier) and, due to their lower costs in comparison with other anti-cancer drug delivery methods, present a feasible alternative to synthetics. Ph-EXs have been developed with many engineering efforts, including novel ways to load therapeutic agents onto exosomes as well as surface functionalization. There are several challenges associated with translating Ph-EXs into the clinical setting; these include: potential variability in effect depending on the botanicals they were extracted from, standardization of extraction and characterization methods, and regulatory obstacles for clinical implementation. This review identifies critical knowledge gaps and proposes priority research directions to advance Ph-EX-based platforms toward clinical use.},
}
RevDate: 2026-04-12
Gut microbiome impact on systemic therapy outcomes in metastatic renal cell carcinoma: a systematic review.
World journal of urology, 44(1):.
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@article {pmid41966656,
year = {2026},
author = {Gavi, F and Bracco, M and Testori, N and Rossi, F and Fettucciari, D and Panio, E and Assumma, S and Russo, P and Gandi, C and Foschi, N and Ragonese, M and Turri, F and Bientinesi, R and Palermo, G and Ciccarese, C and Iacovelli, R and Kröner, PT and Gasbarrini, A and Sighinolfi, MC and Rocco, B},
title = {Gut microbiome impact on systemic therapy outcomes in metastatic renal cell carcinoma: a systematic review.},
journal = {World journal of urology},
volume = {44},
number = {1},
pages = {},
pmid = {41966656},
issn = {1433-8726},
}
RevDate: 2026-04-12
Plant-microbe interactions under drought stress: Unlocking new pathways for sustainable agricultural resilience.
Microbiological research, 309:128516 pii:S0944-5013(26)00080-7 [Epub ahead of print].
Drought stress is among the most significant abiotic constraints on agricultural productivity, a challenge that is intensifying under climate change. Translating the microbial mechanisms under drought into a holistic and systemic strategy remains largely unexplored. This review addresses this gap by advancing the plant-microbiome holobiont framework, which integrates such mechanisms into a unified approach to enhance drought tolerance. The framework constitutes four interrelated pillars which include (1) microbes induced modulation of host physiology and molecular responses through nutrient cycling, phytohormone regulation, osmotic adjustment, biofilm formation, and priming of systemic stress resistance, (2) Root exudates as signal-rich mediators that dynamically shape rhizosphere microbial communities and facilitate the recruitment and activity of drought-adaptive microbes and (3) the evaluation of emerging technological interventions to manipulate the plant-microbe dialogue. These interventions include genetic engineering which enables targeted modification of root exudation patterns and stress-responsive genes to enhance beneficial microbial recruitment, SynComs combining functionally complementary microbes to improve water-use efficiency and nutrient uptake, and mGWAS studies to identify plant genetic loci influencing microbiome composition and interactions, supporting the breeding of cultivars that preferentially associate with beneficial microbes under drought conditions. While (4) modulation of carbon pool, nutrient uptake and resistance priming upon leveraging microbial functions. Explicitly integrating these pillars, framework offers a practical roadmap for transitioning from mechanistic knowledge to targeted advancement of resilient agroecosystems. Harnessing the plant-microbiome holobiont through this integrated approach offers an innovative and sustainable pathway to sustain crop productivity and soil health in increasingly water-limited environments.
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@article {pmid41966784,
year = {2026},
author = {Haider, S and Munyaneza, V and Zhang, W and Ren, L and Song, H and Ahmad, IA and Mehran, M and Liu, S and Xu, F and Kant, S and Yang, J and Yang, C and Ding, G},
title = {Plant-microbe interactions under drought stress: Unlocking new pathways for sustainable agricultural resilience.},
journal = {Microbiological research},
volume = {309},
number = {},
pages = {128516},
doi = {10.1016/j.micres.2026.128516},
pmid = {41966784},
issn = {1618-0623},
abstract = {Drought stress is among the most significant abiotic constraints on agricultural productivity, a challenge that is intensifying under climate change. Translating the microbial mechanisms under drought into a holistic and systemic strategy remains largely unexplored. This review addresses this gap by advancing the plant-microbiome holobiont framework, which integrates such mechanisms into a unified approach to enhance drought tolerance. The framework constitutes four interrelated pillars which include (1) microbes induced modulation of host physiology and molecular responses through nutrient cycling, phytohormone regulation, osmotic adjustment, biofilm formation, and priming of systemic stress resistance, (2) Root exudates as signal-rich mediators that dynamically shape rhizosphere microbial communities and facilitate the recruitment and activity of drought-adaptive microbes and (3) the evaluation of emerging technological interventions to manipulate the plant-microbe dialogue. These interventions include genetic engineering which enables targeted modification of root exudation patterns and stress-responsive genes to enhance beneficial microbial recruitment, SynComs combining functionally complementary microbes to improve water-use efficiency and nutrient uptake, and mGWAS studies to identify plant genetic loci influencing microbiome composition and interactions, supporting the breeding of cultivars that preferentially associate with beneficial microbes under drought conditions. While (4) modulation of carbon pool, nutrient uptake and resistance priming upon leveraging microbial functions. Explicitly integrating these pillars, framework offers a practical roadmap for transitioning from mechanistic knowledge to targeted advancement of resilient agroecosystems. Harnessing the plant-microbiome holobiont through this integrated approach offers an innovative and sustainable pathway to sustain crop productivity and soil health in increasingly water-limited environments.},
}
RevDate: 2026-04-12
Protocol for the assessment of the impact of mycotoxins and glyphosate residues on the gut microbiome and resistome of European fallow deer.
STAR protocols, 7(2):104498 pii:S2666-1667(26)00151-6 [Epub ahead of print].
Here, we present a protocol to describe the bacteriome of the intestinal content of toxin-exposed fallow deer. We describe steps for measuring fecal mycotoxin (deoxynivalenol, zearalenone, fumonisin B1, and aflatoxin B1) levels using liquid chromatography-mass spectrometry, as well as serum glyphosate. We then detail a short-read shotgun DNA sequencing-based bioinformatic pipeline for the toxin level-associated analysis of the bacteriome and resistome and the construction of metagenome-assembled bacterial genomes. This protocol has potential applications in further toxin level-associated metagenome studies. For complete details on the use and execution of this protocol, please refer to Tóth et al.[1].
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@article {pmid41966829,
year = {2026},
author = {Tóth, AG and Paholcsek, M and Solymosi, N and Stágel, A and Gömbös, P and Posta, K and Lakatos, I and Nagy, SÁ and Ferenczi, S and Szőke, Z},
title = {Protocol for the assessment of the impact of mycotoxins and glyphosate residues on the gut microbiome and resistome of European fallow deer.},
journal = {STAR protocols},
volume = {7},
number = {2},
pages = {104498},
doi = {10.1016/j.xpro.2026.104498},
pmid = {41966829},
issn = {2666-1667},
abstract = {Here, we present a protocol to describe the bacteriome of the intestinal content of toxin-exposed fallow deer. We describe steps for measuring fecal mycotoxin (deoxynivalenol, zearalenone, fumonisin B1, and aflatoxin B1) levels using liquid chromatography-mass spectrometry, as well as serum glyphosate. We then detail a short-read shotgun DNA sequencing-based bioinformatic pipeline for the toxin level-associated analysis of the bacteriome and resistome and the construction of metagenome-assembled bacterial genomes. This protocol has potential applications in further toxin level-associated metagenome studies. For complete details on the use and execution of this protocol, please refer to Tóth et al.[1].},
}
RevDate: 2026-04-12
Disentangling the gut microbiome and inflammation in inflammatory bowel diseases: longitudinal observations from the IBSEN III study.
Inflammatory bowel diseases pii:8650432 [Epub ahead of print].
BACKGROUND AND AIM: Despite the well-established involvement of the gut microbiome in inflammatory bowel disease (IBD), less is known about how the gut microbiome changes over time and how it varies with clinical disease activity and fecal calprotectin (f-calprotectin). To address this gap, we utilized samples from the population-based inception cohort of the Inflammatory Bowel Disease in South-Eastern Norway III (IBSEN III) study.
METHODS: Data and stool samples from study participants with IBD and symptomatic controls were collected at diagnosis and after 3, 6, and 12 months. Microbiome profiling of stool samples was performed targeting the V3-V4 region of the 16S rRNA gene, and a consensus-based approach of mixed models was employed for the longitudinal microbiome analysis.
RESULTS: We included 1251 samples from 744 patients with ulcerative colitis, 618 samples from 356 patients with Crohn' s disease and 266 samples from 164 symptomatic non-IBD controls. In the IBD population, we observed that levels of f-calprotectin decreased over time, as did the patient-reported disease activity (P < .001). Distinct changes in the gut microbiome of IBD patients were observed throughout the first year, such as increased alpha diversity (P < .001) and significant taxonomic changes.Notably, there was no covariation between the changes in alpha diversity and f-calprotectin or symptom score.
CONCLUSION: The gut microbiome during the first year after IBD diagnosis showed changes that paralleled inflammation and clinical disease activity, albeit without covariation, suggesting that there may be a disease-driving impact of gut microbiome independent of inflammation and inflammation-driven symptoms.
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@article {pmid41966990,
year = {2026},
author = {Maseng, MG and Hansen, SH and Grännö, O and Bang, C and Lund, C and Huppertz-Hauss, G and Perminow, G and Valeur, J and Bengtson, MB and Opheim, R and Boyar, R and Frigstad, SO and Aabrekk, TB and Detlie, TE and Kristensen, VA and Strande, V and Hovde, Ø and Asak, Ø and Franke, A and Halfvarsson, J and Høivik, ML and Hov, JR},
title = {Disentangling the gut microbiome and inflammation in inflammatory bowel diseases: longitudinal observations from the IBSEN III study.},
journal = {Inflammatory bowel diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/ibd/izag051},
pmid = {41966990},
issn = {1536-4844},
support = {//Takeda Pharmaceuticals, Pfizer, Ferring Pharmaceuticals, Tillotts Pharma, Foundation Dam, and the Norwegian South-Eastern Health Authorities/ ; 90569 to J.H.//NordForsk/ ; 2019-01185 to JH//Vinnova/ ; 2988039 to MLH//Research Council of Norway/ ; No: 2020066//Regional Health Authorities South-Eastern Norway/ ; //DFG Excellence Cluster 2167 "Precision Medicine in Chronic Inflammation" (PMI) and the DFG Research Unit 5042 "miTarget"/ ; no: 327634//Research Council of Norway/ ; },
abstract = {BACKGROUND AND AIM: Despite the well-established involvement of the gut microbiome in inflammatory bowel disease (IBD), less is known about how the gut microbiome changes over time and how it varies with clinical disease activity and fecal calprotectin (f-calprotectin). To address this gap, we utilized samples from the population-based inception cohort of the Inflammatory Bowel Disease in South-Eastern Norway III (IBSEN III) study.
METHODS: Data and stool samples from study participants with IBD and symptomatic controls were collected at diagnosis and after 3, 6, and 12 months. Microbiome profiling of stool samples was performed targeting the V3-V4 region of the 16S rRNA gene, and a consensus-based approach of mixed models was employed for the longitudinal microbiome analysis.
RESULTS: We included 1251 samples from 744 patients with ulcerative colitis, 618 samples from 356 patients with Crohn' s disease and 266 samples from 164 symptomatic non-IBD controls. In the IBD population, we observed that levels of f-calprotectin decreased over time, as did the patient-reported disease activity (P < .001). Distinct changes in the gut microbiome of IBD patients were observed throughout the first year, such as increased alpha diversity (P < .001) and significant taxonomic changes.Notably, there was no covariation between the changes in alpha diversity and f-calprotectin or symptom score.
CONCLUSION: The gut microbiome during the first year after IBD diagnosis showed changes that paralleled inflammation and clinical disease activity, albeit without covariation, suggesting that there may be a disease-driving impact of gut microbiome independent of inflammation and inflammation-driven symptoms.},
}
RevDate: 2026-04-12
Immunotherapy with Guts: A review of microbial therapeutic adjuncts for immunotherapy in solid tumors.
The oncologist pii:8650660 [Epub ahead of print].
BACKGROUND: Immunotherapy has transformed the management of some solid tumor types, but its impact has been limited to the subset of cancer patients who have 'hot' or immunogenic tumors. Numerous studies are based on strategies for turning 'cold', or immune-unresponsive, tumors into a 'hot' state. The gut microbiome has emerged as a potential co-therapy for standard immune checkpoint inhibitors (ICIs) to achieve this goal. Recent approaches have primarily focused on the use of probiotics, microbial consortia, or fecal microbiota transplantations in combination with anti-PD-1 and anti-CTLA-4 antibodies.
METHODS: This review highlights the current status of microbiome modulation and its potential impact on clinical practice. Probiotics, such as CMB588, and microbial consortia have been selected following successful preclinical studies. These taxa may initiate T cell infiltration and are commonly found in the microbial profiles of individuals who have previously responded to immunotherapy.
RESULTS: Several trials with these therapies have had success and noted minimal safety concerns compared to monotherapy treatments. Fecal microbiota transplantation (FMT), originally used to treat Clostridium difficile infections, has also demonstrated promising results in increasing immune checkpoint inhibitor (ICI) efficacy across various cancer types and is being utilized in multiple ongoing trials.
CONCLUSION: These therapeutics form the foundation for exciting possibilities in immunotherapy and improving patient outcomes.
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@article {pmid41967083,
year = {2026},
author = {Pum, K and Lou, E and Goffredo, P and Jahansouz, C and Subramanian, S and Prakash, A},
title = {Immunotherapy with Guts: A review of microbial therapeutic adjuncts for immunotherapy in solid tumors.},
journal = {The oncologist},
volume = {},
number = {},
pages = {},
doi = {10.1093/oncolo/oyag131},
pmid = {41967083},
issn = {1549-490X},
abstract = {BACKGROUND: Immunotherapy has transformed the management of some solid tumor types, but its impact has been limited to the subset of cancer patients who have 'hot' or immunogenic tumors. Numerous studies are based on strategies for turning 'cold', or immune-unresponsive, tumors into a 'hot' state. The gut microbiome has emerged as a potential co-therapy for standard immune checkpoint inhibitors (ICIs) to achieve this goal. Recent approaches have primarily focused on the use of probiotics, microbial consortia, or fecal microbiota transplantations in combination with anti-PD-1 and anti-CTLA-4 antibodies.
METHODS: This review highlights the current status of microbiome modulation and its potential impact on clinical practice. Probiotics, such as CMB588, and microbial consortia have been selected following successful preclinical studies. These taxa may initiate T cell infiltration and are commonly found in the microbial profiles of individuals who have previously responded to immunotherapy.
RESULTS: Several trials with these therapies have had success and noted minimal safety concerns compared to monotherapy treatments. Fecal microbiota transplantation (FMT), originally used to treat Clostridium difficile infections, has also demonstrated promising results in increasing immune checkpoint inhibitor (ICI) efficacy across various cancer types and is being utilized in multiple ongoing trials.
CONCLUSION: These therapeutics form the foundation for exciting possibilities in immunotherapy and improving patient outcomes.},
}
RevDate: 2026-04-12
GC-MS method development and validation for the determination of Short Chain Fatty Acids in human feces.
Journal of pharmaceutical and biomedical analysis, 277:117488 pii:S0731-7085(26)00156-1 [Epub ahead of print].
Short Chain Fatty Acids (SCFAs), the end products of microbial fermentation of dietary fibers, appear to be key mediators of the beneficial effects elicited by the gut microbiome and have been shown to exert multiple effects on metabolism. In this study, we developed and validated a sensitive, accurate, and reproducible GC-MS method for the simultaneous quantification of SCFAs (Acetic acid (C2), propionic acid (C3), butyric acid (C4), isobutyric acid and isovaleric acid) in human feces. Sample preparation was simplified while maintaining robustness, following systematic evaluation of homogenization, extraction solvents, and acidification conditions. The optimized method demonstrated high analytical performance, with limits of detection ranging from 0.01 to 0.52 μmol/g and good precision and accuracy in accordance with FDA and EMA bioanalytical guidelines Stability studies revealed that SCFAs remain stable in acidified fecal samples for up to 10 days without cold-chain requirements, while -80 °C storage was optimal for long-term preservation and 4 °C suitable for short-term handling. The applicability of the method was confirmed through analysis of samples collected from healthy volunteers. Overall, the developed approach provides a practical, high-throughput, and scalable tool for SCFA analysis, supporting applications in clinical research, metabolomics, and large-scale microbiome studies.
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@article {pmid41967141,
year = {2026},
author = {Vasiliki, G and Konstantina, F and Olga, B and Georgios, T and Helen, G and Chistina, V},
title = {GC-MS method development and validation for the determination of Short Chain Fatty Acids in human feces.},
journal = {Journal of pharmaceutical and biomedical analysis},
volume = {277},
number = {},
pages = {117488},
doi = {10.1016/j.jpba.2026.117488},
pmid = {41967141},
issn = {1873-264X},
abstract = {Short Chain Fatty Acids (SCFAs), the end products of microbial fermentation of dietary fibers, appear to be key mediators of the beneficial effects elicited by the gut microbiome and have been shown to exert multiple effects on metabolism. In this study, we developed and validated a sensitive, accurate, and reproducible GC-MS method for the simultaneous quantification of SCFAs (Acetic acid (C2), propionic acid (C3), butyric acid (C4), isobutyric acid and isovaleric acid) in human feces. Sample preparation was simplified while maintaining robustness, following systematic evaluation of homogenization, extraction solvents, and acidification conditions. The optimized method demonstrated high analytical performance, with limits of detection ranging from 0.01 to 0.52 μmol/g and good precision and accuracy in accordance with FDA and EMA bioanalytical guidelines Stability studies revealed that SCFAs remain stable in acidified fecal samples for up to 10 days without cold-chain requirements, while -80 °C storage was optimal for long-term preservation and 4 °C suitable for short-term handling. The applicability of the method was confirmed through analysis of samples collected from healthy volunteers. Overall, the developed approach provides a practical, high-throughput, and scalable tool for SCFA analysis, supporting applications in clinical research, metabolomics, and large-scale microbiome studies.},
}
RevDate: 2026-04-12
Microbiome and multi-omics insights into sustainable aquaculture: A triennial systematic review.
Comparative biochemistry and physiology. Part D, Genomics & proteomics, 59:101830 pii:S1744-117X(26)00089-4 [Epub ahead of print].
Aquaculture is the fastest-growing food production sector, yet intensive practices drive disease outbreaks, antibiotic resistance, and environmental degradation, threatening long-term sustainability. The aquaculture microbiome, encompassing host-associated and environmental microbial communities, regulates nutrient cycling, pathogen suppression, immunity, and overall system resilience. This triennial systematic review (2023-2025), conducted according to PRISMA guidelines, synthesized 19 highly relevant peer-reviewed studies that applied multi-omics approaches (metagenomics, transcriptomics, metabolomics, SNP genotyping, and their integration) to aquaculture microbiomes across shrimp, finfish, and hybrid species. The studies collectively revealed diverse host-microbe-metabolite interactions underpinning growth, immunity, and disease resistance, with representative examples including microbial-metabolite-host signaling axes and microbiome-mediated immune modulation, as seen in Salinivibrio-AMP-mTOR axis, EHP-resistant shrimp via metabolic reprogramming and stable microbiota, and Bacillus-mediated diglyceride production. Beneficial taxa such as Cetobacterium and Salinivibrio, heritable microbiome traits, and sustainable interventions including insect-meal feeds, phytogenic additives, and organic copper consistently improved growth, immunity, and microbial stability while reducing dysbiosis under stress. Environmental stressors and pathogens induced reproducible shifts in microbial diversity, functional pathways, and host metabolism. These findings demonstrate that multi-omics integration is transforming aquaculture into a precision discipline, enabling microbiome-informed selective breeding, targeted probiotics, and environmentally sound nutrition. To translate these insights into practice, future research must emphasize functional validation, machine learning-driven predictive models, and ecosystem-level assessments to achieve resilient, antibiotic-reduced, and sustainable aquaculture systems.
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@article {pmid41967167,
year = {2026},
author = {Okoye, CO and Okoye, KC and Ezenwanne, BC and Olalowo, OO and Andong, FA and Echude, D and Chukwudozie, KI and Emencheta, SC and Ezeonyejiaku, CD and Ikele, CB},
title = {Microbiome and multi-omics insights into sustainable aquaculture: A triennial systematic review.},
journal = {Comparative biochemistry and physiology. Part D, Genomics & proteomics},
volume = {59},
number = {},
pages = {101830},
doi = {10.1016/j.cbd.2026.101830},
pmid = {41967167},
issn = {1878-0407},
abstract = {Aquaculture is the fastest-growing food production sector, yet intensive practices drive disease outbreaks, antibiotic resistance, and environmental degradation, threatening long-term sustainability. The aquaculture microbiome, encompassing host-associated and environmental microbial communities, regulates nutrient cycling, pathogen suppression, immunity, and overall system resilience. This triennial systematic review (2023-2025), conducted according to PRISMA guidelines, synthesized 19 highly relevant peer-reviewed studies that applied multi-omics approaches (metagenomics, transcriptomics, metabolomics, SNP genotyping, and their integration) to aquaculture microbiomes across shrimp, finfish, and hybrid species. The studies collectively revealed diverse host-microbe-metabolite interactions underpinning growth, immunity, and disease resistance, with representative examples including microbial-metabolite-host signaling axes and microbiome-mediated immune modulation, as seen in Salinivibrio-AMP-mTOR axis, EHP-resistant shrimp via metabolic reprogramming and stable microbiota, and Bacillus-mediated diglyceride production. Beneficial taxa such as Cetobacterium and Salinivibrio, heritable microbiome traits, and sustainable interventions including insect-meal feeds, phytogenic additives, and organic copper consistently improved growth, immunity, and microbial stability while reducing dysbiosis under stress. Environmental stressors and pathogens induced reproducible shifts in microbial diversity, functional pathways, and host metabolism. These findings demonstrate that multi-omics integration is transforming aquaculture into a precision discipline, enabling microbiome-informed selective breeding, targeted probiotics, and environmentally sound nutrition. To translate these insights into practice, future research must emphasize functional validation, machine learning-driven predictive models, and ecosystem-level assessments to achieve resilient, antibiotic-reduced, and sustainable aquaculture systems.},
}
RevDate: 2026-04-12
Cross-niche metabolite-microbiome interactions orchestrate systemic soybean resistance to Fusarium root rot.
The ISME journal pii:8650985 [Epub ahead of print].
Fusarium root rot, predominantly caused by Fusarium falciforme, poses a significant threat to soybean productivity globally. Microbiome-based strategies offer sustainable alternatives, but the mechanisms underlying multi-niche interactions remain elusive. Here, we found that a tolerant soybean cultivar (GXD2) coordinates spatially resolved metabolite signals to recruit beneficial microbes across the rhizosphere, root endosphere, and leaf endosphere. Specifically, formononetin and maltol selectively enrich Bacillus and Massilia in the rhizosphere; arctigenin and isovanillic acid recruit Bacillus and Streptomyces to the root endosphere; and flavonoids such as diosmetin attract Penicillium and Aspergillus to the leaf endosphere. Leveraging these interactions, we constructed different types of synthetic communities (SynComs) via top-down (host-selected taxa) and bottom-up (antagonist-based) strategies. Both SynComs suppressed root rot in susceptible cultivars, with foliar application of top-down SynComs significantly enhancing shoot growth. Transcriptomics revealed distinct modes of actions, that top-down SynComs activated mitogen-activated protein kinase (MAPK)-linked terpenoid and flavonoid pathways, whereas bottom-up SynComs primarily modulated host carbon-nitrogen allocation, effectively limiting pathogen resources. Our findings unveil a "metabolite-mediated, multi-niche collaborative defense" model, presenting a robust framework for microbiome-based disease management and paving the way toward sustainable crop protection strategies.
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@article {pmid41967481,
year = {2026},
author = {Liu, Q and Cheng, L and Zhang, E and Ling, L and Tan, W and Liang, S and Shu, C and Ma, Q and Zhao, S and Wei, J and Wang, Y and Nian, H and Cheng, Y and Lian, T},
title = {Cross-niche metabolite-microbiome interactions orchestrate systemic soybean resistance to Fusarium root rot.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag080},
pmid = {41967481},
issn = {1751-7370},
abstract = {Fusarium root rot, predominantly caused by Fusarium falciforme, poses a significant threat to soybean productivity globally. Microbiome-based strategies offer sustainable alternatives, but the mechanisms underlying multi-niche interactions remain elusive. Here, we found that a tolerant soybean cultivar (GXD2) coordinates spatially resolved metabolite signals to recruit beneficial microbes across the rhizosphere, root endosphere, and leaf endosphere. Specifically, formononetin and maltol selectively enrich Bacillus and Massilia in the rhizosphere; arctigenin and isovanillic acid recruit Bacillus and Streptomyces to the root endosphere; and flavonoids such as diosmetin attract Penicillium and Aspergillus to the leaf endosphere. Leveraging these interactions, we constructed different types of synthetic communities (SynComs) via top-down (host-selected taxa) and bottom-up (antagonist-based) strategies. Both SynComs suppressed root rot in susceptible cultivars, with foliar application of top-down SynComs significantly enhancing shoot growth. Transcriptomics revealed distinct modes of actions, that top-down SynComs activated mitogen-activated protein kinase (MAPK)-linked terpenoid and flavonoid pathways, whereas bottom-up SynComs primarily modulated host carbon-nitrogen allocation, effectively limiting pathogen resources. Our findings unveil a "metabolite-mediated, multi-niche collaborative defense" model, presenting a robust framework for microbiome-based disease management and paving the way toward sustainable crop protection strategies.},
}
RevDate: 2026-04-12
Microbiome assembly statistics toward ecosystem-scale insights, forecasting, and management.
The ISME journal pii:8650967 [Epub ahead of print].
Microbiomes are increasingly recognized as key to addressing global challenges in health and sustainability, as they can provide emergent biological functions unattainable with single microbial species. However, microbial communities occasionally undergo abrupt shifts in species composition despite their intrinsic steadiness, making it difficult to maintain highly functional microbiome states. Here, we outline emerging statistical frameworks that integrate ecological stability theory with empirical analyses of microbiome structure and function. Approaches inspired by the concept of "stability landscapes" now enable inference of how the relationship between community structure and assembly potential changes along environmental gradients. Such empirical analyses offer bird's-eye perspectives for maintaining or restoring community states with desirable microbiome functions. Moreover, identifying the attractors of microbiome dynamics facilitates forecasting of abrupt transitions into dysfunctional states (i.e., dysbiosis). Bridging classic ecological theory and empirical microbiome analyses will deepen our understanding of the principles governing species-rich community assembly, expanding the scope of microbiome-based solutions across medical, industrial, agricultural, and environmental sciences.
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@article {pmid41967489,
year = {2026},
author = {Toju, H and Suzuki, K and Sánchez-Pinillos, M and Shima, G and Kageyama, T and Hayashi, I and Noguchi, M and Fujita, H and Goto, Y and Nakaoka, S and Ushio, M and Ichihashi, Y and Fricke, WF and Mizumoto, K and Takayasu, L and Suda, W and Takayasu, M and Yamamichi, M and Weckwerth, W},
title = {Microbiome assembly statistics toward ecosystem-scale insights, forecasting, and management.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag085},
pmid = {41967489},
issn = {1751-7370},
abstract = {Microbiomes are increasingly recognized as key to addressing global challenges in health and sustainability, as they can provide emergent biological functions unattainable with single microbial species. However, microbial communities occasionally undergo abrupt shifts in species composition despite their intrinsic steadiness, making it difficult to maintain highly functional microbiome states. Here, we outline emerging statistical frameworks that integrate ecological stability theory with empirical analyses of microbiome structure and function. Approaches inspired by the concept of "stability landscapes" now enable inference of how the relationship between community structure and assembly potential changes along environmental gradients. Such empirical analyses offer bird's-eye perspectives for maintaining or restoring community states with desirable microbiome functions. Moreover, identifying the attractors of microbiome dynamics facilitates forecasting of abrupt transitions into dysfunctional states (i.e., dysbiosis). Bridging classic ecological theory and empirical microbiome analyses will deepen our understanding of the principles governing species-rich community assembly, expanding the scope of microbiome-based solutions across medical, industrial, agricultural, and environmental sciences.},
}
RevDate: 2026-04-12
Small intestinal microbiome, the underrated maestro of SIMO disease.
FEMS microbiology reviews pii:8651073 [Epub ahead of print].
Small intestinal microbial overgrowth (SIMO) results from a breakdown in the delicate equilibrium between luminal environment, gut motility, and microbial ecology. Despite extensive research, these factors have largely been investigated as separate entities, with limited integrative insights into their interplay. This review is the first comprehensive synthesis of physicochemical, mechanical, and microbial parameters shaping SIMO pathogenesis. By reviewing both clinical and experimental data, we reveal how alterations in pH, transit time, digestive secretion dynamics, bile acid composition and impaired intestinal absorption collectively reshape microbial load, diversity, and metabolic output, establishing a self-perpetuating loop of dysfunction. We further discuss the limitations of current diagnostic tools and the transformative potential of emerging approaches, from sampling capsules enabling molecular analyses, to in vitro models simulating human small intestinal ecosystem. This integrative perspective shifts the paradigm from a microbe-centered to an ecosystem-based understanding of SIMO, outlining key challenges and opportunities for personalized diagnostics, mechanistic research, and microbiota-targeted next-generation therapeutics including pre-, pro-, postbiotics and faecal transplantation.
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@article {pmid41967501,
year = {2026},
author = {Deschamps, C and Tronel, A and Bailly, E and Tanfede, MRS and Gilibert, S and Denis, S and Soranzo, T and Van De Wiele, T and Marinelli, L and Blanquet-Diot, S},
title = {Small intestinal microbiome, the underrated maestro of SIMO disease.},
journal = {FEMS microbiology reviews},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsre/fuag016},
pmid = {41967501},
issn = {1574-6976},
abstract = {Small intestinal microbial overgrowth (SIMO) results from a breakdown in the delicate equilibrium between luminal environment, gut motility, and microbial ecology. Despite extensive research, these factors have largely been investigated as separate entities, with limited integrative insights into their interplay. This review is the first comprehensive synthesis of physicochemical, mechanical, and microbial parameters shaping SIMO pathogenesis. By reviewing both clinical and experimental data, we reveal how alterations in pH, transit time, digestive secretion dynamics, bile acid composition and impaired intestinal absorption collectively reshape microbial load, diversity, and metabolic output, establishing a self-perpetuating loop of dysfunction. We further discuss the limitations of current diagnostic tools and the transformative potential of emerging approaches, from sampling capsules enabling molecular analyses, to in vitro models simulating human small intestinal ecosystem. This integrative perspective shifts the paradigm from a microbe-centered to an ecosystem-based understanding of SIMO, outlining key challenges and opportunities for personalized diagnostics, mechanistic research, and microbiota-targeted next-generation therapeutics including pre-, pro-, postbiotics and faecal transplantation.},
}
RevDate: 2026-04-12
Models of neuroprotection in Parkinson's disease: Exploring cellular, molecular, and microenvironmental targets.
Experimental neurology pii:S0014-4886(26)00127-5 [Epub ahead of print].
Parkinson's disease (PD), the second most common neurodegenerative disorder in the world, is characterized by the chronic and progressive death of dopaminergic neurons. Several intraneuronal mechanisms, as well as microenvironmental factors, are involved in neurodegeneration. Currently, the care for PD patients is focused on controlling motor symptoms. Designing interventions that help stop neurodegeneration remains a major challenge in PD management. This review analyzes various neuroprotective approaches that could promote neuronal survival. We explore innovative strategies, such as gene therapy, the use of exosomes, microbiome modulation, and vagus nerve stimulation. The study emphasizes that these interventions could prevent cellular damage and potentially restore neuronal function. Furthermore, the study emphasizes the importance of understanding the underlying molecular mechanisms in order to develop combined therapies. The research considers critical factors, such as suppressing neuroinflammation and the role of sex hormones in neuron survival. Thus, this review focuses on the molecular mechanisms of neuroprotective strategies under investigation to aid in developing new therapeutic interventions.
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@article {pmid41967563,
year = {2026},
author = {Álvarez-Luquín, DD and González-Fernández, RR and Ichikawa-Escamilla, E and Torres-Velasco, ME and Martínez-Martínez, E and Arce-Sillas, A and Juárez-Vaquera, VH and Miranda-Narvaez, CL and Hernández, M and Adalid-Peralta, L},
title = {Models of neuroprotection in Parkinson's disease: Exploring cellular, molecular, and microenvironmental targets.},
journal = {Experimental neurology},
volume = {},
number = {},
pages = {115764},
doi = {10.1016/j.expneurol.2026.115764},
pmid = {41967563},
issn = {1090-2430},
abstract = {Parkinson's disease (PD), the second most common neurodegenerative disorder in the world, is characterized by the chronic and progressive death of dopaminergic neurons. Several intraneuronal mechanisms, as well as microenvironmental factors, are involved in neurodegeneration. Currently, the care for PD patients is focused on controlling motor symptoms. Designing interventions that help stop neurodegeneration remains a major challenge in PD management. This review analyzes various neuroprotective approaches that could promote neuronal survival. We explore innovative strategies, such as gene therapy, the use of exosomes, microbiome modulation, and vagus nerve stimulation. The study emphasizes that these interventions could prevent cellular damage and potentially restore neuronal function. Furthermore, the study emphasizes the importance of understanding the underlying molecular mechanisms in order to develop combined therapies. The research considers critical factors, such as suppressing neuroinflammation and the role of sex hormones in neuron survival. Thus, this review focuses on the molecular mechanisms of neuroprotective strategies under investigation to aid in developing new therapeutic interventions.},
}
RevDate: 2026-04-13
Nitrogen-Containing Steroidal Alkaloids and the Gut Microbiome: A Steroid-Xenobiotic Axis Perspective for Drug Discovery and Therapeutic Modulation.
Steroids, 231-232:109789 pii:S0039-128X(26)00051-6 [Epub ahead of print].
Drug metabolism has traditionally emphasized hepatic pathways; however, the gut microbiome introduces a parallel system of biochemical modification that profoundly affects drug efficacy, safety, and variability. This review integrates the emerging steroid-xenobiotic-microbiome axis, emphasizing nitrogen-containing steroidal alkaloids (NSAs) as pivotal modulators. These compounds, combining a hydrophobic steroidal scaffold with nitrogen-based polarity, exhibit unique bioactivities through microbial biotransformation. Gut microbes enzymatically modify steroids and xenobiotics via reduction, deconjugation, and oxidation, shaping pharmacokinetics and receptor signaling. Conversely, steroidal scaffolds regulate microbial enzyme expression, forming reciprocal metabolic feedback. Case studies on digoxin, solanine, and veratramine illustrate this interplay. Understanding how nitrogen incorporation governs structure activity relationships and microbial interactions offers a new avenues for precision pharmacology, biomarker discovery, and rational drug design. This integrated perspective bridges medicinal chemistry, microbiome science, and steroid pharmacology to develop next generation therapeutics guided by host-microbe metabolic crosstalk.
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@article {pmid41967658,
year = {2026},
author = {Ganamurali, N and Sabarathinam, S and Narasimhan, MK and S, ES},
title = {Nitrogen-Containing Steroidal Alkaloids and the Gut Microbiome: A Steroid-Xenobiotic Axis Perspective for Drug Discovery and Therapeutic Modulation.},
journal = {Steroids},
volume = {231-232},
number = {},
pages = {109789},
doi = {10.1016/j.steroids.2026.109789},
pmid = {41967658},
issn = {1878-5867},
abstract = {Drug metabolism has traditionally emphasized hepatic pathways; however, the gut microbiome introduces a parallel system of biochemical modification that profoundly affects drug efficacy, safety, and variability. This review integrates the emerging steroid-xenobiotic-microbiome axis, emphasizing nitrogen-containing steroidal alkaloids (NSAs) as pivotal modulators. These compounds, combining a hydrophobic steroidal scaffold with nitrogen-based polarity, exhibit unique bioactivities through microbial biotransformation. Gut microbes enzymatically modify steroids and xenobiotics via reduction, deconjugation, and oxidation, shaping pharmacokinetics and receptor signaling. Conversely, steroidal scaffolds regulate microbial enzyme expression, forming reciprocal metabolic feedback. Case studies on digoxin, solanine, and veratramine illustrate this interplay. Understanding how nitrogen incorporation governs structure activity relationships and microbial interactions offers a new avenues for precision pharmacology, biomarker discovery, and rational drug design. This integrated perspective bridges medicinal chemistry, microbiome science, and steroid pharmacology to develop next generation therapeutics guided by host-microbe metabolic crosstalk.},
}
RevDate: 2026-04-12
DTH: A nonparametric test for homogeneity of multivariate dispersions.
Bioinformatics (Oxford, England) pii:8651108 [Epub ahead of print].
MOTIVATION: Testing for differences in within-group dispersion is a fundamental problem in multivariate data analysis, with direct implications for interpreting group structure and validating statistical assumptions of other analysis such as ANOVA. Existing methods typically construct test statistics either based on the distance of each observation from the group center or on the mean of pairwise dissimilarities among observations within a group. Both approaches can fail when the mean within-group distance is similar across groups but the distributions of the within-group distances differ. This issue is particularly relevant in high-dimensional microbiome data, where outliers and overdispersion can distort the performance of mean-dissimilarity-based tests.
RESULTS: We introduce the non-parametric Distance-based Test for Homogeneity (DTH), which measures dispersion of a group by computing within-group dissimilarity. Difference in dispersion across groups is tested by comparing the distributions of the within-group dissimilarity across different groups. A combination of Kolmogorov-Smirnov and Wasserstein distances are used to construct the difference between the distributions. For more than two groups, pairwise group tests are combined using a permutation-based p-value. Through simulations, we show that our method has higher power than existing tests for homogeneity in certain situations and comparable power in others. For continuous covariates, we offer an heuristic extension of DTH that showed good performance in simulations.
The DTH package, along with the code for reproducing all simulations, analyses, and an accompanying vignette, is available at https://github.com/asmita112358/DTH.
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@article {pmid41967847,
year = {2026},
author = {Roy, A and Lu, J and Satten, GA and Zhao, N},
title = {DTH: A nonparametric test for homogeneity of multivariate dispersions.},
journal = {Bioinformatics (Oxford, England)},
volume = {},
number = {},
pages = {},
doi = {10.1093/bioinformatics/btag178},
pmid = {41967847},
issn = {1367-4811},
abstract = {MOTIVATION: Testing for differences in within-group dispersion is a fundamental problem in multivariate data analysis, with direct implications for interpreting group structure and validating statistical assumptions of other analysis such as ANOVA. Existing methods typically construct test statistics either based on the distance of each observation from the group center or on the mean of pairwise dissimilarities among observations within a group. Both approaches can fail when the mean within-group distance is similar across groups but the distributions of the within-group distances differ. This issue is particularly relevant in high-dimensional microbiome data, where outliers and overdispersion can distort the performance of mean-dissimilarity-based tests.
RESULTS: We introduce the non-parametric Distance-based Test for Homogeneity (DTH), which measures dispersion of a group by computing within-group dissimilarity. Difference in dispersion across groups is tested by comparing the distributions of the within-group dissimilarity across different groups. A combination of Kolmogorov-Smirnov and Wasserstein distances are used to construct the difference between the distributions. For more than two groups, pairwise group tests are combined using a permutation-based p-value. Through simulations, we show that our method has higher power than existing tests for homogeneity in certain situations and comparable power in others. For continuous covariates, we offer an heuristic extension of DTH that showed good performance in simulations.
The DTH package, along with the code for reproducing all simulations, analyses, and an accompanying vignette, is available at https://github.com/asmita112358/DTH.},
}
RevDate: 2026-04-12
Response to letter to the editor regarding methodological refinement and microbiome-centric endpoints.
Additional Links: PMID-41968003
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@article {pmid41968003,
year = {2026},
author = {Kalia, S and Nath, P and Anand, AC and Mallick, B and Praharaj, D and Panigrahi, SC and Sahu, SK and Giri, S and Acharya, SK},
title = {Response to letter to the editor regarding methodological refinement and microbiome-centric endpoints.},
journal = {Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.pan.2026.04.013},
pmid = {41968003},
issn = {1424-3911},
}
RevDate: 2026-04-12
Dietary inulin modulates pork quality and systemic health via gut microbiome and metabolome changes in finishing pigs.
Animal microbiome pii:10.1186/s42523-026-00566-5 [Epub ahead of print].
Additional Links: PMID-41968347
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@article {pmid41968347,
year = {2026},
author = {Wang, Y and Ko, K and Kim, E and Kačániová, M and Lee, Y and Zhang, G},
title = {Dietary inulin modulates pork quality and systemic health via gut microbiome and metabolome changes in finishing pigs.},
journal = {Animal microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s42523-026-00566-5},
pmid = {41968347},
issn = {2524-4671},
support = {2019YFE0107700, NRF-2019K1A3A1A20081146//National Key R&D Program of China-Korea cooperative project/ ; WRS2023075//the key project for foreign experts of Shandong Province/ ; SDAIT-23-05//the Forage Industrial Innovation Team Project/ ; 2022TZXD0018//the Key R&D Program of Shandong Province/ ; NRF-2020R1A2C2004144, RS-2024-00334577//the National Research Foundation Grant of Korea/ ; RS-2024-00410255//Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Education/ ; },
}
RevDate: 2026-04-12
Rhizobacteria-Mediated Plant Resilience to Abiotic Stresses: Drought, Salinity, and Heat.
Plant, cell & environment [Epub ahead of print].
The frequent occurrence of drought, salinity and heat disasters due to global climate change has become a problem that cannot be ignored and seriously restricts food security and sustainable agricultural development. The role of rhizobacteria in the response of plants to abiotic stress has an important guiding significance in improving plant growth. This paper summarizes the response of plant rhizosphere microbial communities to abiotic stress, analyzes the mechanism by which rhizosphere-related bacteria assist plants to resist abiotic stress, and expounds on the interaction between soil physical and chemical properties, the plant root metabolome, and the rhizosphere microbiome under abiotic stress. This review systematically summarizes the core roles and mechanisms of rhizobacteria in plants' defense against abiotic stress. Stress reshapes the rhizosphere microecology, with drought enriching Firmicutes and Actinobacteria, salt stress increasing Bacteroidetes abundance, and heat stress expanding the dominance of thermotolerant bacteria. Microbial diversity and network structure undergo adaptive reorganization. Streptomyces and Bacillus, as the twin stars aiding plants in enhancing stress resistance, provide medium- to long-term protection through rich secondary metabolites and mycelial networks, while Bacillus achieves acute responses via rapid spore germination, signal induction, and nutrient competition. Rhizobacteria improve soil nutrient availability by regulating carbon, nitrogen, and phosphorus cycles, secreting organic acids and enzymes, and induce plant osmotic adjustment, antioxidant, and anti-ethylene signaling networks through extracellular polysaccharides, volatile organic compounds, plant hormones, and 1-aminocyclopropane-1-carboxylic acid (ACC) deaminase pathways, thereby systematically enhancing the host's water use efficiency and membrane stability. Future research should integrate multi-omics and field validation to precisely construct rhizosphere bacterial communities, providing theoretical basis and technical routes for green agriculture.
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@article {pmid41968366,
year = {2026},
author = {Pang, F and Solanki, MK and Dong, D and Li, F and Wang, Z},
title = {Rhizobacteria-Mediated Plant Resilience to Abiotic Stresses: Drought, Salinity, and Heat.},
journal = {Plant, cell & environment},
volume = {},
number = {},
pages = {},
doi = {10.1111/pce.70532},
pmid = {41968366},
issn = {1365-3040},
support = {2023GXNSFAA026182//Guangxi Natural Science Foundation (CN)/ ; 2022GXNSFDA035074//Guangxi Natural Science Foundation (CN)/ ; 32101836//National Natural Science Foundation of China/ ; },
abstract = {The frequent occurrence of drought, salinity and heat disasters due to global climate change has become a problem that cannot be ignored and seriously restricts food security and sustainable agricultural development. The role of rhizobacteria in the response of plants to abiotic stress has an important guiding significance in improving plant growth. This paper summarizes the response of plant rhizosphere microbial communities to abiotic stress, analyzes the mechanism by which rhizosphere-related bacteria assist plants to resist abiotic stress, and expounds on the interaction between soil physical and chemical properties, the plant root metabolome, and the rhizosphere microbiome under abiotic stress. This review systematically summarizes the core roles and mechanisms of rhizobacteria in plants' defense against abiotic stress. Stress reshapes the rhizosphere microecology, with drought enriching Firmicutes and Actinobacteria, salt stress increasing Bacteroidetes abundance, and heat stress expanding the dominance of thermotolerant bacteria. Microbial diversity and network structure undergo adaptive reorganization. Streptomyces and Bacillus, as the twin stars aiding plants in enhancing stress resistance, provide medium- to long-term protection through rich secondary metabolites and mycelial networks, while Bacillus achieves acute responses via rapid spore germination, signal induction, and nutrient competition. Rhizobacteria improve soil nutrient availability by regulating carbon, nitrogen, and phosphorus cycles, secreting organic acids and enzymes, and induce plant osmotic adjustment, antioxidant, and anti-ethylene signaling networks through extracellular polysaccharides, volatile organic compounds, plant hormones, and 1-aminocyclopropane-1-carboxylic acid (ACC) deaminase pathways, thereby systematically enhancing the host's water use efficiency and membrane stability. Future research should integrate multi-omics and field validation to precisely construct rhizosphere bacterial communities, providing theoretical basis and technical routes for green agriculture.},
}
RevDate: 2026-04-12
CmpDate: 2026-04-13
Bacterial Infections Role in Gynecological Cancers Development: Narrative Review.
Cancer reports (Hoboken, N.J.), 9(4):e70499.
BACKGROUND: Gynecological cancers are among the most common cancers in women that affect female reproductive organs. The most common gynecological cancers are ovarian, cervical, uterine/endometrial, vaginal, and vulvar cancer. Women's reproductive organs have a dynamic and relative microbial balance. The disruption in the balance of the microbiome could result in numerous gynecological diseases, as well as, gynecological cancers. In this study, we aimed to review new findings on the role of different bacterial infections in various types of gynecological cancers.
RECENT FINDINGS: The role of bacterial infection, as an external factor, has been established in several cancers. However, the ways in which bacteria can promote the development of cancer are not fully understood. It seems that inflammation induced by bacterial infections could promote carcinogenesis. In addition, bacterial toxins and effector proteins play important roles in the progression of cancer. In this review, we attempt to present the different bacterial infections, which have been linked to gynecological cancers development. According to different researches, Chlamydia, Mycoplasma, and Bacteroides spp. are the most common bacterial infections associated with gynecological cancers.
CONCLUSION: Evaluation of microbiome in reproductive organs of the patients with gynecological cancer and studies on prevention and control of the infections in the patients could be useful in verification of pathogenesis of the diseases and also founding suitable therapeutic interventions.
Additional Links: PMID-41968380
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PubMed:
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@article {pmid41968380,
year = {2026},
author = {Azargun, R and Azargoon, M and Asefy, Z and Yekani, M and Tarhriz, V and Yeganeh, F and Memar, MY and Eyvazi, S},
title = {Bacterial Infections Role in Gynecological Cancers Development: Narrative Review.},
journal = {Cancer reports (Hoboken, N.J.)},
volume = {9},
number = {4},
pages = {e70499},
doi = {10.1002/cnr2.70499},
pmid = {41968380},
issn = {2573-8348},
mesh = {Humans ; Female ; *Genital Neoplasms, Female/microbiology/pathology/etiology ; Microbiota/immunology ; *Bacterial Infections/complications/microbiology ; },
abstract = {BACKGROUND: Gynecological cancers are among the most common cancers in women that affect female reproductive organs. The most common gynecological cancers are ovarian, cervical, uterine/endometrial, vaginal, and vulvar cancer. Women's reproductive organs have a dynamic and relative microbial balance. The disruption in the balance of the microbiome could result in numerous gynecological diseases, as well as, gynecological cancers. In this study, we aimed to review new findings on the role of different bacterial infections in various types of gynecological cancers.
RECENT FINDINGS: The role of bacterial infection, as an external factor, has been established in several cancers. However, the ways in which bacteria can promote the development of cancer are not fully understood. It seems that inflammation induced by bacterial infections could promote carcinogenesis. In addition, bacterial toxins and effector proteins play important roles in the progression of cancer. In this review, we attempt to present the different bacterial infections, which have been linked to gynecological cancers development. According to different researches, Chlamydia, Mycoplasma, and Bacteroides spp. are the most common bacterial infections associated with gynecological cancers.
CONCLUSION: Evaluation of microbiome in reproductive organs of the patients with gynecological cancer and studies on prevention and control of the infections in the patients could be useful in verification of pathogenesis of the diseases and also founding suitable therapeutic interventions.},
}
MeSH Terms:
show MeSH Terms
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Humans
Female
*Genital Neoplasms, Female/microbiology/pathology/etiology
Microbiota/immunology
*Bacterial Infections/complications/microbiology
RevDate: 2026-04-12
Cultivation and Molecular Profiling Reveal Ammonia-Oxidizing Archaea as Skin Commensals.
The ISME journal pii:8651589 [Epub ahead of print].
Ammonia-oxidizing archaea (AOA) have repeatedly been detected with molecular methods on human skin, yet their persistence, physiological traits, and adaptations remain poorly understood. This is mostly owed to a lack of cultured representatives of AOA taxa from healthy human skin. Using a customized enrichment scheme, we cultivated two autotrophic strains, Candidatus Nitrosocosmicus epidermidis and Ca. Nitrosocosmicus unguis, from human skin samples. Genomic analyses revealed specific adaptations for skin colonization, including genomic islands, and expanded gene families linked to interactions with host proteins, and signaling pathways, distinguishing these AOA from their soil-dwelling relatives. Profiling of more than 700 samples from 8 body sites in cross-sectional, and longitudinal cohorts consistently validated the detection of Nitrosocosmicus species with up to 100% prevalence in a longitudinal cohort, and particularly in sebaceous areas. Co-occurrence patterns with specific bacterial taxa reinforce their role as stable components of the skin microbiome. Our results establish Nitrosocosmicus species as common skin commensals, that are evolutionarily capable of transitioning from soil to human skin. They likely play a critical role in the skin ecosystem by recovering nitrogen from the sebum through utilisation of urea and ammonia. This sheds new light on the role of archaeal species in maintaining the nitrogen balance in the human skin microbiome which might be of importance maintaining a healthy skin.
Additional Links: PMID-41968400
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PubMed:
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@article {pmid41968400,
year = {2026},
author = {Mahnert, A and Dreer, M and Perier, Ü and Melcher, M and Duller, S and Lehnen, A and Goessler, T and Brunner, D and Graier, T and Wolf, P and Ponce-Toledo, RI and Hodgskiss, LH and Kerou, M and Moissl-Eichinger, C and Schleper, C},
title = {Cultivation and Molecular Profiling Reveal Ammonia-Oxidizing Archaea as Skin Commensals.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag078},
pmid = {41968400},
issn = {1751-7370},
abstract = {Ammonia-oxidizing archaea (AOA) have repeatedly been detected with molecular methods on human skin, yet their persistence, physiological traits, and adaptations remain poorly understood. This is mostly owed to a lack of cultured representatives of AOA taxa from healthy human skin. Using a customized enrichment scheme, we cultivated two autotrophic strains, Candidatus Nitrosocosmicus epidermidis and Ca. Nitrosocosmicus unguis, from human skin samples. Genomic analyses revealed specific adaptations for skin colonization, including genomic islands, and expanded gene families linked to interactions with host proteins, and signaling pathways, distinguishing these AOA from their soil-dwelling relatives. Profiling of more than 700 samples from 8 body sites in cross-sectional, and longitudinal cohorts consistently validated the detection of Nitrosocosmicus species with up to 100% prevalence in a longitudinal cohort, and particularly in sebaceous areas. Co-occurrence patterns with specific bacterial taxa reinforce their role as stable components of the skin microbiome. Our results establish Nitrosocosmicus species as common skin commensals, that are evolutionarily capable of transitioning from soil to human skin. They likely play a critical role in the skin ecosystem by recovering nitrogen from the sebum through utilisation of urea and ammonia. This sheds new light on the role of archaeal species in maintaining the nitrogen balance in the human skin microbiome which might be of importance maintaining a healthy skin.},
}
RevDate: 2026-04-13
Unravelling the Regulatory Paradox of Probiotics: Challenges in Standardization, Clinical Validation, and Global Acceptance.
Recent advances in food, nutrition & agriculture pii:RAFNA-EPUB-154679 [Epub ahead of print].
Age-specific probiotic-drug hybrid formulations represent an emerging class of therapeutics that combine live microorganisms with pharmaceutical agents to enhance clinical efficacy, minimize adverse effects, and maintain gut microbiome homeostasis across different age groups. Despite their potential, these hybrids face significant regulatory challenges due to their dual identity as both biologics and drugs, creating ambiguity in classification, evaluation, and approval. Global regulatory agencies, including the U.S. Food and Drug Administration (FDA), European Medicines Agency (EMA), and Central Drugs Standard Control Organization (CDSCO), lack harmonized guidelines for such formulations, resulting in fragmented standards and delayed market entry. This study provides a comprehensive review of existing regulatory frameworks to identify gaps in safety assessment, clinical validation, manufacturing, and postmarket surveillance of probiotic-drug hybrids. A comparative decision matrix is developed to map and contrast the FDA, EMA, and CDSCO approval pathways, highlighting differences in evidentiary and procedural requirements. Building on this analysis, an age-stratified regulatory roadmap is proposed to account for physiological, metabolic, and microbiome-related variations among pediatric, adult, and geriatric populations. The roadmap emphasizes adaptive trial designs, long-term safety monitoring, and age-appropriate dosage and labeling requirements. By integrating scientific, clinical, and regulatory perspectives, this paper provides a structured foundation for harmonizing international approval processes and guiding future policy development. The findings aim to support regulatory convergence, enhance safety assurance, and facilitate the ethical and efficient advancement of probiotic-drug hybrid formulations in global healthcare.
Additional Links: PMID-41968561
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PubMed:
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@article {pmid41968561,
year = {2026},
author = {Nayan, S and Baghel Chauhan, S and Singh, I and Jain, C},
title = {Unravelling the Regulatory Paradox of Probiotics: Challenges in Standardization, Clinical Validation, and Global Acceptance.},
journal = {Recent advances in food, nutrition & agriculture},
volume = {},
number = {},
pages = {},
doi = {10.2174/012772574X441445251207215223},
pmid = {41968561},
issn = {2772-5758},
abstract = {Age-specific probiotic-drug hybrid formulations represent an emerging class of therapeutics that combine live microorganisms with pharmaceutical agents to enhance clinical efficacy, minimize adverse effects, and maintain gut microbiome homeostasis across different age groups. Despite their potential, these hybrids face significant regulatory challenges due to their dual identity as both biologics and drugs, creating ambiguity in classification, evaluation, and approval. Global regulatory agencies, including the U.S. Food and Drug Administration (FDA), European Medicines Agency (EMA), and Central Drugs Standard Control Organization (CDSCO), lack harmonized guidelines for such formulations, resulting in fragmented standards and delayed market entry. This study provides a comprehensive review of existing regulatory frameworks to identify gaps in safety assessment, clinical validation, manufacturing, and postmarket surveillance of probiotic-drug hybrids. A comparative decision matrix is developed to map and contrast the FDA, EMA, and CDSCO approval pathways, highlighting differences in evidentiary and procedural requirements. Building on this analysis, an age-stratified regulatory roadmap is proposed to account for physiological, metabolic, and microbiome-related variations among pediatric, adult, and geriatric populations. The roadmap emphasizes adaptive trial designs, long-term safety monitoring, and age-appropriate dosage and labeling requirements. By integrating scientific, clinical, and regulatory perspectives, this paper provides a structured foundation for harmonizing international approval processes and guiding future policy development. The findings aim to support regulatory convergence, enhance safety assurance, and facilitate the ethical and efficient advancement of probiotic-drug hybrid formulations in global healthcare.},
}
RevDate: 2026-04-13
Delivery System Based on Akkermansia Muciniphila Loaded Salidroside for the Treatment of Osteoporosis in Zebrafish Model.
Advanced healthcare materials [Epub ahead of print].
Glucocorticoid-induced osteoporosis (GIOP) is a frequent cost of dexamethasone (Dex) therapy; salidroside (SAL) shows promise but suffers from rapid clearance and poor oral bioavailability. We present an oral, living co-therapy in which viable Akkermansia muciniphila is vacuum-loaded with intracellular SAL and protected by a pH-responsive Eudragit L100 enteric coat (SAL@AKK@EL100). This construct effectively retains probiotic activity, shields the cargo through gastric transit, and shows prolonged intracellular retention with gradual release. In Dex-challenged zebrafish, SAL@AKK@EL100 reversed behavioral dysregulation and improved skeletal mineralization, outperforming SAL or AKK alone. Integrative RNA-seq/16S analysis revealed that SAL@AKK@EL100 treatment was associated with modulation of pathways related to tight junctions, ECM-receptor interaction, actin cytoskeleton, glutathione metabolism, and unsaturated fatty acid biosynthesis, alongside remodeling of the gut microbiota. SAL@AKK@EL100 establishes a modular, microbiome-anchored platform that couples probiotic viability with drug gradual release for promising oral management of GIOP.
Additional Links: PMID-41968607
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PubMed:
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@article {pmid41968607,
year = {2026},
author = {Ma, J and Ruan, J and Yi, J and Zhang, S and Ma, Y and Chen, R and Wang, H and Luo, L and Fang, B and Wu, W and Yang, Q and Sun, D},
title = {Delivery System Based on Akkermansia Muciniphila Loaded Salidroside for the Treatment of Osteoporosis in Zebrafish Model.},
journal = {Advanced healthcare materials},
volume = {},
number = {},
pages = {e04437},
doi = {10.1002/adhm.202504437},
pmid = {41968607},
issn = {2192-2659},
support = {//Scientific Research Cultivation Project of the College of Life and Environmental Sciences/ ; SHPY2025010//Wenzhou University/ ; 2025ZY01039//Central Government Funds for Guiding Local Scientific and Technological Development/ ; JFLKYXM202303AZ-204//JinFeng Laboratory of Chongqing/ ; },
abstract = {Glucocorticoid-induced osteoporosis (GIOP) is a frequent cost of dexamethasone (Dex) therapy; salidroside (SAL) shows promise but suffers from rapid clearance and poor oral bioavailability. We present an oral, living co-therapy in which viable Akkermansia muciniphila is vacuum-loaded with intracellular SAL and protected by a pH-responsive Eudragit L100 enteric coat (SAL@AKK@EL100). This construct effectively retains probiotic activity, shields the cargo through gastric transit, and shows prolonged intracellular retention with gradual release. In Dex-challenged zebrafish, SAL@AKK@EL100 reversed behavioral dysregulation and improved skeletal mineralization, outperforming SAL or AKK alone. Integrative RNA-seq/16S analysis revealed that SAL@AKK@EL100 treatment was associated with modulation of pathways related to tight junctions, ECM-receptor interaction, actin cytoskeleton, glutathione metabolism, and unsaturated fatty acid biosynthesis, alongside remodeling of the gut microbiota. SAL@AKK@EL100 establishes a modular, microbiome-anchored platform that couples probiotic viability with drug gradual release for promising oral management of GIOP.},
}
RevDate: 2026-04-13
Bromocriptine Attenuated Ulcerative Colitis and Colonic Inflammation by Inhibiting IL-1β, Likely through NF-κB Down-regulation: Integrated Network Pharmacology and in vivo Experimental Validation.
Current pharmaceutical design pii:CPD-EPUB-154769 [Epub ahead of print].
INTRODUCTION: Gastrointestinal dopamine (DA) plays a crucial role in maintaining gut homeostasis. In patients with ulcerative colitis (UC), a decrease in DA levels due to changes in the gut microbiome can activate immune cells in the colon's mucosal layer, leading to the secretion of various inflammatory mediators and ultimately causing damage to the colonic mucosa. In the present study, we initially analysed integrated network pharmacology and investigated the protective effect of bromocriptine (BRO), a dopamine D2 receptor (D2R) agonist, on acetic acid (AA)-induced UC in rats.
METHODS: Wistar rats were randomly divided into six groups (N=6/group). The intrarectal administration of AA induced UC. Treatment groups (III-IV) received three doses (2, 5, and 10 mg/kg) of BRO once daily for seven days. Group VI animals were administered mesalamine. On the eighth day, the animals were sacrificed to evaluate the lesion scores, ulcer indices, histopathological findings, nitric oxide (NO) levels, and myeloperoxidase (MPO). Finally, tissue levels of interleukin (IL-1β) and nuclear factor kappa B (NF-κB) were measured using ELISA.
RESULTS: BRO treatment effectively improved the disease severity index (DAI), colonic lesion score, and ulcer index in rats with AA-induced UC. Histopathological studies revealed that treatment with BRO limited mucosal damage and neutrophil extravasation in colonic tissue. Moreover, biochemical assessments of MPO and NO showed a significant decrease in the levels of both inflammatory mediators following treatment with BRO. Additionally, the results indicated a reduction in the expression of IL-1β and NF-κB in colonic tissue, further supporting the amelioration of colonic inflammation caused by BRO.
DISCUSSION: The present research demonstrated that BRO exerts a protective effect by influencing the expression of IL-1β and NF-κB in rats with AA-induced UC, thus restricting the activity of immune cells in the colonic mucosa.
CONCLUSION: Findings of this research suggest that BRO may be a promising therapeutic agent for the management of UC.
Additional Links: PMID-41968668
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PubMed:
Citation:
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@article {pmid41968668,
year = {2026},
author = {Saha, S and Mondal, S and Chatterjee, O and Devroy, P and Sur, D and Bala, A},
title = {Bromocriptine Attenuated Ulcerative Colitis and Colonic Inflammation by Inhibiting IL-1β, Likely through NF-κB Down-regulation: Integrated Network Pharmacology and in vivo Experimental Validation.},
journal = {Current pharmaceutical design},
volume = {},
number = {},
pages = {},
doi = {10.2174/0113816128418229260223013818},
pmid = {41968668},
issn = {1873-4286},
abstract = {INTRODUCTION: Gastrointestinal dopamine (DA) plays a crucial role in maintaining gut homeostasis. In patients with ulcerative colitis (UC), a decrease in DA levels due to changes in the gut microbiome can activate immune cells in the colon's mucosal layer, leading to the secretion of various inflammatory mediators and ultimately causing damage to the colonic mucosa. In the present study, we initially analysed integrated network pharmacology and investigated the protective effect of bromocriptine (BRO), a dopamine D2 receptor (D2R) agonist, on acetic acid (AA)-induced UC in rats.
METHODS: Wistar rats were randomly divided into six groups (N=6/group). The intrarectal administration of AA induced UC. Treatment groups (III-IV) received three doses (2, 5, and 10 mg/kg) of BRO once daily for seven days. Group VI animals were administered mesalamine. On the eighth day, the animals were sacrificed to evaluate the lesion scores, ulcer indices, histopathological findings, nitric oxide (NO) levels, and myeloperoxidase (MPO). Finally, tissue levels of interleukin (IL-1β) and nuclear factor kappa B (NF-κB) were measured using ELISA.
RESULTS: BRO treatment effectively improved the disease severity index (DAI), colonic lesion score, and ulcer index in rats with AA-induced UC. Histopathological studies revealed that treatment with BRO limited mucosal damage and neutrophil extravasation in colonic tissue. Moreover, biochemical assessments of MPO and NO showed a significant decrease in the levels of both inflammatory mediators following treatment with BRO. Additionally, the results indicated a reduction in the expression of IL-1β and NF-κB in colonic tissue, further supporting the amelioration of colonic inflammation caused by BRO.
DISCUSSION: The present research demonstrated that BRO exerts a protective effect by influencing the expression of IL-1β and NF-κB in rats with AA-induced UC, thus restricting the activity of immune cells in the colonic mucosa.
CONCLUSION: Findings of this research suggest that BRO may be a promising therapeutic agent for the management of UC.},
}
RevDate: 2026-04-13
Peptidomics: A New Dimension in Microbiome Research.
Protein and peptide letters pii:PPL-EPUB-154754 [Epub ahead of print].
The human gut microbiome is now recognised as a major determinant of health, with roles extending beyond digestion to influence neurodegeneration, metabolism, immunity, and pharmacological responses. Clinical studies link microbial imbalances to Alzheimer's disease, Parkinson's disease, depression, and cardiovascular disorders, yet the underlying mechanisms remain only partly understood. Methodological advances have progressively deepened our insight. DNA-based sequencing (metagenomics) catalogues microbial genes but reveals only potential functions. RNA-based sequencing (metatranscriptomics) highlights active gene expression, but instability of transcripts and poor correlation with protein activity limit its predictive value. Metabolomics measures small-molecule end products, providing direct evidence of microbial biochemistry and identifying disease-linked metabolites such as urolithin A, trimethylamine N-oxide, and equol. These approaches together have transformed microbiome science, but they remain incomplete. A critical and underutilised dimension is peptidomics: the systematic analysis of endogenous peptides in the gut and circulation. Enabled by peptide-enriching, protease-inhibiting workflows and high-resolution liquid chromatography-tandem mass spectrometry (LC-MS/MS), peptidomics directly captures unstable signaling peptides and proteolytic fragments that are often invisible to conventional proteomics. Coupled with emerging gut-specific peptide databases, such as MetaPep, and Artificial Intelligence (AI) assisted de novo sequencing and spectral prediction for non-human peptides, this provides a concrete technical route to reading out the functional peptide layer of the microbiome. Peptidomics can capture functional signals of host-microbiome interaction, reveal context-specific biomarkers, and provide mechanistic insight into disease. Recent studies demonstrate that peptide-level resolution uncovers microbial contributions to gut inflammation, modulates the gut-brain axis, and enables peptide-based disease stratification in conditions such as inflammatory bowel disease. However, despite these promising examples, peptidomics remains largely absent from mainstream microbiome research, which needs to be changed. Integrating peptidomics with existing genomic, transcriptomic, and metabolomic approaches will generate a more complete and functional picture of the microbiome. This shift will accelerate biomarker discovery, refine diagnostics, and expand the search for peptide-based therapeutics, positioning peptidomics as an essential next step in microbiome science.
Additional Links: PMID-41968748
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PubMed:
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@article {pmid41968748,
year = {2026},
author = {Hilpert, K},
title = {Peptidomics: A New Dimension in Microbiome Research.},
journal = {Protein and peptide letters},
volume = {},
number = {},
pages = {},
doi = {10.2174/0109298665436241260327111926},
pmid = {41968748},
issn = {1875-5305},
abstract = {The human gut microbiome is now recognised as a major determinant of health, with roles extending beyond digestion to influence neurodegeneration, metabolism, immunity, and pharmacological responses. Clinical studies link microbial imbalances to Alzheimer's disease, Parkinson's disease, depression, and cardiovascular disorders, yet the underlying mechanisms remain only partly understood. Methodological advances have progressively deepened our insight. DNA-based sequencing (metagenomics) catalogues microbial genes but reveals only potential functions. RNA-based sequencing (metatranscriptomics) highlights active gene expression, but instability of transcripts and poor correlation with protein activity limit its predictive value. Metabolomics measures small-molecule end products, providing direct evidence of microbial biochemistry and identifying disease-linked metabolites such as urolithin A, trimethylamine N-oxide, and equol. These approaches together have transformed microbiome science, but they remain incomplete. A critical and underutilised dimension is peptidomics: the systematic analysis of endogenous peptides in the gut and circulation. Enabled by peptide-enriching, protease-inhibiting workflows and high-resolution liquid chromatography-tandem mass spectrometry (LC-MS/MS), peptidomics directly captures unstable signaling peptides and proteolytic fragments that are often invisible to conventional proteomics. Coupled with emerging gut-specific peptide databases, such as MetaPep, and Artificial Intelligence (AI) assisted de novo sequencing and spectral prediction for non-human peptides, this provides a concrete technical route to reading out the functional peptide layer of the microbiome. Peptidomics can capture functional signals of host-microbiome interaction, reveal context-specific biomarkers, and provide mechanistic insight into disease. Recent studies demonstrate that peptide-level resolution uncovers microbial contributions to gut inflammation, modulates the gut-brain axis, and enables peptide-based disease stratification in conditions such as inflammatory bowel disease. However, despite these promising examples, peptidomics remains largely absent from mainstream microbiome research, which needs to be changed. Integrating peptidomics with existing genomic, transcriptomic, and metabolomic approaches will generate a more complete and functional picture of the microbiome. This shift will accelerate biomarker discovery, refine diagnostics, and expand the search for peptide-based therapeutics, positioning peptidomics as an essential next step in microbiome science.},
}
RevDate: 2026-04-13
How the gut microbiome affects the immunotherapy response in hepatocellular carcinoma.
Cancer biology & medicine pii:j.issn.2095-3941.2025.0761 [Epub ahead of print].
Hepatocellular carcinoma (HCC) remains a major global health challenge with limited long-term survival despite advances in surgical, locoregional, and systemic treatments. Although immune checkpoint blockade (ICB) has reshaped HCC therapy, only a subset of patients achieves durable responses, reflecting substantial heterogeneity in tumor biology and immune microenvironments. Dysbiosis, involving the loss of beneficial bacteria, like Lactobacillus reuteri and Akkermansia muciniphila, and the expansion of pathogens, such as Klebsiella pneumoniae and Catenibacterium mitsuokai, drives HCC by promoting microbial translocation and chronic inflammation. This process is mediated by microbiota-derived metabolites. Pro-carcinogenic agents, like deoxycholic acid (DCA) and quinolinic acid, induce inflammation and activate oncogenic pathways, while protective short-chain fatty acids (SCFAs), like acetate and butyrate, modulate T-cell and ILC3 responses to influence antitumor immunity. Tryptophan catabolites, acting via the aryl hydrocarbon receptor (AhR), further fine tune immune and barrier functions. In addition, emerging data implicate intratumoral microbiota as active modulators of immune suppression and metastatic behavior. These mechanistic insights have accelerated the development of microbiome-targeted interventions, such as probiotics, prebiotics, engineered bacterial strains, and fecal microbiota transplantation, to enhance ICB responsiveness. This review synthesizes current advances linking the gut microbiome to HCC immunobiology and highlights emerging therapeutic strategies aimed at optimizing immunotherapy through precise microbial modulation.
Additional Links: PMID-41968757
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PubMed:
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@article {pmid41968757,
year = {2026},
author = {Wu, M and Zhang, Y and Yu, J},
title = {How the gut microbiome affects the immunotherapy response in hepatocellular carcinoma.},
journal = {Cancer biology & medicine},
volume = {},
number = {},
pages = {},
doi = {10.20892/j.issn.2095-3941.2025.0761},
pmid = {41968757},
issn = {2095-3941},
support = {2023ZD0500200//Non-communicable Chronic Diseases-National Science and Technology Major Project/ ; 3133344//Strategic Seed Funding Collaboration Research Scheme CUHK/ ; 3135509//Strategic Impact Enhancement Fund CUHK/ ; 3134277//Impact Case for RAE CUHK/ ; },
abstract = {Hepatocellular carcinoma (HCC) remains a major global health challenge with limited long-term survival despite advances in surgical, locoregional, and systemic treatments. Although immune checkpoint blockade (ICB) has reshaped HCC therapy, only a subset of patients achieves durable responses, reflecting substantial heterogeneity in tumor biology and immune microenvironments. Dysbiosis, involving the loss of beneficial bacteria, like Lactobacillus reuteri and Akkermansia muciniphila, and the expansion of pathogens, such as Klebsiella pneumoniae and Catenibacterium mitsuokai, drives HCC by promoting microbial translocation and chronic inflammation. This process is mediated by microbiota-derived metabolites. Pro-carcinogenic agents, like deoxycholic acid (DCA) and quinolinic acid, induce inflammation and activate oncogenic pathways, while protective short-chain fatty acids (SCFAs), like acetate and butyrate, modulate T-cell and ILC3 responses to influence antitumor immunity. Tryptophan catabolites, acting via the aryl hydrocarbon receptor (AhR), further fine tune immune and barrier functions. In addition, emerging data implicate intratumoral microbiota as active modulators of immune suppression and metastatic behavior. These mechanistic insights have accelerated the development of microbiome-targeted interventions, such as probiotics, prebiotics, engineered bacterial strains, and fecal microbiota transplantation, to enhance ICB responsiveness. This review synthesizes current advances linking the gut microbiome to HCC immunobiology and highlights emerging therapeutic strategies aimed at optimizing immunotherapy through precise microbial modulation.},
}
RevDate: 2026-04-13
CmpDate: 2026-04-13
Comparative characteristics of the microbiota of diverticula in complicated diverticulitis.
The new microbiologica, 49(1):65-70.
We present a comparison of the mucosal microbiota within different diverticula in a patient with diverticular disease (DD) complicated by diverticulitis and pelvic abscess. The conventional culture method and the 16S rRNA-based sequencing approach were employed to characterize the microbiota of perforated diverticulum (PD) and adjacent visually intact diverticulum (ID) from the same surgically resected colonic segment. Compared to PD, the microbiota of ID demonstrated depletion in butyrate-producing genera and increased abundances of Proteobacteria, Enterobacteriaceae, and Bacteroides. The predominantly pro-inflammatory character of the microbiota in ID suggests its probable pathological role in the progression of DD towards more complicated forms, up to inflammatory destruction (perforation) of the diverticulum wall. The insights of this study pave the way for the development of forthcoming clinical trials focusing on microbiota-related therapies, including the use of antibiotics, probiotics, and fecal microbiota transplantation (FMT), to potentially treat or manage DD and its complications.
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@article {pmid41969116,
year = {2026},
author = {Shakirov, R and Pankratova, Y and Shakurov, A and Senina, A and Boulygina, E and Grigoryeva, T and Yarullina, D and Karpukhin, O},
title = {Comparative characteristics of the microbiota of diverticula in complicated diverticulitis.},
journal = {The new microbiologica},
volume = {49},
number = {1},
pages = {65-70},
pmid = {41969116},
issn = {1121-7138},
mesh = {Humans ; *Diverticulitis/microbiology/complications ; Male ; *Gastrointestinal Microbiome ; *Bacteria/classification/isolation & purification/genetics ; Middle Aged ; *Diverticulum/microbiology/complications ; Aged ; RNA, Ribosomal, 16S/genetics ; Female ; },
abstract = {We present a comparison of the mucosal microbiota within different diverticula in a patient with diverticular disease (DD) complicated by diverticulitis and pelvic abscess. The conventional culture method and the 16S rRNA-based sequencing approach were employed to characterize the microbiota of perforated diverticulum (PD) and adjacent visually intact diverticulum (ID) from the same surgically resected colonic segment. Compared to PD, the microbiota of ID demonstrated depletion in butyrate-producing genera and increased abundances of Proteobacteria, Enterobacteriaceae, and Bacteroides. The predominantly pro-inflammatory character of the microbiota in ID suggests its probable pathological role in the progression of DD towards more complicated forms, up to inflammatory destruction (perforation) of the diverticulum wall. The insights of this study pave the way for the development of forthcoming clinical trials focusing on microbiota-related therapies, including the use of antibiotics, probiotics, and fecal microbiota transplantation (FMT), to potentially treat or manage DD and its complications.},
}
MeSH Terms:
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Humans
*Diverticulitis/microbiology/complications
Male
*Gastrointestinal Microbiome
*Bacteria/classification/isolation & purification/genetics
Middle Aged
*Diverticulum/microbiology/complications
Aged
RNA, Ribosomal, 16S/genetics
Female
RevDate: 2026-04-12
CmpDate: 2026-04-11
Results of the Ninth Scientific Workshop of the European Crohn's and Colitis Organisation (ECCO): Artificial Intelligence in medical management and precision medicine.
Journal of Crohn's & colitis, 20(4):.
BACKGROUND AND AIMS: Artificial intelligence (AI) is increasingly being applied in various fields of medicine, including inflammatory bowel diseases (IBD). This systematic review, conducted as part of the ECCO 9th Scientific Workshop on AI in IBD, explores AI applications in multiomics precision medicine, large language models (LLMs) for textual tasks, and utilization of wearable and remote care technologies.
METHODS: A comprehensive systematic analysis of the literature was undertaken, emphasizing three topics: multiomics predictive models in IBD; natural language processing (NLP) and LLMs for clinical practice, research and patient communication; and the role of remote monitoring and wearable devices.
RESULTS: Key areas of promise include the implementation of NLP and LLMs for case identification and differentiation, tracking disease activity, pharmacovigilance, quality assurance, and patient support. Multiomic approaches, integrating genomics, transcriptomics, proteomics, metabolomics, and metagenomics, show potential for developing more accurate diagnostic and risk prediction models and improving treatment response prediction and detection of actionable drug targets for future therapeutics. Wearables and remote monitoring technologies can transform IBD management from episodic assessments to continuous, less biased tracking of patient-reported outcomes and physiological biomarkers.
CONCLUSIONS: While AI and multiomics approaches hold substantial promise for advancing IBD management and research, further refinement is necessary to ensure content validity and address safety concerns, thereby allowing integration of AI into clinical workflows and safeguarding of data privacy. Future research should prioritize the integration of diverse omic data, conduct of longitudinal studies, and validation in large and diverse cohorts.
Additional Links: PMID-40796214
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@article {pmid40796214,
year = {2026},
author = {Kopylov, U and Verstockt, B and Marigorta, UM and Noviello, D and Bossuyt, P and Mookhoek, A and Sinonquel, P and El-Hussuna, A and Sahnan, K and Baumgart, DC and Noor, NM and Allocca, M and Carter, D and Ensari, A and Iacucci, M and Pellino, G and Soriano, A and de Laffolie, J and Daperno, M and Raine, T and Cleynen, I and Sebastian, S},
title = {Results of the Ninth Scientific Workshop of the European Crohn's and Colitis Organisation (ECCO): Artificial Intelligence in medical management and precision medicine.},
journal = {Journal of Crohn's & colitis},
volume = {20},
number = {4},
pages = {},
doi = {10.1093/ecco-jcc/jjaf134},
pmid = {40796214},
issn = {1876-4479},
mesh = {Humans ; *Artificial Intelligence ; *Precision Medicine/methods ; *Inflammatory Bowel Diseases/therapy/diagnosis ; Natural Language Processing ; Wearable Electronic Devices ; *Crohn Disease/therapy ; Telemedicine ; },
abstract = {BACKGROUND AND AIMS: Artificial intelligence (AI) is increasingly being applied in various fields of medicine, including inflammatory bowel diseases (IBD). This systematic review, conducted as part of the ECCO 9th Scientific Workshop on AI in IBD, explores AI applications in multiomics precision medicine, large language models (LLMs) for textual tasks, and utilization of wearable and remote care technologies.
METHODS: A comprehensive systematic analysis of the literature was undertaken, emphasizing three topics: multiomics predictive models in IBD; natural language processing (NLP) and LLMs for clinical practice, research and patient communication; and the role of remote monitoring and wearable devices.
RESULTS: Key areas of promise include the implementation of NLP and LLMs for case identification and differentiation, tracking disease activity, pharmacovigilance, quality assurance, and patient support. Multiomic approaches, integrating genomics, transcriptomics, proteomics, metabolomics, and metagenomics, show potential for developing more accurate diagnostic and risk prediction models and improving treatment response prediction and detection of actionable drug targets for future therapeutics. Wearables and remote monitoring technologies can transform IBD management from episodic assessments to continuous, less biased tracking of patient-reported outcomes and physiological biomarkers.
CONCLUSIONS: While AI and multiomics approaches hold substantial promise for advancing IBD management and research, further refinement is necessary to ensure content validity and address safety concerns, thereby allowing integration of AI into clinical workflows and safeguarding of data privacy. Future research should prioritize the integration of diverse omic data, conduct of longitudinal studies, and validation in large and diverse cohorts.},
}
MeSH Terms:
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Humans
*Artificial Intelligence
*Precision Medicine/methods
*Inflammatory Bowel Diseases/therapy/diagnosis
Natural Language Processing
Wearable Electronic Devices
*Crohn Disease/therapy
Telemedicine
RevDate: 2026-04-10
CmpDate: 2026-04-10
Bacillus mojavensis postbiotics: transcriptomic and anticancer effects in colon cancer cells.
AMB Express, 16(1):.
UNLABELLED: Probiotics have been shown to exert antiproliferative effects on colon cancer cells. While these effects are often attributed to microbiome regulation, they may also result from bioactive metabolites produced by probiotic bacteria. In the present study, we investigated the impact of a cell-free extract, hereafter referred to as a postbiotic, derived from Bacillus mojavensis, a strain isolated from aguamiel (a traditional Mexican beverage). The antiproliferative activity was evaluated in SW480 human colon cancer cells using MTT and crystal violet assays, while antimigratory effects were assessed through a wound-healing assay. In addition, the ability of the postbiotic to counteract inflammatory proliferation was evaluated in SW480 cells treated with lipopolysaccharide (LPS). Biosafety was tested using peripheral blood mononuclear cells (PBMCs) from healthy donors. Results demonstrated that treatment with 25–50 µg/mL of B. mojavensis postbiotic reduced SW480 cell viability by 75.15% and 79.3%, respectively, and significantly inhibited cell migration after 24 h. Moreover, the postbiotic decreased LPS-induced proliferation without exerting any cytotoxic effect on PBMCs, underscoring its selectivity toward malignant cells. To elucidate the underlying mechanisms, transcriptomic profiling was performed, revealing extensive modulation of oncogenes and tumor suppressors, with enrichment of PI3K–Akt, MAPK, apoptosis, and cytokine receptor pathways. In conclusion, postbiotics from B. mojavensis isolated from aguamiel exhibit selective anticancer activity by inhibiting proliferation, migration, and inflammation-induced growth in colorectal cancer cells. Transcriptomic findings further support these effects.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13568-026-02018-4.
Additional Links: PMID-41779268
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Citation:
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@article {pmid41779268,
year = {2026},
author = {Trujillo-López, MA and Muñoz-Olivos, C and Garduño-Vargas, MÁ and Sánchez-López, JM and Martínez-Ortiz, VM and Pérez-Armendáriz, B and El-Kassis, EG and Bautista-Rodriguez, E},
title = {Bacillus mojavensis postbiotics: transcriptomic and anticancer effects in colon cancer cells.},
journal = {AMB Express},
volume = {16},
number = {1},
pages = {},
pmid = {41779268},
issn = {2191-0855},
support = {CBF-2025-I-3072//SECIHTI/ ; },
abstract = {UNLABELLED: Probiotics have been shown to exert antiproliferative effects on colon cancer cells. While these effects are often attributed to microbiome regulation, they may also result from bioactive metabolites produced by probiotic bacteria. In the present study, we investigated the impact of a cell-free extract, hereafter referred to as a postbiotic, derived from Bacillus mojavensis, a strain isolated from aguamiel (a traditional Mexican beverage). The antiproliferative activity was evaluated in SW480 human colon cancer cells using MTT and crystal violet assays, while antimigratory effects were assessed through a wound-healing assay. In addition, the ability of the postbiotic to counteract inflammatory proliferation was evaluated in SW480 cells treated with lipopolysaccharide (LPS). Biosafety was tested using peripheral blood mononuclear cells (PBMCs) from healthy donors. Results demonstrated that treatment with 25–50 µg/mL of B. mojavensis postbiotic reduced SW480 cell viability by 75.15% and 79.3%, respectively, and significantly inhibited cell migration after 24 h. Moreover, the postbiotic decreased LPS-induced proliferation without exerting any cytotoxic effect on PBMCs, underscoring its selectivity toward malignant cells. To elucidate the underlying mechanisms, transcriptomic profiling was performed, revealing extensive modulation of oncogenes and tumor suppressors, with enrichment of PI3K–Akt, MAPK, apoptosis, and cytokine receptor pathways. In conclusion, postbiotics from B. mojavensis isolated from aguamiel exhibit selective anticancer activity by inhibiting proliferation, migration, and inflammation-induced growth in colorectal cancer cells. Transcriptomic findings further support these effects.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13568-026-02018-4.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
Alistipes and Eggerthella shape the response to oncolytic adenovirus therapy in mice and humans through short-chain fatty acid metabolism.
Oncoimmunology, 15(1):2656514.
Accumulating evidence implicates the microbiome as an important determinant of clinical outcomes in cancer therapies; however, the role of the microbiome in oncolytic virus therapy remains largely unexplored. We investigated the gut microbiome of cancer patients following treatment with the oncolytic adenovirus igrelimogene litadenorepvec (Ad5/3-E2F-d24-hTNF-IRES-hIL2; TILT-123). Baseline fecal samples from phase I clinical trials (NCT04695327 and NCT05271318) were analyzed using shotgun metagenomic sequencing and compared to treatment outcomes. A higher relative abundance of Alistipes was observed in patients with treatment benefit, while elevated Eggerthella was observed with reduced benefit. These associations were validated in a preclinical mouse model where administration of Alistipes shahii improved the efficacy of adenovirus therapy. In addition, enrichment analysis in patient samples showed a positive correlation between higher relative abundance of Alistipes and elevated short-chain fatty acids in both feces and serum, which in turn revealed higher circulating neutrophil counts. Finally, in a case study, we observed that adenovirus treatment resulted in increased Alistipes relative abundance and reduced Eggerthella relative abundance, indicating that adenovirus therapy may beneficially modulate the microbiome. Overall, our findings reveal a novel association between Alistipes, Eggerthella, and the therapeutic response to oncolytic adenovirus therapy, highlighting their potential as biomarkers or targets for microbiome-based interventions such as pre-, pro-, or postbiotics.
Additional Links: PMID-41957950
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PubMed:
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@article {pmid41957950,
year = {2026},
author = {van der Heijden, M and Clubb, JHA and Erawijantari, PP and Ronkainen, A and Arias, V and Jirovec, E and Kudling, T and Pakola, SA and Ojala, N and Haybout, L and Basnet, S and Grönberg-Vähä-Koskela, S and Karoliina Raatikainen, S and Hemminki, O and Kanerva, A and Quixabeira, DCA and Cervera-Carrascon, V and Manuel Dos Santos, J and Lahti, L and Hemminki, A},
title = {Alistipes and Eggerthella shape the response to oncolytic adenovirus therapy in mice and humans through short-chain fatty acid metabolism.},
journal = {Oncoimmunology},
volume = {15},
number = {1},
pages = {2656514},
doi = {10.1080/2162402X.2026.2656514},
pmid = {41957950},
issn = {2162-402X},
mesh = {*Oncolytic Virotherapy/methods ; Humans ; Animals ; Mice ; *Adenoviridae/genetics ; *Fatty Acids, Volatile/metabolism ; *Gastrointestinal Microbiome ; *Oncolytic Viruses ; Feces/microbiology ; Female ; *Neoplasms/therapy/microbiology ; Male ; },
abstract = {Accumulating evidence implicates the microbiome as an important determinant of clinical outcomes in cancer therapies; however, the role of the microbiome in oncolytic virus therapy remains largely unexplored. We investigated the gut microbiome of cancer patients following treatment with the oncolytic adenovirus igrelimogene litadenorepvec (Ad5/3-E2F-d24-hTNF-IRES-hIL2; TILT-123). Baseline fecal samples from phase I clinical trials (NCT04695327 and NCT05271318) were analyzed using shotgun metagenomic sequencing and compared to treatment outcomes. A higher relative abundance of Alistipes was observed in patients with treatment benefit, while elevated Eggerthella was observed with reduced benefit. These associations were validated in a preclinical mouse model where administration of Alistipes shahii improved the efficacy of adenovirus therapy. In addition, enrichment analysis in patient samples showed a positive correlation between higher relative abundance of Alistipes and elevated short-chain fatty acids in both feces and serum, which in turn revealed higher circulating neutrophil counts. Finally, in a case study, we observed that adenovirus treatment resulted in increased Alistipes relative abundance and reduced Eggerthella relative abundance, indicating that adenovirus therapy may beneficially modulate the microbiome. Overall, our findings reveal a novel association between Alistipes, Eggerthella, and the therapeutic response to oncolytic adenovirus therapy, highlighting their potential as biomarkers or targets for microbiome-based interventions such as pre-, pro-, or postbiotics.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Oncolytic Virotherapy/methods
Humans
Animals
Mice
*Adenoviridae/genetics
*Fatty Acids, Volatile/metabolism
*Gastrointestinal Microbiome
*Oncolytic Viruses
Feces/microbiology
Female
*Neoplasms/therapy/microbiology
Male
RevDate: 2026-04-12
CmpDate: 2026-04-10
Social Structure and Interactions Differentially Shape Aerotolerant and Anaerobic Gut Microbiomes in a Cooperative Breeding Species.
Molecular ecology, 35(7):e70304.
Social transmission of microbes has profound impacts on disease epidemiology and host health. However, how social factors influence gut microbiome (GM) transmission in wild populations is not well understood. Here, we use a wild population of the Seychelles warbler, a facultative cooperatively breeding passerine, to determine whether cooperative breeding behaviour influences the GM. Specifically, we hypothesise that close social interactions as part of cooperative breeding should encourage the sharing of anaerobic microbes, which may be less likely to transmit indirectly through the environment. We found that GM composition was more similar within versus between social groups, and this effect was driven by sharing both aerotolerant and anaerobic bacterial genera. As predicted, the similarity of anaerobic, but not aerotolerant, GM communities between pairs of individuals within a group was positively correlated with the strength of their social interactions (defined by their cooperative breeding status). Specifically, anaerobic GM composition was more similar between pairs of individuals that cooperate at the nest (dominant breeders and dominant-helper pairs) than for non-cooperative pairs (involving non-helping subordinate individuals). This is likely because breeders and helpers directly interact while caring for offspring at a nest. This work reveals how cooperative social interactions lead to microbial transmission and thus contribute to shaping specific components of a host's gut microbiome.
Additional Links: PMID-41958318
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Citation:
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@article {pmid41958318,
year = {2026},
author = {Lee, CZ and Worsley, SF and Burke, T and Komdeur, J and Hildebrand, F and Dugdale, HL and Richardson, DS},
title = {Social Structure and Interactions Differentially Shape Aerotolerant and Anaerobic Gut Microbiomes in a Cooperative Breeding Species.},
journal = {Molecular ecology},
volume = {35},
number = {7},
pages = {e70304},
pmid = {41958318},
issn = {1365-294X},
support = {BB/T008717/1/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; BB/X011054/1/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; BBS/E/F/000PR13631/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; NE/S010939/1//Natural Environment Research Council/ ; ECF-2023-433//Leverhulme Trust/ ; erc-stg-948219 EPYC/ERC_/European Research Council/International ; BBX011089/1//Earlham Institute ISP Decoding Biodiversity/ ; BBS/E/ER/230002A//Earlham Institute ISP Decoding Biodiversity/ ; BBS/E/ER/230002B//Earlham Institute ISP Decoding Biodiversity/ ; ALWOP.531//Nederlandse Organisatie voor Wetenschappelijk Onderzoek/ ; 854.11.003//Nederlandse Organisatie voor Wetenschappelijk Onderzoek/ ; 823.01.014//Nederlandse Organisatie voor Wetenschappelijk Onderzoek/ ; //Rosalind Franklin Institute/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/genetics ; *Songbirds/microbiology ; *Cooperative Behavior ; Breeding ; Anaerobiosis ; Female ; Male ; Social Behavior ; Seychelles ; },
abstract = {Social transmission of microbes has profound impacts on disease epidemiology and host health. However, how social factors influence gut microbiome (GM) transmission in wild populations is not well understood. Here, we use a wild population of the Seychelles warbler, a facultative cooperatively breeding passerine, to determine whether cooperative breeding behaviour influences the GM. Specifically, we hypothesise that close social interactions as part of cooperative breeding should encourage the sharing of anaerobic microbes, which may be less likely to transmit indirectly through the environment. We found that GM composition was more similar within versus between social groups, and this effect was driven by sharing both aerotolerant and anaerobic bacterial genera. As predicted, the similarity of anaerobic, but not aerotolerant, GM communities between pairs of individuals within a group was positively correlated with the strength of their social interactions (defined by their cooperative breeding status). Specifically, anaerobic GM composition was more similar between pairs of individuals that cooperate at the nest (dominant breeders and dominant-helper pairs) than for non-cooperative pairs (involving non-helping subordinate individuals). This is likely because breeders and helpers directly interact while caring for offspring at a nest. This work reveals how cooperative social interactions lead to microbial transmission and thus contribute to shaping specific components of a host's gut microbiome.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Gastrointestinal Microbiome/genetics
*Songbirds/microbiology
*Cooperative Behavior
Breeding
Anaerobiosis
Female
Male
Social Behavior
Seychelles
RevDate: 2026-04-10
CmpDate: 2026-04-10
Insights Into Variations in the Gut Virome of Tibetan Macaques (Macaca thibetana) Across Wild, Captive, and Semi-Provisioned Environments.
American journal of primatology, 88(4):e70148.
Viruses are integral components of the mammalian gut ecosystem, playing crucial roles in regulating the gut microbiome and maintaining host health. However, the impact of human activity on the gut virome of mammals remains poorly understood. This study investigated the gut viromes of Tibetan macaques (Macaca thibetana), a primate species endemic to China, under three distinct human-influenced environments (wild, semi-provisioned, and captive) using metagenomic sequencing. Our results revealed that semi-provisioned macaques supported the highest viral diversity, while captive and wild groups exhibited lower diversity, with distinct functional shifts among groups. Furthermore, the co-variation and highly coupled KEGG functional profiles between viral and bacterial communities suggest they function as an integrated synergistic network, where changes in one directly impact the metabolic output of the other. Co-occurrence network analysis further demonstrated that the virus-bacterium interaction network in the captive group was the most fragile, with a structure indicative of a high risk of micro-ecosystem imbalance. Microbial system imbalance is characterized by alterations in both community composition and function, resulting in diminished resilience and stability, which may ultimately compromise host intestinal health. Our results demonstrate that captivity and provisioning drive divergence in the Tibetan macaque gut virome. The fragile, skewed networks in captive individuals highlight a potential cost to microbial health, which may underlie broader health and adaptation risks such as heightened pathogen susceptibility and diminished capacity to cope with environmental perturbations. Thus, monitoring the virome offers a novel early-warning system, informing strategies to enhance welfare and conservation outcomes.
Additional Links: PMID-41958322
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@article {pmid41958322,
year = {2026},
author = {Yang, D and Bao, C and Xia, Y and Ling, Y and Zhang, F and Ji, R and Zhong, J and Zhang, T and Tian, H and Xu, X and Sun, B},
title = {Insights Into Variations in the Gut Virome of Tibetan Macaques (Macaca thibetana) Across Wild, Captive, and Semi-Provisioned Environments.},
journal = {American journal of primatology},
volume = {88},
number = {4},
pages = {e70148},
doi = {10.1002/ajp.70148},
pmid = {41958322},
issn = {1098-2345},
support = {32171488//National Natural Science Foundation of China/ ; 32300400//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; *Macaca/virology/microbiology ; *Virome ; Tibet ; Male ; Animals, Zoo/virology ; Female ; },
abstract = {Viruses are integral components of the mammalian gut ecosystem, playing crucial roles in regulating the gut microbiome and maintaining host health. However, the impact of human activity on the gut virome of mammals remains poorly understood. This study investigated the gut viromes of Tibetan macaques (Macaca thibetana), a primate species endemic to China, under three distinct human-influenced environments (wild, semi-provisioned, and captive) using metagenomic sequencing. Our results revealed that semi-provisioned macaques supported the highest viral diversity, while captive and wild groups exhibited lower diversity, with distinct functional shifts among groups. Furthermore, the co-variation and highly coupled KEGG functional profiles between viral and bacterial communities suggest they function as an integrated synergistic network, where changes in one directly impact the metabolic output of the other. Co-occurrence network analysis further demonstrated that the virus-bacterium interaction network in the captive group was the most fragile, with a structure indicative of a high risk of micro-ecosystem imbalance. Microbial system imbalance is characterized by alterations in both community composition and function, resulting in diminished resilience and stability, which may ultimately compromise host intestinal health. Our results demonstrate that captivity and provisioning drive divergence in the Tibetan macaque gut virome. The fragile, skewed networks in captive individuals highlight a potential cost to microbial health, which may underlie broader health and adaptation risks such as heightened pathogen susceptibility and diminished capacity to cope with environmental perturbations. Thus, monitoring the virome offers a novel early-warning system, informing strategies to enhance welfare and conservation outcomes.},
}
MeSH Terms:
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hide MeSH Terms
Animals
*Gastrointestinal Microbiome
*Macaca/virology/microbiology
*Virome
Tibet
Male
Animals, Zoo/virology
Female
RevDate: 2026-04-10
CmpDate: 2026-04-10
Weight loss and metabolic improvements dominate the microbiome response in the MIND diet intervention: a randomized controlled trial.
Alzheimer's & dementia (New York, N. Y.), 12(2):e70239.
INTRODUCTION: Observational studies link the MIND diet to reduced risk of Alzheimer's disease (AD) and slower cognitive decline. However, a recent randomized controlled trial found no differential cognitive benefit of the MIND diet over a control diet in the context of shared caloric restriction. Given that both groups achieved significant weight loss and metabolic improvements, this study aimed to disentangle the impact of the MIND diet and host metabolic improvements on the intestinal microbiome.
METHODS: A subset of participants (n = 213) from the MIND trial were analyzed in this study. Clinical data and stool samples were collected at baseline, Year 1, Year 2, and Year 3, and longitudinal changes in microbiome composition were assessed via shotgun metagenomics.
RESULTS: Both groups exhibited significant, transient microbiome remodeling at Year 1 (the period of most active weight loss). The control group demonstrated a broad range of altered metabolic pathways, whereas the MIND diet group showed only one, suggesting a functional buffering effect of the MIND diet. Prospective modeling independent of diet group revealed that a poorer cognitive trajectory was significantly associated with increased inositol degradation (PWY-7237) and purine nucleotide salvage (PWY66-409); conversely, a better cognitive trajectory was associated with increased degradation of deoxy sugars (FUC-RHAMCAT-PWY).
DISCUSSION: Caloric restriction, weight loss, and host metabolic improvement are the dominant factors shaping the intestinal microbiome, overshadowing diet-specific taxonomic shifts. The MIND diet appeared to provide a modest stabilizing effect on the microbial functional profile against perturbations during active weight loss; however, these dietary associations did not persist in covariate-adjusted models, suggesting that host metabolic improvements remained the primary driver of functional shifts.
Additional Links: PMID-41958469
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Citation:
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@article {pmid41958469,
year = {2026},
author = {Voigt, RM and Chaudhary, A and Naqib, A and Engen, PA and Adnan, D and Dhana, K and Green, SJ and Villanueva, M and Agarwal, P and Barnes, LL and Sacks, F and Keshavarzian, A},
title = {Weight loss and metabolic improvements dominate the microbiome response in the MIND diet intervention: a randomized controlled trial.},
journal = {Alzheimer's & dementia (New York, N. Y.)},
volume = {12},
number = {2},
pages = {e70239},
pmid = {41958469},
issn = {2352-8737},
abstract = {INTRODUCTION: Observational studies link the MIND diet to reduced risk of Alzheimer's disease (AD) and slower cognitive decline. However, a recent randomized controlled trial found no differential cognitive benefit of the MIND diet over a control diet in the context of shared caloric restriction. Given that both groups achieved significant weight loss and metabolic improvements, this study aimed to disentangle the impact of the MIND diet and host metabolic improvements on the intestinal microbiome.
METHODS: A subset of participants (n = 213) from the MIND trial were analyzed in this study. Clinical data and stool samples were collected at baseline, Year 1, Year 2, and Year 3, and longitudinal changes in microbiome composition were assessed via shotgun metagenomics.
RESULTS: Both groups exhibited significant, transient microbiome remodeling at Year 1 (the period of most active weight loss). The control group demonstrated a broad range of altered metabolic pathways, whereas the MIND diet group showed only one, suggesting a functional buffering effect of the MIND diet. Prospective modeling independent of diet group revealed that a poorer cognitive trajectory was significantly associated with increased inositol degradation (PWY-7237) and purine nucleotide salvage (PWY66-409); conversely, a better cognitive trajectory was associated with increased degradation of deoxy sugars (FUC-RHAMCAT-PWY).
DISCUSSION: Caloric restriction, weight loss, and host metabolic improvement are the dominant factors shaping the intestinal microbiome, overshadowing diet-specific taxonomic shifts. The MIND diet appeared to provide a modest stabilizing effect on the microbial functional profile against perturbations during active weight loss; however, these dietary associations did not persist in covariate-adjusted models, suggesting that host metabolic improvements remained the primary driver of functional shifts.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
Artificial intelligence-driven gastrointestinal functional assessment: multimodal imaging, digital biomarkers, and real-time monitoring.
Frontiers in physiology, 17:1778235.
Gastrointestinal (GI) functional disorders and chronic inflammatory diseases impose a substantial health burden, yet their assessment remains challenging because symptoms reflect dynamic interactions among motility, visceral sensation, immune-microbiome regulation, and brain-gut signaling. Artificial intelligence (AI) is rapidly reshaping GI functional medicine by enabling scalable, quantitative interpretation of complex data generated from multimodal imaging, physiological sensing, and real-world patient monitoring. This review synthesizes advances across three tightly connected pillars that map onto a physiology-informed "assessment-to-action" loop: (i) AI-assisted multimodal GI imaging for quantitative phenotyping and integrated diagnosis; (ii) AI-enabled discovery and validation of digital biomarkers that capture dynamic GI function in naturalistic settings; and (iii) real-time monitoring platforms that support early warning, longitudinal assessment, and adaptive management. We summarize representative applications in functional GI disorders, inflammatory bowel disease (IBD), and GI oncology, highlighting methodological themes including multimodal fusion, temporal modeling, uncertainty estimation, and explainable AI. We then discuss barriers to translation-standardization and interoperability, external validation under dataset shift, privacy and governance, and workflow integration-and outline practical directions for building clinically trustworthy AI systems for GI functional assessment. Collectively, physiology-centered AI approaches have the potential to transform GI care from episodic testing to longitudinal, mechanism-aware monitoring and personalized intervention.
Additional Links: PMID-41958528
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Citation:
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@article {pmid41958528,
year = {2026},
author = {Li, L and Lv, F and Du, C and Yang, L and Pa, C and Dai, Y},
title = {Artificial intelligence-driven gastrointestinal functional assessment: multimodal imaging, digital biomarkers, and real-time monitoring.},
journal = {Frontiers in physiology},
volume = {17},
number = {},
pages = {1778235},
pmid = {41958528},
issn = {1664-042X},
abstract = {Gastrointestinal (GI) functional disorders and chronic inflammatory diseases impose a substantial health burden, yet their assessment remains challenging because symptoms reflect dynamic interactions among motility, visceral sensation, immune-microbiome regulation, and brain-gut signaling. Artificial intelligence (AI) is rapidly reshaping GI functional medicine by enabling scalable, quantitative interpretation of complex data generated from multimodal imaging, physiological sensing, and real-world patient monitoring. This review synthesizes advances across three tightly connected pillars that map onto a physiology-informed "assessment-to-action" loop: (i) AI-assisted multimodal GI imaging for quantitative phenotyping and integrated diagnosis; (ii) AI-enabled discovery and validation of digital biomarkers that capture dynamic GI function in naturalistic settings; and (iii) real-time monitoring platforms that support early warning, longitudinal assessment, and adaptive management. We summarize representative applications in functional GI disorders, inflammatory bowel disease (IBD), and GI oncology, highlighting methodological themes including multimodal fusion, temporal modeling, uncertainty estimation, and explainable AI. We then discuss barriers to translation-standardization and interoperability, external validation under dataset shift, privacy and governance, and workflow integration-and outline practical directions for building clinically trustworthy AI systems for GI functional assessment. Collectively, physiology-centered AI approaches have the potential to transform GI care from episodic testing to longitudinal, mechanism-aware monitoring and personalized intervention.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
Gut microbiome differences by serostatus in rheumatoid arthritis: a systematic review.
Frontiers in immunology, 17:1722255.
BACKGROUND: Rheumatoid arthritis (RA) is a heterogeneous autoimmune disease in which serological status, defined by rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPA), influences disease course. Alterations of the gut microbiome have been implicated in RA, but differences between seropositive and seronegative patients, and between seropositive RA and healthy controls, have not been systematically reviewed.
METHODS: PubMed, Scopus, Web of Science, and the Cochrane Library were searched to July 2025 for observational studies of adult RA patients reporting RF and/or ACPA status with gut microbiome analysis. Two reviewers independently screened, extracted data, and assessed quality using the Newcastle-Ottawa Scale (NOS).
RESULTS: Eight studies published between 2016 and 2024 met the inclusion criteria. Six investigated both RF and ACPA, while two focused primarily on ACPA. In seropositive RA, higher abundances of Collinsella and Blautia and lower levels of Faecalibacterium were consistently reported. Several studies demonstrated reduced α-diversity in seropositive patients compared with seronegative RA or healthy controls, particularly in preclinical or early disease, while established RA showed no consistent differences. Findings for β-diversity were heterogeneous, with some cohorts reporting significant associations with serostatus, whereas others found no clear separation.
CONCLUSIONS: Seropositive RA, especially ACPA-positive, is frequently associated with reduced microbial diversity and distinct compositional shifts compared with seronegative RA and healthy controls. Larger standardized studies are required to validate these associations and assess their biomarker potential.
https://www.crd.york.ac.uk/prospero/, identifier CRD420251140715.
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@article {pmid41958652,
year = {2026},
author = {Nurgaziyev, M and Kozhakhmetov, S and Issilbayeva, A and Jarmukhanov, Z and Nurgaziyeva, A and Sergazy, S and Kuantkhan, M and Chulenbayeva, L and Kushugulova, A},
title = {Gut microbiome differences by serostatus in rheumatoid arthritis: a systematic review.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1722255},
pmid = {41958652},
issn = {1664-3224},
mesh = {Humans ; *Arthritis, Rheumatoid/immunology/microbiology/blood ; *Gastrointestinal Microbiome/immunology ; Anti-Citrullinated Protein Antibodies/blood/immunology ; Rheumatoid Factor/blood/immunology ; },
abstract = {BACKGROUND: Rheumatoid arthritis (RA) is a heterogeneous autoimmune disease in which serological status, defined by rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPA), influences disease course. Alterations of the gut microbiome have been implicated in RA, but differences between seropositive and seronegative patients, and between seropositive RA and healthy controls, have not been systematically reviewed.
METHODS: PubMed, Scopus, Web of Science, and the Cochrane Library were searched to July 2025 for observational studies of adult RA patients reporting RF and/or ACPA status with gut microbiome analysis. Two reviewers independently screened, extracted data, and assessed quality using the Newcastle-Ottawa Scale (NOS).
RESULTS: Eight studies published between 2016 and 2024 met the inclusion criteria. Six investigated both RF and ACPA, while two focused primarily on ACPA. In seropositive RA, higher abundances of Collinsella and Blautia and lower levels of Faecalibacterium were consistently reported. Several studies demonstrated reduced α-diversity in seropositive patients compared with seronegative RA or healthy controls, particularly in preclinical or early disease, while established RA showed no consistent differences. Findings for β-diversity were heterogeneous, with some cohorts reporting significant associations with serostatus, whereas others found no clear separation.
CONCLUSIONS: Seropositive RA, especially ACPA-positive, is frequently associated with reduced microbial diversity and distinct compositional shifts compared with seronegative RA and healthy controls. Larger standardized studies are required to validate these associations and assess their biomarker potential.
https://www.crd.york.ac.uk/prospero/, identifier CRD420251140715.},
}
MeSH Terms:
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Humans
*Arthritis, Rheumatoid/immunology/microbiology/blood
*Gastrointestinal Microbiome/immunology
Anti-Citrullinated Protein Antibodies/blood/immunology
Rheumatoid Factor/blood/immunology
RevDate: 2026-04-10
CmpDate: 2026-04-10
Microbe-driven immune suppression in colorectal cancer: the Fusobacterium nucleatum playbook.
Frontiers in immunology, 17:1795703.
Fusobacterium nucleatum, a key oral-pathobiont in colorectal cancer (CRC), has evolved from a presumed "passenger" to an active "co-conspirator" in tumorigenesis. This review systematically delineates its core role as an "architect of the immune microenvironment," whereby it remodels T-cell immune responses through precise mechanisms to establish an immunosuppressive tumor microenvironment. Specifically, F. nucleatum employs virulence factors such as Fap2 and FadA for specific colonization, and achieves immune evasion by inhibiting NK and T-cell function and recruiting myeloid-derived suppressor cells (MDSCs). Post-colonization, it further fine-tunes T-cell subsets: driving Th17 polarization to create a pro-inflammatory milieu while suppressing the infiltration and function of CD8[+] T cells and promoting their exhaustion. Intriguingly, it upregulates programmed death-ligand 1 (PD-L1) expression, which may conversely enhance tumor sensitivity to anti-PD-1/PD-L1 immunotherapy. Moreover, it collaborates with other microbes via quorum sensing and the oral-gut axis to construct a procarcinogenic ecosystem. Based on these mechanisms, F. nucleatum exhibits substantial clinical translational potential. Its load serves as an effective non-invasive diagnostic biomarker and a prognostic predictor, and may help predict responses to immune checkpoint inhibitors. Therapeutically, strategies targeting the eradication or inhibition of F. nucleatum-including antibiotics, specific phages, virulence factor inhibitors, and combination immunotherapy-represent highly promising novel directions. Despite existing challenges, future efforts to deepen mechanistic understanding, develop precision intervention tools, and establish integrated patient stratification systems hold the potential to revolutionize CRC prevention, diagnosis, and combination therapy by targeting F. nucleatum.
Additional Links: PMID-41958661
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@article {pmid41958661,
year = {2026},
author = {Wuyi, W and Tao, P},
title = {Microbe-driven immune suppression in colorectal cancer: the Fusobacterium nucleatum playbook.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1795703},
pmid = {41958661},
issn = {1664-3224},
mesh = {Humans ; *Colorectal Neoplasms/immunology/microbiology/therapy ; *Fusobacterium nucleatum/immunology ; Tumor Microenvironment/immunology ; Animals ; *Fusobacterium Infections/immunology/microbiology ; },
abstract = {Fusobacterium nucleatum, a key oral-pathobiont in colorectal cancer (CRC), has evolved from a presumed "passenger" to an active "co-conspirator" in tumorigenesis. This review systematically delineates its core role as an "architect of the immune microenvironment," whereby it remodels T-cell immune responses through precise mechanisms to establish an immunosuppressive tumor microenvironment. Specifically, F. nucleatum employs virulence factors such as Fap2 and FadA for specific colonization, and achieves immune evasion by inhibiting NK and T-cell function and recruiting myeloid-derived suppressor cells (MDSCs). Post-colonization, it further fine-tunes T-cell subsets: driving Th17 polarization to create a pro-inflammatory milieu while suppressing the infiltration and function of CD8[+] T cells and promoting their exhaustion. Intriguingly, it upregulates programmed death-ligand 1 (PD-L1) expression, which may conversely enhance tumor sensitivity to anti-PD-1/PD-L1 immunotherapy. Moreover, it collaborates with other microbes via quorum sensing and the oral-gut axis to construct a procarcinogenic ecosystem. Based on these mechanisms, F. nucleatum exhibits substantial clinical translational potential. Its load serves as an effective non-invasive diagnostic biomarker and a prognostic predictor, and may help predict responses to immune checkpoint inhibitors. Therapeutically, strategies targeting the eradication or inhibition of F. nucleatum-including antibiotics, specific phages, virulence factor inhibitors, and combination immunotherapy-represent highly promising novel directions. Despite existing challenges, future efforts to deepen mechanistic understanding, develop precision intervention tools, and establish integrated patient stratification systems hold the potential to revolutionize CRC prevention, diagnosis, and combination therapy by targeting F. nucleatum.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Colorectal Neoplasms/immunology/microbiology/therapy
*Fusobacterium nucleatum/immunology
Tumor Microenvironment/immunology
Animals
*Fusobacterium Infections/immunology/microbiology
RevDate: 2026-04-10
CmpDate: 2026-04-10
Gut microbe Terrisporobacter promotes papillary thyroid carcinoma progression by upregulating the NTRK1 oncogene and fostering an immunosuppressive tumor microenvironment.
Frontiers in immunology, 17:1740257.
Growing evidence suggests a link between the gut microbiome and papillary thyroid carcinoma (PTC), but the causal relationships and the impact on the tumor immune microenvironment (TME) are poorly understood. This study aimed to elucidate the causal role of specific gut microbes in PTC and uncover the underlying immunological and molecular mechanisms. We employed a multi-stage design, beginning with a two-sample Mendelian randomization (MR) analysis using large-scale GWAS data to infer causality. Findings were then validated in 450 PTC patients from The Cancer Genome Atlas (TCGA) by analyzing correlations between microbial abundance, gene expression, immune cell infiltration, and survival. Finally, the core mechanism was confirmed through extensive in vitro experiments with PTC cell lines. Our MR analysis identified a causal association between a genetically predicted higher abundance of the genus Terrisporobacter and an increased risk of PTC (Odds Ratio [OR] = 2.06, 95% Confidence Interval [CI]: 1.34-3.16). In the TCGA cohort, higher intratumoral signals of Terrisporobacter was significantly correlated with an immunosuppressive TME, characterized by increased infiltration of M2 macrophages (ρ = 0.25, p < 0.001) and decreased CD8+ T cells (ρ = -0.19, p = 0.008). Mechanistically, Terrisporobacter abundance was also strongly associated with the upregulation of the oncogene NTRK1 (ρ = 0.35, p < 0.001), which independently predicted poorer overall survival (Hazard Ratio [HR] = 2.15, p = 0.004). In vitro experiments confirmed that supernatant from Terrisporobacter culture not only upregulated NTRK1 expression and promoted PTC cell proliferation but also enhanced invasion and induced cell de-differentiation. Importantly, pharmacological inhibition of TRK signaling reversed the bacteria-induced aggressive phenotype. Our integrated analysis provides robust, multi-layered evidence for a causal role of Terrisporobacter in promoting PTC progression. We define a novel gut-thyroid axis where Terrisporobacter contributes to PTC development by upregulating the NTRK1 oncogene and shaping a pro-tumorigenic, immunosuppressive microenvironment. These findings reveal a new dimension of host-microbe interaction in thyroid cancer and highlight the TME as a key downstream target of microbial influence.
Additional Links: PMID-41958678
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@article {pmid41958678,
year = {2026},
author = {Li, J and Shen, J and Lu, D and Ding, E and Wei, L},
title = {Gut microbe Terrisporobacter promotes papillary thyroid carcinoma progression by upregulating the NTRK1 oncogene and fostering an immunosuppressive tumor microenvironment.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1740257},
pmid = {41958678},
issn = {1664-3224},
mesh = {Humans ; *Tumor Microenvironment/immunology ; *Thyroid Cancer, Papillary/immunology/pathology/genetics/microbiology ; *Gastrointestinal Microbiome/immunology ; *Thyroid Neoplasms/immunology/pathology/microbiology/genetics ; *Receptor, trkA/genetics/metabolism ; Disease Progression ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Up-Regulation ; },
abstract = {Growing evidence suggests a link between the gut microbiome and papillary thyroid carcinoma (PTC), but the causal relationships and the impact on the tumor immune microenvironment (TME) are poorly understood. This study aimed to elucidate the causal role of specific gut microbes in PTC and uncover the underlying immunological and molecular mechanisms. We employed a multi-stage design, beginning with a two-sample Mendelian randomization (MR) analysis using large-scale GWAS data to infer causality. Findings were then validated in 450 PTC patients from The Cancer Genome Atlas (TCGA) by analyzing correlations between microbial abundance, gene expression, immune cell infiltration, and survival. Finally, the core mechanism was confirmed through extensive in vitro experiments with PTC cell lines. Our MR analysis identified a causal association between a genetically predicted higher abundance of the genus Terrisporobacter and an increased risk of PTC (Odds Ratio [OR] = 2.06, 95% Confidence Interval [CI]: 1.34-3.16). In the TCGA cohort, higher intratumoral signals of Terrisporobacter was significantly correlated with an immunosuppressive TME, characterized by increased infiltration of M2 macrophages (ρ = 0.25, p < 0.001) and decreased CD8+ T cells (ρ = -0.19, p = 0.008). Mechanistically, Terrisporobacter abundance was also strongly associated with the upregulation of the oncogene NTRK1 (ρ = 0.35, p < 0.001), which independently predicted poorer overall survival (Hazard Ratio [HR] = 2.15, p = 0.004). In vitro experiments confirmed that supernatant from Terrisporobacter culture not only upregulated NTRK1 expression and promoted PTC cell proliferation but also enhanced invasion and induced cell de-differentiation. Importantly, pharmacological inhibition of TRK signaling reversed the bacteria-induced aggressive phenotype. Our integrated analysis provides robust, multi-layered evidence for a causal role of Terrisporobacter in promoting PTC progression. We define a novel gut-thyroid axis where Terrisporobacter contributes to PTC development by upregulating the NTRK1 oncogene and shaping a pro-tumorigenic, immunosuppressive microenvironment. These findings reveal a new dimension of host-microbe interaction in thyroid cancer and highlight the TME as a key downstream target of microbial influence.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Tumor Microenvironment/immunology
*Thyroid Cancer, Papillary/immunology/pathology/genetics/microbiology
*Gastrointestinal Microbiome/immunology
*Thyroid Neoplasms/immunology/pathology/microbiology/genetics
*Receptor, trkA/genetics/metabolism
Disease Progression
Cell Line, Tumor
Gene Expression Regulation, Neoplastic
Up-Regulation
RevDate: 2026-04-11
Bayesian Multinomial Logistic Normal Models through Marginally Latent Matrix-T Processes.
Journal of machine learning research : JMLR, 23:.
Bayesian multinomial logistic-normal (MLN) models are popular for the analysis of sequence count data (e.g., microbiome or gene expression data) due to their ability to model multivariate count data with complex covariance structure. However, existing implementations of MLN models are limited to small datasets due to the non-conjugacy of the multinomial and logistic-normal distributions. Motivated by the need to develop efficient inference for Bayesian MLN models, we develop two key ideas. First, we develop the class of Marginally Latent Matrix-T Process (Marginally LTP) models. We demonstrate that many popular MLN models, including those with latent linear, non-linear, and dynamic linear structure are special cases of this class. Second, we develop an efficient inference scheme for Marginally LTP models with specific accelerations for the MLN subclass. Through application to MLN models, we demonstrate that our inference scheme are both highly accurate and often 4-5 orders of magnitude faster than MCMC.
Additional Links: PMID-41958966
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@article {pmid41958966,
year = {2022},
author = {Silverman, JD and Roche, K and Holmes, ZC and David, LA and Mukherjee, S},
title = {Bayesian Multinomial Logistic Normal Models through Marginally Latent Matrix-T Processes.},
journal = {Journal of machine learning research : JMLR},
volume = {23},
number = {},
pages = {},
pmid = {41958966},
issn = {1532-4435},
support = {R01 DK116187/DK/NIDDK NIH HHS/United States ; T32 GM007171/GM/NIGMS NIH HHS/United States ; },
abstract = {Bayesian multinomial logistic-normal (MLN) models are popular for the analysis of sequence count data (e.g., microbiome or gene expression data) due to their ability to model multivariate count data with complex covariance structure. However, existing implementations of MLN models are limited to small datasets due to the non-conjugacy of the multinomial and logistic-normal distributions. Motivated by the need to develop efficient inference for Bayesian MLN models, we develop two key ideas. First, we develop the class of Marginally Latent Matrix-T Process (Marginally LTP) models. We demonstrate that many popular MLN models, including those with latent linear, non-linear, and dynamic linear structure are special cases of this class. Second, we develop an efficient inference scheme for Marginally LTP models with specific accelerations for the MLN subclass. Through application to MLN models, we demonstrate that our inference scheme are both highly accurate and often 4-5 orders of magnitude faster than MCMC.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
Characterisation of vaginal Lactobacillus isolates from South African women towards the development of a biotherapeutic to optimise the vaginal microbiome.
bioRxiv : the preprint server for biology pii:2026.03.26.714511.
UNLABELLED: HIV remains among the world's most serious healthcare challenges, with adolescent girls and young women in sub-Saharan Africa at particularly high risk of infection. Bacterial vaginosis (BV) is a key risk factor for HIV acquisition, however current treatment strategies are limited. Optimal vaginal Lactobacillus spp. protect against BV and HIV, largely through immunoregulatory and antimicrobial activities mediated in part by lactic acid. Towards the development of a Lactobacillus -containing live biotherapeutic for African women, we sampled 181 vaginal Lactobacillus isolates from 25 BV-negative South African women. Fifty isolates were selected for evaluation of inflammatory responses using vaginal epithelial cells, D- and L-lactate and lactic acid production and culture acidification. Aside from a single Lactobacillus salivarius strain, L. crispatus isolates acidified the culture media the most and produced the most D- and L-lactic acid. Inflammatory cytokine responses to Lactobacillus strains were variable, with L. crispatus eliciting the lowest levels of cytokine production. When all properties were evaluated collectively, L. crispatus strains exhibited the most desirable biotherapeutic characteristics. Whole genome sequence analysis of ten L. crispatus isolates showed that the majority were more closely related to one another than to isolates from other geographical regions. This supports the need for live biotherapeutics to be tailored for the population of intended use. No antimicrobial resistance elements were detected, while putative bacteriocins and intact prophage sequences were identified in all isolates. L. crispatus isolates displayed characteristics essential for optimal live biotherapeutic performance, however additional analysis is required to determine the functionality of identified putative prophages.
IMPORTANCE: HIV is a leading cause of morbidity and mortality in sub-Saharan Africa, where adolescent girls and young women are three times more likely to acquire HIV than their male counterparts. A key risk factor for HIV is bacterial vaginosis (BV), a condition characterised by the loss of beneficial Lactobacillus species and increased abundance of non-optimal, inflammatory bacteria. Although BV affects approximately 25% of women in sub-Saharan Africa, effective therapeutics are lacking. Live biotherapeutics containing optimal Lactobacillus spp. represent a promising strategy to improve BV treatment outcomes and reduce HIV infection risk. We isolated 181 vaginal Lactobacillus spp. from 25 BV-negative South African women and characterized 50 selected isolates. This led to the identification of live biotherapeutic candidates for African women with distinct genomes compared to isolates from other geographical regions. This study contributes to current knowledge of the characteristics that should be considered when screening novel isolates for this purpose.
Additional Links: PMID-41959050
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@article {pmid41959050,
year = {2026},
author = {Wilson, J and Amir Hamzah, AS and Jordan, C and Hayward, JA and Kullin, B and Manhanzva, MT and Tyssen, D and Mehou-Loko, C and Abrahams, AG and Radzey, N and Harryparsad, R and Meyer, B and Hearps, AC and Ziemann, M and Humphries, H and Mkhize, P and Bekker, LG and Passmore, JS and Jaspan, HB and Sheppard, AE and Tachedjian, G and Masson, L},
title = {Characterisation of vaginal Lactobacillus isolates from South African women towards the development of a biotherapeutic to optimise the vaginal microbiome.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.26.714511},
pmid = {41959050},
issn = {2692-8205},
abstract = {UNLABELLED: HIV remains among the world's most serious healthcare challenges, with adolescent girls and young women in sub-Saharan Africa at particularly high risk of infection. Bacterial vaginosis (BV) is a key risk factor for HIV acquisition, however current treatment strategies are limited. Optimal vaginal Lactobacillus spp. protect against BV and HIV, largely through immunoregulatory and antimicrobial activities mediated in part by lactic acid. Towards the development of a Lactobacillus -containing live biotherapeutic for African women, we sampled 181 vaginal Lactobacillus isolates from 25 BV-negative South African women. Fifty isolates were selected for evaluation of inflammatory responses using vaginal epithelial cells, D- and L-lactate and lactic acid production and culture acidification. Aside from a single Lactobacillus salivarius strain, L. crispatus isolates acidified the culture media the most and produced the most D- and L-lactic acid. Inflammatory cytokine responses to Lactobacillus strains were variable, with L. crispatus eliciting the lowest levels of cytokine production. When all properties were evaluated collectively, L. crispatus strains exhibited the most desirable biotherapeutic characteristics. Whole genome sequence analysis of ten L. crispatus isolates showed that the majority were more closely related to one another than to isolates from other geographical regions. This supports the need for live biotherapeutics to be tailored for the population of intended use. No antimicrobial resistance elements were detected, while putative bacteriocins and intact prophage sequences were identified in all isolates. L. crispatus isolates displayed characteristics essential for optimal live biotherapeutic performance, however additional analysis is required to determine the functionality of identified putative prophages.
IMPORTANCE: HIV is a leading cause of morbidity and mortality in sub-Saharan Africa, where adolescent girls and young women are three times more likely to acquire HIV than their male counterparts. A key risk factor for HIV is bacterial vaginosis (BV), a condition characterised by the loss of beneficial Lactobacillus species and increased abundance of non-optimal, inflammatory bacteria. Although BV affects approximately 25% of women in sub-Saharan Africa, effective therapeutics are lacking. Live biotherapeutics containing optimal Lactobacillus spp. represent a promising strategy to improve BV treatment outcomes and reduce HIV infection risk. We isolated 181 vaginal Lactobacillus spp. from 25 BV-negative South African women and characterized 50 selected isolates. This led to the identification of live biotherapeutic candidates for African women with distinct genomes compared to isolates from other geographical regions. This study contributes to current knowledge of the characteristics that should be considered when screening novel isolates for this purpose.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
Infant gut microbiomes contribute to metabolic states that impact brain function.
bioRxiv : the preprint server for biology pii:2026.03.09.710596.
Alterations in the gut microbiome are associated with neurodevelopmental disorders, but causal mechanisms and therapeutic strategies remain undefined. Here, we demonstrate that human infant microbiomes isolated during the first six months of life drive behavioral impairments in mice and that microbiota-based interventions restore mice to normal behavior. Early-life microbiomes from twelve infants who later exhibited cognitive deficits at 2 years old (low-scoring) transferred adverse metabolic, brain, and behavioral phenotypes to mice, in contrast to microbiomes from twenty-three cognitively typical or high-scoring infants. Deficits in mice were rescued by fecal microbiota transplant from high-scoring infants or a rationally designed consortium that promoted amino acid levels. We confirmed lower fecal amino acid concentrations in low-scoring infants and replicated the association between early-life microbiome composition and cognitive outcomes in a second geographically independent infant cohort. Altogether, we discovered an early-life microbiome-mediated metabolic state causally linked to cognitive deficits and amenable to microbial intervention.
Additional Links: PMID-41959053
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@article {pmid41959053,
year = {2026},
author = {Midani, FS and Lee, DH and Moon, Y and Seale, M and Horvath, TD and Ardis, AK and Cantú, J and Coles, E and Pizzini, JD and Zhu, D and Dooling, SW and Ahern, GJ and Ardis, CK and Beckford, A and Ruggiero, NM and Shin, J and Joos, R and Stanton, C and Ross, RP and Dai, DLY and Mandhane, PJ and Petersen, C and Turvey, SE and Kiely, ME and Murray, DM and Costa-Mattioli, M and Tolias, KF and Britton, RA and Danhof, HA},
title = {Infant gut microbiomes contribute to metabolic states that impact brain function.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.09.710596},
pmid = {41959053},
issn = {2692-8205},
abstract = {Alterations in the gut microbiome are associated with neurodevelopmental disorders, but causal mechanisms and therapeutic strategies remain undefined. Here, we demonstrate that human infant microbiomes isolated during the first six months of life drive behavioral impairments in mice and that microbiota-based interventions restore mice to normal behavior. Early-life microbiomes from twelve infants who later exhibited cognitive deficits at 2 years old (low-scoring) transferred adverse metabolic, brain, and behavioral phenotypes to mice, in contrast to microbiomes from twenty-three cognitively typical or high-scoring infants. Deficits in mice were rescued by fecal microbiota transplant from high-scoring infants or a rationally designed consortium that promoted amino acid levels. We confirmed lower fecal amino acid concentrations in low-scoring infants and replicated the association between early-life microbiome composition and cognitive outcomes in a second geographically independent infant cohort. Altogether, we discovered an early-life microbiome-mediated metabolic state causally linked to cognitive deficits and amenable to microbial intervention.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
A Droplet Digital PCR Assay for Quantification of Bacteriophage Viral Vector Titer and Purity.
bioRxiv : the preprint server for biology pii:2024.11.20.624577.
PURPOSE: Bacteriophage (phage) based vectors offer considerable promise as tools for tuning the microbiome with molecular and genetic precision. However, standardized methods to rigorously characterize phage vectors remain lacking. Here, we present an optimized digital droplet PCR (ddPCR)-based assay for quantifying both the purity and potency of phage vector preparations.
METHODS: We utilized central composite design to develop a ddPCR assay capable of quantifying the number of phage vector capsids packed with the phage vector genome or packed with the transgenic DNA of interest. This assay targets 2 unique DNA barcodes, designed to be biologically inert and maximally orthogonal to existing DNA sequences.
RESULTS: Through stringent optimization, we were able to achieve assay conditions that enable a dynamic range of nearly 3 orders of magnitude and correct for systemic error in the assay. We then show that biological activity assays consistently underestimate transgene-packed vectors titers, leading to overestimation of true transduction efficiency, particularly when contamination by genome-packed vectors is high. We further demonstrate how this approach facilitates optimization of vector production conditions and substantially improves the precision and reproducibility of phage vector transduction.
CONCLUSION: Compared to assays of biological activity, this optimized ddPCR assay has improved accuracy and, through design of experiments optimization, high precision (CVs = 5.5 ± 1.3% and 4.5 ± 1.0% for the genome and transgene barcodes, respectively). This assay can be broadly adopted to characterize and quality control vector preparations for various applications.
Additional Links: PMID-41959059
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@article {pmid41959059,
year = {2026},
author = {Voorhees, PJ and Ponek, RM and Liu, JD and Lai, SK},
title = {A Droplet Digital PCR Assay for Quantification of Bacteriophage Viral Vector Titer and Purity.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2024.11.20.624577},
pmid = {41959059},
issn = {2692-8205},
abstract = {PURPOSE: Bacteriophage (phage) based vectors offer considerable promise as tools for tuning the microbiome with molecular and genetic precision. However, standardized methods to rigorously characterize phage vectors remain lacking. Here, we present an optimized digital droplet PCR (ddPCR)-based assay for quantifying both the purity and potency of phage vector preparations.
METHODS: We utilized central composite design to develop a ddPCR assay capable of quantifying the number of phage vector capsids packed with the phage vector genome or packed with the transgenic DNA of interest. This assay targets 2 unique DNA barcodes, designed to be biologically inert and maximally orthogonal to existing DNA sequences.
RESULTS: Through stringent optimization, we were able to achieve assay conditions that enable a dynamic range of nearly 3 orders of magnitude and correct for systemic error in the assay. We then show that biological activity assays consistently underestimate transgene-packed vectors titers, leading to overestimation of true transduction efficiency, particularly when contamination by genome-packed vectors is high. We further demonstrate how this approach facilitates optimization of vector production conditions and substantially improves the precision and reproducibility of phage vector transduction.
CONCLUSION: Compared to assays of biological activity, this optimized ddPCR assay has improved accuracy and, through design of experiments optimization, high precision (CVs = 5.5 ± 1.3% and 4.5 ± 1.0% for the genome and transgene barcodes, respectively). This assay can be broadly adopted to characterize and quality control vector preparations for various applications.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
Sleeve gastrectomy protects lean mice from future obesity.
bioRxiv : the preprint server for biology pii:2026.03.09.710623.
BACKGROUND: Obesity and metabolic disease drive premature aging and reduced lifespan. While metabolic interventions like calorie restriction, protein restriction, and time restricted feeding have been shown to improved lifespan, they are either not effective or sustainable for most humans. Bariatric surgery is the most efficacious metabolic intervention available and is associated with increased lifespan. However, whether its longevity benefits derive solely from weight reduction or reflect surgery-specific metabolic reprogramming remains unknown.
METHODS: We employed a lean mouse model of sleeve gastrectomy (SG) in which young, lean male C57BL/6J mice underwent SG or sham operation while maintained on low-fat chow, then were challenged with high-fat diet (HFD) in midlife. We assessed glucose metabolism, body composition, energy expenditure, hepatic histology, adipose tissue inflammation, and cecal microbiome composition.
RESULTS: Despite identical weight and food intake on low-fat chow, SG mice demonstrated improved glucose tolerance and insulin sensitivity prior to HFD challenge. Upon HFD exposure, SG animals exhibited enhanced metabolic flexibility with greater capacity for fat oxidation, increased energy expenditure, attenuated weight gain, and reduced adiposity compared to sham controls. SG further reduced hepatic lipid accumulation and attenuated visceral adipose tissue inflammation, marked by decreased pro-inflammatory cytokine expression and reduced macrophage infiltration. These metabolic benefits occurred independently of caloric intake. Cecal microbiome profiling revealed surgery-specific remodeling characterized by Lactobacillus enrichment and reductions in Verrucomicrobia and Clostridia - a pattern distinct from caloric restriction and consistent with prior SG studies.
CONCLUSIONS: Early-life SG confers durable, weight-loss-independent protection against midlife metabolic deterioration. Gut microbiome remodeling, particularly enrichment of Lactobacillus species, represents a candidate mediating mechanism and a potential therapeutic target for aging and metabolic disease.
Additional Links: PMID-41959063
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@article {pmid41959063,
year = {2026},
author = {Moscalu, A and Babygirijia, R and Mathew, T and Chaudhari, SN and Zhang, D and Zhou, L and Sheu, EG and Harris, DA},
title = {Sleeve gastrectomy protects lean mice from future obesity.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.09.710623},
pmid = {41959063},
issn = {2692-8205},
abstract = {BACKGROUND: Obesity and metabolic disease drive premature aging and reduced lifespan. While metabolic interventions like calorie restriction, protein restriction, and time restricted feeding have been shown to improved lifespan, they are either not effective or sustainable for most humans. Bariatric surgery is the most efficacious metabolic intervention available and is associated with increased lifespan. However, whether its longevity benefits derive solely from weight reduction or reflect surgery-specific metabolic reprogramming remains unknown.
METHODS: We employed a lean mouse model of sleeve gastrectomy (SG) in which young, lean male C57BL/6J mice underwent SG or sham operation while maintained on low-fat chow, then were challenged with high-fat diet (HFD) in midlife. We assessed glucose metabolism, body composition, energy expenditure, hepatic histology, adipose tissue inflammation, and cecal microbiome composition.
RESULTS: Despite identical weight and food intake on low-fat chow, SG mice demonstrated improved glucose tolerance and insulin sensitivity prior to HFD challenge. Upon HFD exposure, SG animals exhibited enhanced metabolic flexibility with greater capacity for fat oxidation, increased energy expenditure, attenuated weight gain, and reduced adiposity compared to sham controls. SG further reduced hepatic lipid accumulation and attenuated visceral adipose tissue inflammation, marked by decreased pro-inflammatory cytokine expression and reduced macrophage infiltration. These metabolic benefits occurred independently of caloric intake. Cecal microbiome profiling revealed surgery-specific remodeling characterized by Lactobacillus enrichment and reductions in Verrucomicrobia and Clostridia - a pattern distinct from caloric restriction and consistent with prior SG studies.
CONCLUSIONS: Early-life SG confers durable, weight-loss-independent protection against midlife metabolic deterioration. Gut microbiome remodeling, particularly enrichment of Lactobacillus species, represents a candidate mediating mechanism and a potential therapeutic target for aging and metabolic disease.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
Increased S. epidermidis in the airway-gut microbiome of infants with bronchopulmonary dysplasia.
bioRxiv : the preprint server for biology pii:2026.04.03.715941.
RATIONALE: Bronchopulmonary dysplasia (BPD), the lung disease associated with premature birth, is a significant health problem, often with long-term respiratory consequences. Recent research has highlighted the potential role of the lung and gut microbiome in the development and progression of BPD, yet it is unclear what aspects of the microbiome may contribute to BPD susceptibility.
OBJECTIVES: To comprehensively characterize the lung and gut microbiomes of preterm infants and identify shared microbial taxa that are associated with BPD development.
METHODS: Tracheal aspirate and stool samples were collected from 39 premature infants over the first month of life. To assess the taxonomic microbial composition of the lung and gut, samples were analyzed using shotgun metagenomic sequencing. BPD classification was determined using the National Institute of Child Health and Human Development severity-based definition at 36 weeks postmenstrual age.
MEASUREMENTS AND MAIN RESULTS: Microbial communities of the lung and gut were significantly different between infants who went on to develop BPD and those who did not, with an enrichment of skin-associated microbial genera such as Staphylococcus, Corynebacterium, and Cutibacterium in infants who developed BPD. Specifically, Staphylococcus epidermidis was enriched in premature infants who developed BPD and was the most prominent species shared between lung and gut communities. Temporal changes in gut microbial communities co-occurred with feeding practices and antibiotic exposure, suggesting an influence of external factors on microbiome composition.
CONCLUSIONS: Our findings provide evidence that certain microbial colonization patterns among premature infants are closely associated with the pathogenesis and progression of BPD.
Additional Links: PMID-41959121
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@article {pmid41959121,
year = {2026},
author = {Solomon, Z and Eno, M and Thompson, SC and Rager, SL and Jin, JC and Zeng, MY and Keerthy, D and Worgall, S and Johnson, EL and Heras, A},
title = {Increased S. epidermidis in the airway-gut microbiome of infants with bronchopulmonary dysplasia.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.04.03.715941},
pmid = {41959121},
issn = {2692-8205},
abstract = {RATIONALE: Bronchopulmonary dysplasia (BPD), the lung disease associated with premature birth, is a significant health problem, often with long-term respiratory consequences. Recent research has highlighted the potential role of the lung and gut microbiome in the development and progression of BPD, yet it is unclear what aspects of the microbiome may contribute to BPD susceptibility.
OBJECTIVES: To comprehensively characterize the lung and gut microbiomes of preterm infants and identify shared microbial taxa that are associated with BPD development.
METHODS: Tracheal aspirate and stool samples were collected from 39 premature infants over the first month of life. To assess the taxonomic microbial composition of the lung and gut, samples were analyzed using shotgun metagenomic sequencing. BPD classification was determined using the National Institute of Child Health and Human Development severity-based definition at 36 weeks postmenstrual age.
MEASUREMENTS AND MAIN RESULTS: Microbial communities of the lung and gut were significantly different between infants who went on to develop BPD and those who did not, with an enrichment of skin-associated microbial genera such as Staphylococcus, Corynebacterium, and Cutibacterium in infants who developed BPD. Specifically, Staphylococcus epidermidis was enriched in premature infants who developed BPD and was the most prominent species shared between lung and gut communities. Temporal changes in gut microbial communities co-occurred with feeding practices and antibiotic exposure, suggesting an influence of external factors on microbiome composition.
CONCLUSIONS: Our findings provide evidence that certain microbial colonization patterns among premature infants are closely associated with the pathogenesis and progression of BPD.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
Gut Microbiome Alterations in Canine Idiopathic Epilepsy: A Pairwise Case-Control Study.
bioRxiv : the preprint server for biology pii:2026.04.02.716098.
BACKGROUND: Idiopathic epilepsy (IE) is the most common chronic nervous system disorder of dogs, and its cause is poorly understood. Emerging evidence suggests that microbiome alterations can occur with IE via the microbiota-gut-brain axis. Therefore, we analyzed the fecal microbiomes of 98 dogs (49 IE, 49 control) in a pairwise case-control observational study using 16S rRNA gene sequencing.
RESULTS: Although the microbial community was mostly similar between groups, IE was associated with a modest but significant shift in Weighted-Unifrac distance (P = 0.042). We used six differential abundance (DA) methods to identify differentially abundant amplicon sequencing variants (ASVs) between IE and control groups. Notably, one Collinsella ASV was found to be significantly more abundant in IE dogs by all six methods. The gut microbial compositions varied drastically across households (accounting for about 69% of the total variation), but did not have significant differences between sex, age, or breed. Phenobarbital administration in IE dogs had a significant effect on seizure control, and was not associated with changes in the microbiome.
CONCLUSION: Our findings suggest a relationship between gut microbiomes and IE. However, the specific mechanism needs to be further investigated.
Additional Links: PMID-41959202
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@article {pmid41959202,
year = {2026},
author = {Yang, Y and Nettifee, J and Azcarate-Peril, MA and Muñana, KR and Callahan, B},
title = {Gut Microbiome Alterations in Canine Idiopathic Epilepsy: A Pairwise Case-Control Study.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.04.02.716098},
pmid = {41959202},
issn = {2692-8205},
abstract = {BACKGROUND: Idiopathic epilepsy (IE) is the most common chronic nervous system disorder of dogs, and its cause is poorly understood. Emerging evidence suggests that microbiome alterations can occur with IE via the microbiota-gut-brain axis. Therefore, we analyzed the fecal microbiomes of 98 dogs (49 IE, 49 control) in a pairwise case-control observational study using 16S rRNA gene sequencing.
RESULTS: Although the microbial community was mostly similar between groups, IE was associated with a modest but significant shift in Weighted-Unifrac distance (P = 0.042). We used six differential abundance (DA) methods to identify differentially abundant amplicon sequencing variants (ASVs) between IE and control groups. Notably, one Collinsella ASV was found to be significantly more abundant in IE dogs by all six methods. The gut microbial compositions varied drastically across households (accounting for about 69% of the total variation), but did not have significant differences between sex, age, or breed. Phenobarbital administration in IE dogs had a significant effect on seizure control, and was not associated with changes in the microbiome.
CONCLUSION: Our findings suggest a relationship between gut microbiomes and IE. However, the specific mechanism needs to be further investigated.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
MAAMOUL: Metabolic network-based discovery of microbiome-metabolome shifts in disease.
bioRxiv : the preprint server for biology pii:2026.03.27.714614.
MOTIVATION: A central goal in human gut microbiome research is to identify disease-associated functional shifts, an objective increasingly pursued through metagenomic and metabolomic assays. However, common differential abundance analyses of genes or metabolites often yield long and difficult-to-interpret feature lists. Aggregating features into predefined pathways can improve interpretability but relies on fixed pathway boundaries that may not reflect context-specific functional changes. Moreover, even when paired metagenomic-metabolomic data are available, they are often analyzed separately or linked only through simple statistical associations.
RESULTS: We introduce MAAMOUL, a knowledge-based computational framework that integrates metagenomic and metabolomic data to identify disease-associated, data-driven microbial metabolic modules. Leveraging prior knowledge of bacterial metabolism, MAAMOUL maps disease-association scores onto a global microbiome-wide metabolic network and identifies custom modules enriched for altered genes and metabolites. Applying MAAMOUL to inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) datasets revealed significant disease-associated modules not detected by conventional pathway-level analysis. In IBD, modules reflected disrupted sulfur and aromatic amino acid metabolism and enhanced microbial nucleotide salvage, whereas in IBS they linked purine and nicotinate/nicotinamide metabolism. These results demonstrate that network-guided multi-omic integration can uncover coherent functional shifts in the gut microbiome overlooked by single-omic or purely statistical approaches.
AVAILABILITY: MAAMOUL is available as an R package at https://github.com/borenstein-lab/MAAMOUL .
Additional Links: PMID-41959210
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@article {pmid41959210,
year = {2026},
author = {Muller, E and Baum, S and Borenstein, E},
title = {MAAMOUL: Metabolic network-based discovery of microbiome-metabolome shifts in disease.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.27.714614},
pmid = {41959210},
issn = {2692-8205},
abstract = {MOTIVATION: A central goal in human gut microbiome research is to identify disease-associated functional shifts, an objective increasingly pursued through metagenomic and metabolomic assays. However, common differential abundance analyses of genes or metabolites often yield long and difficult-to-interpret feature lists. Aggregating features into predefined pathways can improve interpretability but relies on fixed pathway boundaries that may not reflect context-specific functional changes. Moreover, even when paired metagenomic-metabolomic data are available, they are often analyzed separately or linked only through simple statistical associations.
RESULTS: We introduce MAAMOUL, a knowledge-based computational framework that integrates metagenomic and metabolomic data to identify disease-associated, data-driven microbial metabolic modules. Leveraging prior knowledge of bacterial metabolism, MAAMOUL maps disease-association scores onto a global microbiome-wide metabolic network and identifies custom modules enriched for altered genes and metabolites. Applying MAAMOUL to inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) datasets revealed significant disease-associated modules not detected by conventional pathway-level analysis. In IBD, modules reflected disrupted sulfur and aromatic amino acid metabolism and enhanced microbial nucleotide salvage, whereas in IBS they linked purine and nicotinate/nicotinamide metabolism. These results demonstrate that network-guided multi-omic integration can uncover coherent functional shifts in the gut microbiome overlooked by single-omic or purely statistical approaches.
AVAILABILITY: MAAMOUL is available as an R package at https://github.com/borenstein-lab/MAAMOUL .},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
Impact of high-fat Western diet on chronic lymphocytic leukemia disease progression and gut microbiome profile in Eμ-TCL1 mice.
bioRxiv : the preprint server for biology pii:2026.03.30.715124.
BACKGROUND: The composition and function of the gut microbiome have been shown to contribute to both health and disease. One of the most powerful modulators of microbial composition and function is diet.
MATERIALS & METHODS: Using the Eμ-TCL1 murine model of B-cell chronic lymphocytic leukemia (CLL), we assigned male and female mice to a high-fat, high-carbohydrate Western diet (HF) or standard chow (CH) diet.
RESULTS: Mice consuming a HF diet had significantly shorter survival than those consuming a CH diet, irrespective of sex, with female mice exhibiting particularly poor outcomes. We also observed a significant increase in splenic involvement by CLL in the HF diet-fed mice at time of sacrifice. Mice receiving the HF diet demonstrated immediate and profound effects on the gut microbiome, marked by reduced alpha diversity and significantly different community composition as measured by beta diversity. Notably, there was a sustained increase in Akkermansia muciniphila and Bacteroidetes thetaiotaomicron in HF diet-fed mice, coupled with a corresponding increase in microbiome functional pathways related to arginine and histidine biosynthesis, chitin degradation, and nucleotide biosynthesis.
DISCUSSION: Collectively our data provides evidence of the profound and sustained impact of a high-fat Western diet upon the gut microbiome community and CLL pathogenesis in the Eμ-TCL1 murine model of CLL.
Additional Links: PMID-41959214
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@article {pmid41959214,
year = {2026},
author = {Skupa, SA and Hernandez, JB and Smith, AL and Drengler, EM and Seth, AK and Rai, SN and Clayton, JB and D'Angelo, CR and El-Gamal, D},
title = {Impact of high-fat Western diet on chronic lymphocytic leukemia disease progression and gut microbiome profile in Eμ-TCL1 mice.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.30.715124},
pmid = {41959214},
issn = {2692-8205},
abstract = {BACKGROUND: The composition and function of the gut microbiome have been shown to contribute to both health and disease. One of the most powerful modulators of microbial composition and function is diet.
MATERIALS & METHODS: Using the Eμ-TCL1 murine model of B-cell chronic lymphocytic leukemia (CLL), we assigned male and female mice to a high-fat, high-carbohydrate Western diet (HF) or standard chow (CH) diet.
RESULTS: Mice consuming a HF diet had significantly shorter survival than those consuming a CH diet, irrespective of sex, with female mice exhibiting particularly poor outcomes. We also observed a significant increase in splenic involvement by CLL in the HF diet-fed mice at time of sacrifice. Mice receiving the HF diet demonstrated immediate and profound effects on the gut microbiome, marked by reduced alpha diversity and significantly different community composition as measured by beta diversity. Notably, there was a sustained increase in Akkermansia muciniphila and Bacteroidetes thetaiotaomicron in HF diet-fed mice, coupled with a corresponding increase in microbiome functional pathways related to arginine and histidine biosynthesis, chitin degradation, and nucleotide biosynthesis.
DISCUSSION: Collectively our data provides evidence of the profound and sustained impact of a high-fat Western diet upon the gut microbiome community and CLL pathogenesis in the Eμ-TCL1 murine model of CLL.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
Blautia wexlerae Transforms Dietary Fatty Acids to Activate Enteroendocrine Signaling and Improve Metabolic Health in Mice and Humans.
bioRxiv : the preprint server for biology pii:2026.03.13.709143.
Metabolites produced by the gut microbiome influence host metabolic health, but how this occurs remains incompletely defined. Here, we report that a common human gut commensal, Blautia wexlerae , converts dietary fats into bioactive metabolites that induce gut hormone production to affect glucose metabolism and suppress appetite. We found that colonization with Blautia wexlerae correlated with healthier eating behaviors in humans. Blautia wexlerae encodes a unique acyl transferase and is capable of producing acyl amines from nutrient substrates. These Blautia acyl amines stimulated human enteroendocrine cells to secrete GLP-1 and other gut peptide hormones more potently than endogenously produced acyl amines. When fed to mice, acyl amines improved glycemic control and decreased appetite. In humans, higher stool levels of Blautia DNA encoding acyl amine synthesis genes correlated with leanness and decreased dietary fat intake. These results define a mechanism of action for how Blautia wexlerae affects host metabolic control.
Additional Links: PMID-41959235
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@article {pmid41959235,
year = {2026},
author = {Zhang, YJ and Tanofsky-Kraff, M and Reyes, MM and Zeve, D and Ehrmann, KJ and Lee, J and Schaan, AP and Prado, A and Ma, XC and Parker, MN and Brady, SM and Saint-Denis, E and Sharma, K and Frintu, B and Richmond, C and Desai, N and Yeliseyev, V and Bry, L and Avila-Pacheco, J and Clish, CB and Quealy, M and Clardy, J and Breault, DT and Ding, Y and Wang, X and Jost, M and Poyet, M and Groussin, M and Yanovski, JA and Lencer, WI and Alm, EJ},
title = {Blautia wexlerae Transforms Dietary Fatty Acids to Activate Enteroendocrine Signaling and Improve Metabolic Health in Mice and Humans.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.13.709143},
pmid = {41959235},
issn = {2692-8205},
abstract = {Metabolites produced by the gut microbiome influence host metabolic health, but how this occurs remains incompletely defined. Here, we report that a common human gut commensal, Blautia wexlerae , converts dietary fats into bioactive metabolites that induce gut hormone production to affect glucose metabolism and suppress appetite. We found that colonization with Blautia wexlerae correlated with healthier eating behaviors in humans. Blautia wexlerae encodes a unique acyl transferase and is capable of producing acyl amines from nutrient substrates. These Blautia acyl amines stimulated human enteroendocrine cells to secrete GLP-1 and other gut peptide hormones more potently than endogenously produced acyl amines. When fed to mice, acyl amines improved glycemic control and decreased appetite. In humans, higher stool levels of Blautia DNA encoding acyl amine synthesis genes correlated with leanness and decreased dietary fat intake. These results define a mechanism of action for how Blautia wexlerae affects host metabolic control.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
C. mastitidis requires the protein Sortase F to colonize the eye.
bioRxiv : the preprint server for biology pii:2026.03.12.711320.
The ocular surface is a mucosal tissue that is constantly exposed to environmental antigens and potential pathogens. Human microbiomes play a critical role in the balance of surveillance and inflammation at sites of colonization. Historically, the investigation of the ocular microbiome has been difficult due to its paucibacterial nature and the inhospitable environment of the ocular surface. Despite this, Corynebacterium mastitidis (C. mast) developed a unique ability to colonize the eye and elicit a protective immune response characterized by induction of IL-17 from γδ T cells and protection from corneal infection. Therefore, we sought to understand the unique bacterial machinery that C. mast utilizes to colonize the eye and how it affects the induction of an eye-specific immune signature. Using a C. mast transposon mutant library, we identified a mutant that completely lacked an ability to form biofilm, colonize the eye, and induce in vivo immunity. Whole genome sequencing revealed a disruption in the sortase F gene, which anchors proteins to the cell wall of C. mast , governing biofilm formation and tethering of adhesins to the cell surface. Additionally, we show that mutation in individual C. mast adhesins does not affect ocular colonization or immune induction. By understanding the molecular mechanism of ocular microbial colonization, this work advances our understanding of how bacteria colonize and induce immune responses on the eye, providing a foundation for developing novel therapeutic strategies against ocular infections.
Additional Links: PMID-41959264
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@article {pmid41959264,
year = {2026},
author = {Rigas, YE and Shane, J and Treat, B and Shanks, RMQ and Leger, AJS},
title = {C. mastitidis requires the protein Sortase F to colonize the eye.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.12.711320},
pmid = {41959264},
issn = {2692-8205},
abstract = {The ocular surface is a mucosal tissue that is constantly exposed to environmental antigens and potential pathogens. Human microbiomes play a critical role in the balance of surveillance and inflammation at sites of colonization. Historically, the investigation of the ocular microbiome has been difficult due to its paucibacterial nature and the inhospitable environment of the ocular surface. Despite this, Corynebacterium mastitidis (C. mast) developed a unique ability to colonize the eye and elicit a protective immune response characterized by induction of IL-17 from γδ T cells and protection from corneal infection. Therefore, we sought to understand the unique bacterial machinery that C. mast utilizes to colonize the eye and how it affects the induction of an eye-specific immune signature. Using a C. mast transposon mutant library, we identified a mutant that completely lacked an ability to form biofilm, colonize the eye, and induce in vivo immunity. Whole genome sequencing revealed a disruption in the sortase F gene, which anchors proteins to the cell wall of C. mast , governing biofilm formation and tethering of adhesins to the cell surface. Additionally, we show that mutation in individual C. mast adhesins does not affect ocular colonization or immune induction. By understanding the molecular mechanism of ocular microbial colonization, this work advances our understanding of how bacteria colonize and induce immune responses on the eye, providing a foundation for developing novel therapeutic strategies against ocular infections.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
Multi-cohort Analysis Reveals Microbiome Signatures Associated with Drug Response in New-Onset Rheumatoid Arthritis.
bioRxiv : the preprint server for biology pii:2026.03.30.715090.
The human gut microbiome influences treatment outcomes, but whether microbiome signatures of drug response generalize across cohorts remains unclear. Here, we perform a multi-cohort analysis (3 cohorts, N=100 patients) to determine whether cross-cohort microbial signatures are associated with methotrexate (MTX) response in new-onset rheumatoid arthritis (RA) patients. Pre-treatment gut microbiome community structure and function differed by future MTX response status, with MTX-nonresponders (MTX-NR) showing Bacteroides caccae depletion and Ruminococcus bromii enrichment. Multiple microbial functions were depleted in MTX-NR, including nucleotide metabolism, one-carbon pool by folate, and histidine metabolism. Notably, candidate MTX-degrading genes were enriched in MTX-NR. Microbiome functional profiles outperformed clinical metrics in predicting future MTX response. These results show that consistent microbiome signatures are associated with MTX response across different RA cohorts and pave the way for microbiome-based precision medicine in newly diagnosed RA patients.
Additional Links: PMID-41959277
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@article {pmid41959277,
year = {2026},
author = {Bodkhe, RL and Blank, RB and Trepka, KR and Orellana, DA and Scher, JU and Turnbaugh, PJ and Nayak, RR},
title = {Multi-cohort Analysis Reveals Microbiome Signatures Associated with Drug Response in New-Onset Rheumatoid Arthritis.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.30.715090},
pmid = {41959277},
issn = {2692-8205},
abstract = {The human gut microbiome influences treatment outcomes, but whether microbiome signatures of drug response generalize across cohorts remains unclear. Here, we perform a multi-cohort analysis (3 cohorts, N=100 patients) to determine whether cross-cohort microbial signatures are associated with methotrexate (MTX) response in new-onset rheumatoid arthritis (RA) patients. Pre-treatment gut microbiome community structure and function differed by future MTX response status, with MTX-nonresponders (MTX-NR) showing Bacteroides caccae depletion and Ruminococcus bromii enrichment. Multiple microbial functions were depleted in MTX-NR, including nucleotide metabolism, one-carbon pool by folate, and histidine metabolism. Notably, candidate MTX-degrading genes were enriched in MTX-NR. Microbiome functional profiles outperformed clinical metrics in predicting future MTX response. These results show that consistent microbiome signatures are associated with MTX response across different RA cohorts and pave the way for microbiome-based precision medicine in newly diagnosed RA patients.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
The Urinary Tract commensal Peptoniphilus spp. Encodes a Novel 17β-Hydroxysteroid Dehydrogenase.
bioRxiv : the preprint server for biology pii:2026.03.29.714803.
UNLABELLED: Microbial steroid metabolism represents an underappreciated extension of the vertebrate endocrine system, with growing evidence that host-associated microbes contribute to the diversity and bioavailability of sex steroids within human tissues. Emerging studies have linked microbial androgen metabolism to urinary microbiome composition and to resistance to androgen deprivation therapy (ADT) in prostate cancer. While microbial pathways capable of converting steroid precursors such as cortisol to androgens, via the steroid-17,20-desmolase pathway, such as DesG-mediated interconversion of androstenedione to testosterone have been reported, the diversity of enzymes mediating downstream androgen interconversion remains incompletely defined. Here, we investigate the androgen-forming capabilities of anaerobic bacteria from the male genitourinary microbiome, focusing on NADPH-dependent 17β-hydroxysteroid dehydrogenases (17β-HSDHs) that catalyze interconversion of androstenedione and testosterone. We isolated androgen-forming bacterial strains from human male urine and identified a previously uncharacterized 17β-HSDH encoded by Peptoniphilus obesi , demonstrated that this enzyme catalyzes the NADPH-dependent reduction of androstenedione to testosterone and the reverse oxidation reaction. Sequence similarity searches further identified a homologous 17β-HSDH in Anaerococcus , which was synthesized and functionally validated, revealing conserved activity despite low sequence identity to the previously characterized urinary tract enzyme DesG. The enzymes were found to have broad substrate specificity for C19 and C18 17keto- and 17β-hydroxysteroids. Together, these findings expand the known diversity of microbial 17β-HSDHs and identify previously unrecognized androgen-forming activities within the genitourinary microbiome.
IMPORTANCE: Microbial steroid-transforming pathways may provide a mechanism by which commensal anaerobes contribute to androgen availability in the genitourinary tract. By identifying novel 17β-hydroxysteroid dehydrogenases from Peptoniphilus and Anaerococcus , genera repeatedly associated with prostate cancer, this study provides mechanistic insight into how microbial steroid metabolism may influence hormone-driven disease.
Additional Links: PMID-41959294
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@article {pmid41959294,
year = {2026},
author = {Binion, B and Ahmad, S and Wang, T and Tang, E and Barnick, B and Olukoya, D and Mbuvi, P and Dutta, D and Erdman, JW and Gaskins, HR and Yang, G and Irudayaraj, J and Ridlon, JM},
title = {The Urinary Tract commensal Peptoniphilus spp. Encodes a Novel 17β-Hydroxysteroid Dehydrogenase.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.29.714803},
pmid = {41959294},
issn = {2692-8205},
abstract = {UNLABELLED: Microbial steroid metabolism represents an underappreciated extension of the vertebrate endocrine system, with growing evidence that host-associated microbes contribute to the diversity and bioavailability of sex steroids within human tissues. Emerging studies have linked microbial androgen metabolism to urinary microbiome composition and to resistance to androgen deprivation therapy (ADT) in prostate cancer. While microbial pathways capable of converting steroid precursors such as cortisol to androgens, via the steroid-17,20-desmolase pathway, such as DesG-mediated interconversion of androstenedione to testosterone have been reported, the diversity of enzymes mediating downstream androgen interconversion remains incompletely defined. Here, we investigate the androgen-forming capabilities of anaerobic bacteria from the male genitourinary microbiome, focusing on NADPH-dependent 17β-hydroxysteroid dehydrogenases (17β-HSDHs) that catalyze interconversion of androstenedione and testosterone. We isolated androgen-forming bacterial strains from human male urine and identified a previously uncharacterized 17β-HSDH encoded by Peptoniphilus obesi , demonstrated that this enzyme catalyzes the NADPH-dependent reduction of androstenedione to testosterone and the reverse oxidation reaction. Sequence similarity searches further identified a homologous 17β-HSDH in Anaerococcus , which was synthesized and functionally validated, revealing conserved activity despite low sequence identity to the previously characterized urinary tract enzyme DesG. The enzymes were found to have broad substrate specificity for C19 and C18 17keto- and 17β-hydroxysteroids. Together, these findings expand the known diversity of microbial 17β-HSDHs and identify previously unrecognized androgen-forming activities within the genitourinary microbiome.
IMPORTANCE: Microbial steroid-transforming pathways may provide a mechanism by which commensal anaerobes contribute to androgen availability in the genitourinary tract. By identifying novel 17β-hydroxysteroid dehydrogenases from Peptoniphilus and Anaerococcus , genera repeatedly associated with prostate cancer, this study provides mechanistic insight into how microbial steroid metabolism may influence hormone-driven disease.},
}
RevDate: 2026-04-10
CmpDate: 2026-04-10
Species-specific prophage induction by ciprofloxacin in human gut metagenomes.
bioRxiv : the preprint server for biology pii:2026.03.11.711154.
UNLABELLED: Antibiotics are known to trigger prophage induction in controlled laboratory settings, but it remains unclear whether this also occurs within microbiomes in nature. Current methods investigating the link between antibiotics and prophage induction within the human gut rely on in vitro culturing of human gut bacterial isolates. Using a metagenomic approach, we aimed to measure prophage induction and whether it is associated with antibiotic exposure. Across two independent human cohorts, we compared prophage to bacterial host read depth ratios (P:H) across known or measured antibiotic exposures. We found that induction is not broadly associated with antibiotic exposures at the level of the overall microbiome, but that ciprofloxacin increases P:H ratios in specific bacterial species. We documented heterogeneous trajectories of P:H ratios over the course of antibiotic exposure, sometimes increasing and remaining high, or returning to baseline. This study complements experimental models by providing in vivo evidence of induction in the human gut.
IMPORTANCE: Bacteriophages are viruses that infect a bacterial host. The lytic and lysogenic cycles are the two classic outcomes of phage infection. In the lytic cycle, the phage immediately replicates and lyses its host to release new viral particles. In the lysogenic cycle, the phage, now called a prophage, integrates its genome into that of its host without killing it. Prophages can switch to the lytic cycle in a process called induction, in which the viral genome is replicated, the host cell is lysed, and viral particles are released. The most immediate consequence of induction is host cell death which can impact bacterial populations and communities. Since prophages are mobile genetic elements that can move between bacteria, they are also an important vehicle for horizontal gene transfer. While induction has been well studied in vitro , whether and how induction occurs within the complex microbial ecosystem in humans is less well characterized. Understanding prophage induction in vivo is therefore critical in corroborating in vitro observations.
Additional Links: PMID-41959308
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@article {pmid41959308,
year = {2026},
author = {Sakdinan, B and Sinha, A and Qadri, F and Khan, AI and Nelson, EJ and Shapiro, BJ},
title = {Species-specific prophage induction by ciprofloxacin in human gut metagenomes.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.11.711154},
pmid = {41959308},
issn = {2692-8205},
abstract = {UNLABELLED: Antibiotics are known to trigger prophage induction in controlled laboratory settings, but it remains unclear whether this also occurs within microbiomes in nature. Current methods investigating the link between antibiotics and prophage induction within the human gut rely on in vitro culturing of human gut bacterial isolates. Using a metagenomic approach, we aimed to measure prophage induction and whether it is associated with antibiotic exposure. Across two independent human cohorts, we compared prophage to bacterial host read depth ratios (P:H) across known or measured antibiotic exposures. We found that induction is not broadly associated with antibiotic exposures at the level of the overall microbiome, but that ciprofloxacin increases P:H ratios in specific bacterial species. We documented heterogeneous trajectories of P:H ratios over the course of antibiotic exposure, sometimes increasing and remaining high, or returning to baseline. This study complements experimental models by providing in vivo evidence of induction in the human gut.
IMPORTANCE: Bacteriophages are viruses that infect a bacterial host. The lytic and lysogenic cycles are the two classic outcomes of phage infection. In the lytic cycle, the phage immediately replicates and lyses its host to release new viral particles. In the lysogenic cycle, the phage, now called a prophage, integrates its genome into that of its host without killing it. Prophages can switch to the lytic cycle in a process called induction, in which the viral genome is replicated, the host cell is lysed, and viral particles are released. The most immediate consequence of induction is host cell death which can impact bacterial populations and communities. Since prophages are mobile genetic elements that can move between bacteria, they are also an important vehicle for horizontal gene transfer. While induction has been well studied in vitro , whether and how induction occurs within the complex microbial ecosystem in humans is less well characterized. Understanding prophage induction in vivo is therefore critical in corroborating in vitro observations.},
}
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RJR Experience and Expertise
Researcher
Robbins holds BS, MS, and PhD degrees in the life sciences. He served as a tenured faculty member in the Zoology and Biological Science departments at Michigan State University. He is currently exploring the intersection between genomics, microbial ecology, and biodiversity — an area that promises to transform our understanding of the biosphere.
Educator
Robbins has extensive experience in college-level education: At MSU he taught introductory biology, genetics, and population genetics. At JHU, he was an instructor for a special course on biological database design. At FHCRC, he team-taught a graduate-level course on the history of genetics. At Bellevue College he taught medical informatics.
Administrator
Robbins has been involved in science administration at both the federal and the institutional levels. At NSF he was a program officer for database activities in the life sciences, at DOE he was a program officer for information infrastructure in the human genome project. At the Fred Hutchinson Cancer Research Center, he served as a vice president for fifteen years.
Technologist
Robbins has been involved with information technology since writing his first Fortran program as a college student. At NSF he was the first program officer for database activities in the life sciences. At JHU he held an appointment in the CS department and served as director of the informatics core for the Genome Data Base. At the FHCRC he was VP for Information Technology.
Publisher
While still at Michigan State, Robbins started his first publishing venture, founding a small company that addressed the short-run publishing needs of instructors in very large undergraduate classes. For more than 20 years, Robbins has been operating The Electronic Scholarly Publishing Project, a web site dedicated to the digital publishing of critical works in science, especially classical genetics.
Speaker
Robbins is well-known for his speaking abilities and is often called upon to provide keynote or plenary addresses at international meetings. For example, in July, 2012, he gave a well-received keynote address at the Global Biodiversity Informatics Congress, sponsored by GBIF and held in Copenhagen. The slides from that talk can be seen HERE.
Facilitator
Robbins is a skilled meeting facilitator. He prefers a participatory approach, with part of the meeting involving dynamic breakout groups, created by the participants in real time: (1) individuals propose breakout groups; (2) everyone signs up for one (or more) groups; (3) the groups with the most interested parties then meet, with reports from each group presented and discussed in a subsequent plenary session.
Designer
Robbins has been engaged with photography and design since the 1960s, when he worked for a professional photography laboratory. He now prefers digital photography and tools for their precision and reproducibility. He designed his first web site more than 20 years ago and he personally designed and implemented this web site. He engages in graphic design as a hobby.
RJR Picks from Around the Web (updated 11 MAY 2018 )
Old Science
Weird Science
Treating Disease with Fecal Transplantation
Fossils of miniature humans (hobbits) discovered in Indonesia
Paleontology
Dinosaur tail, complete with feathers, found preserved in amber.
Astronomy
Mysterious fast radio burst (FRB) detected in the distant universe.
Big Data & Informatics
Big Data: Buzzword or Big Deal?
Hacking the genome: Identifying anonymized human subjects using publicly available data.