Pub Date : 2026-01-27DOI: 10.1080/19490976.2026.2616066
Tyrus J Perdue,Cassandra E Newkirk,Robert Beblavy,Antti E Seppo,Erin C Davis,Michael B Sohn,Kirsi M Järvinen,Cynthia L Monaco
Atopic disease prevalence, including atopic dermatitis, food allergy, asthma, and allergic rhinitis, has risen dramatically in industrialized countries. Traditional, single family farming lifestyles protect against atopic disease, but the mechanisms are incompletely understood. While there are established epidemiologic connections between childhood respiratory viral infections and the infant gut bacterial microbiome with allergic disease development, the influence of the early enteric virome on atopic disease development is unknown. We analyzed the enteric virome in 131 infants from high-atopy-risk urban/suburban environments and low-atopic-risk single-family farming communities. While similar at 12 months, enteric bacteriophage communities significantly differed by farm-life versus urban lifestyle at six weeks and six months of age. A lifestyle protective from atopic disease demonstrated higher colonization rates of Bifidobacterium longum subsp. infantis (B. infantis), an important beneficial commensal, with phageome communities differing in infants colonized by B. infantis at all time points. Simultaneously, Mastadenovirus and Bocaparvovirus were more prevalent in urban infant stools at six months of age. Sparser phage-phage networks were found at all timepoints in infants who later developed atopic disease. These data suggest that the early infant enteric DNA virome develops differently in farming and urban lifestyles and may factor into risk of atopic disease development.
{"title":"The enteric DNA virome differs in infants at risk for atopic disease.","authors":"Tyrus J Perdue,Cassandra E Newkirk,Robert Beblavy,Antti E Seppo,Erin C Davis,Michael B Sohn,Kirsi M Järvinen,Cynthia L Monaco","doi":"10.1080/19490976.2026.2616066","DOIUrl":"https://doi.org/10.1080/19490976.2026.2616066","url":null,"abstract":"Atopic disease prevalence, including atopic dermatitis, food allergy, asthma, and allergic rhinitis, has risen dramatically in industrialized countries. Traditional, single family farming lifestyles protect against atopic disease, but the mechanisms are incompletely understood. While there are established epidemiologic connections between childhood respiratory viral infections and the infant gut bacterial microbiome with allergic disease development, the influence of the early enteric virome on atopic disease development is unknown. We analyzed the enteric virome in 131 infants from high-atopy-risk urban/suburban environments and low-atopic-risk single-family farming communities. While similar at 12 months, enteric bacteriophage communities significantly differed by farm-life versus urban lifestyle at six weeks and six months of age. A lifestyle protective from atopic disease demonstrated higher colonization rates of Bifidobacterium longum subsp. infantis (B. infantis), an important beneficial commensal, with phageome communities differing in infants colonized by B. infantis at all time points. Simultaneously, Mastadenovirus and Bocaparvovirus were more prevalent in urban infant stools at six months of age. Sparser phage-phage networks were found at all timepoints in infants who later developed atopic disease. These data suggest that the early infant enteric DNA virome develops differently in farming and urban lifestyles and may factor into risk of atopic disease development.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"42 1","pages":"2616066"},"PeriodicalIF":12.2,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146056780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-26DOI: 10.1080/19490976.2026.2617694
Alex Peh,Evany Dinakis,Michael Nakai,Rikeish R Muralitharan,Samoda Rupasinghe,Jenny L Wilson,Connie H Y Wong,Hamdi A Jama,Charlotte M O Barker,Mahnaz Modarresi,Barbara K Kemp-Harper,Tenghao Zheng,Francine Z Marques,Brad R S Broughton
Systemic infections are a common cause of complications and death after stroke. These infections can occur due to the breakdown of the gut epithelial barrier and the translocation of bacteria from the gut to peripheral systemic tissues. However, it remains unclear whether gut bacteria also translocate to the brain and contribute to stroke-induced neuronal damage. In this study, we observed a significant number of peptidoglycan- and lipopolysaccharide-positive bacteria in the ischemic hemisphere of mice subjected to either photothrombotic (PT) stroke or middle cerebral artery occlusion (MCAO). In contrast, no bacteria were observed in the ischemic brains of germ-free mice following MCAO. Absolute quantification via PCR also revealed increased bacteria in the ischemic hemisphere and blood of PT mice. Bacterial translocation to the brain is associated with the breakdown of the gut-epithelial and blood-brain barriers. Although inhibition of sympathetic tone reduces gut-epithelial barrier permeability, the bacterial load in the brain and functional deficits poststroke, it does not affect cerebral apoptosis, neuroinflammation or infarct volume. Collectively, these findings indicate that activation of the sympathetic nervous system after stroke promotes the migration of gut-derived bacteria into the ischemic brain, and this process worsens motor function in mice.
{"title":"Gut bacteria presence in the brain is increased after ischemic stroke in mice.","authors":"Alex Peh,Evany Dinakis,Michael Nakai,Rikeish R Muralitharan,Samoda Rupasinghe,Jenny L Wilson,Connie H Y Wong,Hamdi A Jama,Charlotte M O Barker,Mahnaz Modarresi,Barbara K Kemp-Harper,Tenghao Zheng,Francine Z Marques,Brad R S Broughton","doi":"10.1080/19490976.2026.2617694","DOIUrl":"https://doi.org/10.1080/19490976.2026.2617694","url":null,"abstract":"Systemic infections are a common cause of complications and death after stroke. These infections can occur due to the breakdown of the gut epithelial barrier and the translocation of bacteria from the gut to peripheral systemic tissues. However, it remains unclear whether gut bacteria also translocate to the brain and contribute to stroke-induced neuronal damage. In this study, we observed a significant number of peptidoglycan- and lipopolysaccharide-positive bacteria in the ischemic hemisphere of mice subjected to either photothrombotic (PT) stroke or middle cerebral artery occlusion (MCAO). In contrast, no bacteria were observed in the ischemic brains of germ-free mice following MCAO. Absolute quantification via PCR also revealed increased bacteria in the ischemic hemisphere and blood of PT mice. Bacterial translocation to the brain is associated with the breakdown of the gut-epithelial and blood-brain barriers. Although inhibition of sympathetic tone reduces gut-epithelial barrier permeability, the bacterial load in the brain and functional deficits poststroke, it does not affect cerebral apoptosis, neuroinflammation or infarct volume. Collectively, these findings indicate that activation of the sympathetic nervous system after stroke promotes the migration of gut-derived bacteria into the ischemic brain, and this process worsens motor function in mice.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"29 1","pages":"2617694"},"PeriodicalIF":12.2,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146044598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-23DOI: 10.1080/19490976.2026.2620127
Yunfeng Gao,Shima Shahbaz,Shokrollah Elahi,Tanya M Monaghan, ,Dina Kao
Fecal microbiota transplantation (FMT) is highly effective in preventing recurrent Clostridioides difficile infection (rCDI), yet its immunological mechanisms remain poorly defined. While bacterial engraftment and recovery of microbial diversity are central to FMT efficacy, accumulating evidence suggests that host immune reprogramming is involved. In murine models, regulatory CD4⁺ T cells are indispensable for clearing C. difficile. To address this mechanistic gap, we examined systemic immune reprogramming following FMT by performing flow cytometry and single-cell RNA sequencing (scRNA-seq) on a subset of successfully treated participants from a clinical trial comparing lyophilized FMT (LFMT) with lyophilized sterile fecal filtrate (LSFF, no live bacteria) for preventing rCDI. Flow cytometry was performed on peripheral mononuclear cells from 19 LFMT recipients and 18 LSFF recipients, and scRNA-seq analysis was performed on two LFMT recipients. Although flow cytometry results did not show significant changes in the assessed markers after rCDI resolution in either treatment group, exploratory scRNA-seq in the two LFMT recipients revealed distinct LFMT-associated transcriptional signatures across adaptive and innate-like lymphocyte populations. LFMT was associated with upregulated activation and regulatory genes (CD69, STAT1, TOX, RORA, FOXP3) in CD4⁺ and CD8⁺ T cells, suggesting enhanced immune regulation with reduced cytotoxic gene expression (GZMB, PRF1, GNLY). Innate-like lymphocytes displayed broad activation, with natural killer cells showing increased KLRD1, PRF1, and IL2RB and mucosal-associated invariant T cells (MAIT cells) upregulating STAT1, JUN, and RORA while downregulating KLRB1 and STAT3. These transcriptional programs are consistent with recalibration of T cell homeostasis and innate-like lymphocyte activation, potentially driven by microbial restoration. Collectively, this exploratory study provides the first single-cell immune atlas of LFMT in rCDI, identifying coordinated activation of regulatory, effector, and innate immune pathways. Given the small sample size, these findings should be considered hypothesis-generating, requiring validation in larger cohorts.
{"title":"Distinct T and innate-like lymphocyte reprogramming following lyophilized fecal microbiota transplantation in recurrent C. difficile infection.","authors":"Yunfeng Gao,Shima Shahbaz,Shokrollah Elahi,Tanya M Monaghan, ,Dina Kao","doi":"10.1080/19490976.2026.2620127","DOIUrl":"https://doi.org/10.1080/19490976.2026.2620127","url":null,"abstract":"Fecal microbiota transplantation (FMT) is highly effective in preventing recurrent Clostridioides difficile infection (rCDI), yet its immunological mechanisms remain poorly defined. While bacterial engraftment and recovery of microbial diversity are central to FMT efficacy, accumulating evidence suggests that host immune reprogramming is involved. In murine models, regulatory CD4⁺ T cells are indispensable for clearing C. difficile. To address this mechanistic gap, we examined systemic immune reprogramming following FMT by performing flow cytometry and single-cell RNA sequencing (scRNA-seq) on a subset of successfully treated participants from a clinical trial comparing lyophilized FMT (LFMT) with lyophilized sterile fecal filtrate (LSFF, no live bacteria) for preventing rCDI. Flow cytometry was performed on peripheral mononuclear cells from 19 LFMT recipients and 18 LSFF recipients, and scRNA-seq analysis was performed on two LFMT recipients. Although flow cytometry results did not show significant changes in the assessed markers after rCDI resolution in either treatment group, exploratory scRNA-seq in the two LFMT recipients revealed distinct LFMT-associated transcriptional signatures across adaptive and innate-like lymphocyte populations. LFMT was associated with upregulated activation and regulatory genes (CD69, STAT1, TOX, RORA, FOXP3) in CD4⁺ and CD8⁺ T cells, suggesting enhanced immune regulation with reduced cytotoxic gene expression (GZMB, PRF1, GNLY). Innate-like lymphocytes displayed broad activation, with natural killer cells showing increased KLRD1, PRF1, and IL2RB and mucosal-associated invariant T cells (MAIT cells) upregulating STAT1, JUN, and RORA while downregulating KLRB1 and STAT3. These transcriptional programs are consistent with recalibration of T cell homeostasis and innate-like lymphocyte activation, potentially driven by microbial restoration. Collectively, this exploratory study provides the first single-cell immune atlas of LFMT in rCDI, identifying coordinated activation of regulatory, effector, and innate immune pathways. Given the small sample size, these findings should be considered hypothesis-generating, requiring validation in larger cohorts.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"86 1","pages":"2620127"},"PeriodicalIF":12.2,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146021680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-23DOI: 10.1080/19490976.2026.2614054
Eunike Tiffany,Kyoung Su Kim,Panida Sittipo,Dong-Woo Lee,Yun Kyung Lee
Akkermansia muciniphila, Bacteroides thetaiotaomicron, Mediterraneibacter (formerly Ruminococcus) gnavus, and other mucin-degrading (MD) bacteria play pivotal roles in shaping gut microbial ecosystems, maintaining gut barrier function, and mediating host-microbiota crosstalk. These bacteria influence intestinal homeostasis by modulating epithelial cell differentiation, immune responses, and gut microbiota composition through mucin degradation and the production of bioactive metabolites. Their abundance and functional activities fluctuate dynamically in response to dietary components, host immunity, and environmental factors, resulting in context-dependent effects on gastrointestinal and systemic health. This review summarizes current insights into the ecology and metabolic capabilities of MD bacteria, highlighting their dual roles in metabolic disorders, inflammatory diseases, infection susceptibility, and neuroimmune conditions. Understanding the ecological niches and molecular interactions of MD bacteria offers promising approaches for microbiota-targeted therapies aimed at restoring gut and systemic homeostasis.
{"title":"Mucin-degrading gut bacteria: context-dependent roles in intestinal homeostasis and disease.","authors":"Eunike Tiffany,Kyoung Su Kim,Panida Sittipo,Dong-Woo Lee,Yun Kyung Lee","doi":"10.1080/19490976.2026.2614054","DOIUrl":"https://doi.org/10.1080/19490976.2026.2614054","url":null,"abstract":"Akkermansia muciniphila, Bacteroides thetaiotaomicron, Mediterraneibacter (formerly Ruminococcus) gnavus, and other mucin-degrading (MD) bacteria play pivotal roles in shaping gut microbial ecosystems, maintaining gut barrier function, and mediating host-microbiota crosstalk. These bacteria influence intestinal homeostasis by modulating epithelial cell differentiation, immune responses, and gut microbiota composition through mucin degradation and the production of bioactive metabolites. Their abundance and functional activities fluctuate dynamically in response to dietary components, host immunity, and environmental factors, resulting in context-dependent effects on gastrointestinal and systemic health. This review summarizes current insights into the ecology and metabolic capabilities of MD bacteria, highlighting their dual roles in metabolic disorders, inflammatory diseases, infection susceptibility, and neuroimmune conditions. Understanding the ecological niches and molecular interactions of MD bacteria offers promising approaches for microbiota-targeted therapies aimed at restoring gut and systemic homeostasis.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"64 1","pages":"2614054"},"PeriodicalIF":12.2,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146021683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-23DOI: 10.1080/19490976.2026.2615494
Shuyu Guo,Bingyong Mao,Xin Tang,Qiuxiang Zhang,Jianxin Zhao,Wei Chen,Shumao Cui
In natural and engineered ecosystems, diverse species interact in complex ways to form highly efficient microecologies. One key orchestrator of these interactions is autoinducer-2 (AI-2), a signaling molecule that plays a crucial role in microbial community assembly, metabolic flux, and resilience to environmental disturbances. This review provides the systematic synthesis of AI-2's dual structural dynamics (S-THMF-borate/R-THMF interconversion) and its context-dependent roles in mediating bacterial crosstalk. It also reveals the receptor diversity (such as LuxP and LsrB) of AI-2 in bacterial kingdom and the signal transduction mechanism. Systematically elaborated on AI-2's regulation of cellular metabolic flux and its ability to autonomously exhibit a series of coordinated behaviors in response to environmental changes. The review explores the ramifications of AI-2 on bacterial community interactions in synthetic biology and natural ecosystems. The wide application of AI-2-mediated interspecific communication in various fields including host health, agriculture, industry and environmental ecology has also been widely discussed. Factors influencing AI-2 production are thoroughly examined, including internal factors such as strain specificity, cell density, growth form and the phenotypic heterogeneity. Additionally, external biological factors (such as nutritional status and environmental stress) and abiotic factors (aggregation, diffusion, and flow) are discussed in detail. By examining knowledge gaps in AI-2-mediated spatial heterogeneity and multi-QS system coordination, this work charts a roadmap for harnessing microbial communication in chemical engineering and environmental sustainability.
{"title":"Autoinducer 2 as a universal language in microbial consortia: decoding molecular mechanisms, ecological impacts, and application.","authors":"Shuyu Guo,Bingyong Mao,Xin Tang,Qiuxiang Zhang,Jianxin Zhao,Wei Chen,Shumao Cui","doi":"10.1080/19490976.2026.2615494","DOIUrl":"https://doi.org/10.1080/19490976.2026.2615494","url":null,"abstract":"In natural and engineered ecosystems, diverse species interact in complex ways to form highly efficient microecologies. One key orchestrator of these interactions is autoinducer-2 (AI-2), a signaling molecule that plays a crucial role in microbial community assembly, metabolic flux, and resilience to environmental disturbances. This review provides the systematic synthesis of AI-2's dual structural dynamics (S-THMF-borate/R-THMF interconversion) and its context-dependent roles in mediating bacterial crosstalk. It also reveals the receptor diversity (such as LuxP and LsrB) of AI-2 in bacterial kingdom and the signal transduction mechanism. Systematically elaborated on AI-2's regulation of cellular metabolic flux and its ability to autonomously exhibit a series of coordinated behaviors in response to environmental changes. The review explores the ramifications of AI-2 on bacterial community interactions in synthetic biology and natural ecosystems. The wide application of AI-2-mediated interspecific communication in various fields including host health, agriculture, industry and environmental ecology has also been widely discussed. Factors influencing AI-2 production are thoroughly examined, including internal factors such as strain specificity, cell density, growth form and the phenotypic heterogeneity. Additionally, external biological factors (such as nutritional status and environmental stress) and abiotic factors (aggregation, diffusion, and flow) are discussed in detail. By examining knowledge gaps in AI-2-mediated spatial heterogeneity and multi-QS system coordination, this work charts a roadmap for harnessing microbial communication in chemical engineering and environmental sustainability.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"321 1","pages":"2615494"},"PeriodicalIF":12.2,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146021682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Excess energy intake contributes to adiposity in obesity. We investigated whether the human intestinal bacterium Phascolarctobacterium faecium could prevent obesity via enteroendocrine pathways in a mouse model of diet-induced obesity (DIO). Daily administration of P. faecium (2 × 109 cells/mouse) reduced food intake through the early overproduction of the satiety hormone peptide YY (PYY) compared to untreated DIO mice. Moreover, P. faecium increased the intestinal levels of branched-chain amino acids, which, in turn, stimulated PYY secretion in neuroendocrine cell cultures and also modified gut microbiota composition. A pair-feeding study demonstrated that the anorexigenic effect of P. faecium contributes to its effects in attenuating body weight gain in DIO mice, but that other mechanisms are also involved in its metabolic benefits. Specifically, P. faecium accelerated gut transit and serum lipid clearance, thereby limiting adiposity independently of food intake. This study identifies the mode of action of a human intestinal bacterium recently linked to obesity protection, providing valuable insights into host-microbe interactions governing body weight.
{"title":"Phascolarctobacterium faecium reduces food intake via PYY signaling, contributing to the mitigation of body weight gain in diet-induced obese mice.","authors":"Clara Bullich-Vilarrubias,Marina Romaní-Pérez,Inmaculada López-Almela,Carlos Pomares-Díaz,Silvia Basili Franzin,Giuseppe Esposito,Alfonso Benítez-Páez,Verónica Tolosa-Enguís,Yolanda Sanz","doi":"10.1080/19490976.2026.2617691","DOIUrl":"https://doi.org/10.1080/19490976.2026.2617691","url":null,"abstract":"Excess energy intake contributes to adiposity in obesity. We investigated whether the human intestinal bacterium Phascolarctobacterium faecium could prevent obesity via enteroendocrine pathways in a mouse model of diet-induced obesity (DIO). Daily administration of P. faecium (2 × 109 cells/mouse) reduced food intake through the early overproduction of the satiety hormone peptide YY (PYY) compared to untreated DIO mice. Moreover, P. faecium increased the intestinal levels of branched-chain amino acids, which, in turn, stimulated PYY secretion in neuroendocrine cell cultures and also modified gut microbiota composition. A pair-feeding study demonstrated that the anorexigenic effect of P. faecium contributes to its effects in attenuating body weight gain in DIO mice, but that other mechanisms are also involved in its metabolic benefits. Specifically, P. faecium accelerated gut transit and serum lipid clearance, thereby limiting adiposity independently of food intake. This study identifies the mode of action of a human intestinal bacterium recently linked to obesity protection, providing valuable insights into host-microbe interactions governing body weight.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"37 1","pages":"2617691"},"PeriodicalIF":12.2,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146014927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-20DOI: 10.1080/19490976.2026.2617699
Jing Xu,Ziyi Han,Qing Xue,Haoran Wang,Jiyu Song,Yutong Li,Yongfeng Zhang,Di Wang,Min Hu
The link between hyperlipidemia and periodontitis is well-established, but the underlying mechanisms remain incompletely understood. Here, we reveal a critical role for a 'gut-oral' axis in mediating this interaction. Integrating multi-omics analyses of clinical samples and mouse models, we identified that a significant reduction of intestinal Limosilactobacillus mucosae is a key feature of hyperlipidemic periodontitis (HPD). Fecal microbiota transplantation established a causal link between this gut dysbiosis and exacerbated periodontitis. Mechanistically, oral administration of live L. mucosae ameliorates HPD by restoring intestinal levels of the key metabolite, glycerophosphocholine (α-GPC). Notably, supplementation with α-GPC alone recapitulated this protective effect by upregulating the tight junction protein Claudin-1 (CLDN1) in periodontal tissue. This reinforcement of the epithelial barrier curtailed inflammatory infiltration and restored bone homeostasis. Our findings uncover a protective 'L. mucosae-α-GPC-CLDN1' axis, providing mechanistic insight into how gut microbiota mediates metabolism-associated inflammation and proposing a potential therapeutic strategy for HPD.
{"title":"Limosilactobacillus mucosae attenuates hyperlipidemic periodontitis via the gut-oral axis.","authors":"Jing Xu,Ziyi Han,Qing Xue,Haoran Wang,Jiyu Song,Yutong Li,Yongfeng Zhang,Di Wang,Min Hu","doi":"10.1080/19490976.2026.2617699","DOIUrl":"https://doi.org/10.1080/19490976.2026.2617699","url":null,"abstract":"The link between hyperlipidemia and periodontitis is well-established, but the underlying mechanisms remain incompletely understood. Here, we reveal a critical role for a 'gut-oral' axis in mediating this interaction. Integrating multi-omics analyses of clinical samples and mouse models, we identified that a significant reduction of intestinal Limosilactobacillus mucosae is a key feature of hyperlipidemic periodontitis (HPD). Fecal microbiota transplantation established a causal link between this gut dysbiosis and exacerbated periodontitis. Mechanistically, oral administration of live L. mucosae ameliorates HPD by restoring intestinal levels of the key metabolite, glycerophosphocholine (α-GPC). Notably, supplementation with α-GPC alone recapitulated this protective effect by upregulating the tight junction protein Claudin-1 (CLDN1) in periodontal tissue. This reinforcement of the epithelial barrier curtailed inflammatory infiltration and restored bone homeostasis. Our findings uncover a protective 'L. mucosae-α-GPC-CLDN1' axis, providing mechanistic insight into how gut microbiota mediates metabolism-associated inflammation and proposing a potential therapeutic strategy for HPD.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"6 1","pages":"2617699"},"PeriodicalIF":12.2,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146005013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The impact of microplastics (MPs) on the diversity and composition of the gut microbiome has been extensively documented in animal studies, but evidence in humans remains limited. Recognizing the potential differences in MP effects between animal and human gut microbiomes, this review synthesizes current evidence concerning their impact on the human gut microbiota. Furthermore, the potential links between microplastic-induced dysbiosis and the pathogenesis of human diseases were analyzed. Cross-sectional studies have been conducted to explore microplastic exposures (such as in humans who consume hot foods served in disposable plastic tableware) and their associations with gut microbiome functionalities in infants, preschool children and adults. Exposure to MPs increased the abundance of Dethiosulfovibrionaceae, Enterobacteriaceae, Moraxellaceae, Actinomycetota, Pseudomonadota, and Veillonella. On the other hand, MPs decreased the abundances of Bacillota, Bacteroidota, Lactobacillales, Rikenellaceae, Parabacteroides, Roseburia, Coprococcus, Turicibacter, and Eubacterium coprostanoligenes. These changes were associated with a decrease in butyrate production and a decrease in short-chain fatty acid levels. However, for some other bacteria, both inductive (on Oscillospiraceae, Adlercreutzia, Phascolarctobacterium, and Collinsella) and repressive effects (on Streptococcus) have been documented. There are contradictory reports about MP-induced changes in Lachnospiraceae (including the Dorea genus), Alistipes and Faecalibacterium, which may be correlated with obesity, gastrointestinal dysfunction, some cancers, inflammatory bowel disease and Crohn's disease. Potential reasons for these discrepancies are proposed. This review also examines putative mechanisms, with a focus on biofilm formation on selective surfaces, and discusses the inherent limitations of current MP exposure assessments in human gut microbiota studies.
{"title":"Gut microbiome remodeling induced by microplastic exposure in humans.","authors":"Xin-Yue Yang,Zhong-Wei Zhang,Guang-Deng Chen,Shu Yuan","doi":"10.1080/19490976.2026.2617696","DOIUrl":"https://doi.org/10.1080/19490976.2026.2617696","url":null,"abstract":"The impact of microplastics (MPs) on the diversity and composition of the gut microbiome has been extensively documented in animal studies, but evidence in humans remains limited. Recognizing the potential differences in MP effects between animal and human gut microbiomes, this review synthesizes current evidence concerning their impact on the human gut microbiota. Furthermore, the potential links between microplastic-induced dysbiosis and the pathogenesis of human diseases were analyzed. Cross-sectional studies have been conducted to explore microplastic exposures (such as in humans who consume hot foods served in disposable plastic tableware) and their associations with gut microbiome functionalities in infants, preschool children and adults. Exposure to MPs increased the abundance of Dethiosulfovibrionaceae, Enterobacteriaceae, Moraxellaceae, Actinomycetota, Pseudomonadota, and Veillonella. On the other hand, MPs decreased the abundances of Bacillota, Bacteroidota, Lactobacillales, Rikenellaceae, Parabacteroides, Roseburia, Coprococcus, Turicibacter, and Eubacterium coprostanoligenes. These changes were associated with a decrease in butyrate production and a decrease in short-chain fatty acid levels. However, for some other bacteria, both inductive (on Oscillospiraceae, Adlercreutzia, Phascolarctobacterium, and Collinsella) and repressive effects (on Streptococcus) have been documented. There are contradictory reports about MP-induced changes in Lachnospiraceae (including the Dorea genus), Alistipes and Faecalibacterium, which may be correlated with obesity, gastrointestinal dysfunction, some cancers, inflammatory bowel disease and Crohn's disease. Potential reasons for these discrepancies are proposed. This review also examines putative mechanisms, with a focus on biofilm formation on selective surfaces, and discusses the inherent limitations of current MP exposure assessments in human gut microbiota studies.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"41 1","pages":"2617696"},"PeriodicalIF":12.2,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145994918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The incidence of type 1 diabetes (T1D) has risen sharply in recent decades, implicating the role of environmental factors in disease pathogenesis. Diet, a primary driver of gut microbiome development and composition, along with other environmental exposures, has emerged as a potential modulator of T1D risk and progression. While nutrients, such as certain vitamins, may exert protective effects, the roles of other dietary factors (e.g., early exposure to dietary antigens) remain unclear. Importantly, diet shapes the gut microbiome, which produces immunomodulatory metabolites, including secondary bile acids, short-chain fatty acids (SCFAs), and others that directly influence immune responses. This review presents evidence on how specific dietary factors, including macronutrients (fats, carbohydrates, proteins, such as gluten and milk proteins), fibers, and breastfeeding, affect the gut microbiome and T1D. We also discuss the effects of microbiome-targeted interventions, including probiotics, prebiotics, and fecal microbiota transplantation, on T1D and their potential as future therapeutic strategies. Although animal studies provide compelling mechanistic insights, the results from human trials remain inconsistent, underscoring the urgent need for longitudinal and interventional studies to establish causality. Understanding the complex interplay between diet, the gut microbiome, and immune homeostasis is essential for developing personalized strategies to prevent and treat T1D and delay-related complications.
{"title":"Diet, gut microbiome, and type 1 diabetes: from risk to translational opportunity.","authors":"Khyati Girdhar,Sandra Dedrick,Lukas Rhodes,David Kim,Amaya Powis,Caitlin Mahon,Hannah Chapdelaine,Liane Obaid,Meghan McNamara,Emrah Altindis","doi":"10.1080/19490976.2026.2614039","DOIUrl":"https://doi.org/10.1080/19490976.2026.2614039","url":null,"abstract":"The incidence of type 1 diabetes (T1D) has risen sharply in recent decades, implicating the role of environmental factors in disease pathogenesis. Diet, a primary driver of gut microbiome development and composition, along with other environmental exposures, has emerged as a potential modulator of T1D risk and progression. While nutrients, such as certain vitamins, may exert protective effects, the roles of other dietary factors (e.g., early exposure to dietary antigens) remain unclear. Importantly, diet shapes the gut microbiome, which produces immunomodulatory metabolites, including secondary bile acids, short-chain fatty acids (SCFAs), and others that directly influence immune responses. This review presents evidence on how specific dietary factors, including macronutrients (fats, carbohydrates, proteins, such as gluten and milk proteins), fibers, and breastfeeding, affect the gut microbiome and T1D. We also discuss the effects of microbiome-targeted interventions, including probiotics, prebiotics, and fecal microbiota transplantation, on T1D and their potential as future therapeutic strategies. Although animal studies provide compelling mechanistic insights, the results from human trials remain inconsistent, underscoring the urgent need for longitudinal and interventional studies to establish causality. Understanding the complex interplay between diet, the gut microbiome, and immune homeostasis is essential for developing personalized strategies to prevent and treat T1D and delay-related complications.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"141 1","pages":"2614039"},"PeriodicalIF":12.2,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145968388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-13DOI: 10.1080/19490976.2025.2611544
Hyeon Gwon Lee,Ju Yeon Song,Jaekyung Yoon,Yusook Chung,Soon-Kyeong Kwon,Jihyun F Kim
Metagenomic approaches offer unprecedented opportunities to characterize microbial community structure and function, yet several challenges remain unresolved. Inconsistent genome quality impairs reliability of metagenome-assembled genomes, lack of unified taxonomic criteria limits cross-study comparability, and multi-step workflows involving numerous programs and parameters hinder reproducibility and accessibility. We benchmarked existing programs and parameters using simulated metagenomic data to identify optimal configurations. metaFun is an open-source, end-to-end pipeline that integrates quality control, taxonomic profiling, functional profiling, de novo assembly, binning, genome assessment, comparative genomic analysis, pangenome annotation, network analysis, and strain-level microdiversity analysis into a unified framework. Interactive modules support standardized data interpretation and exploratory visualization. The pipeline is implemented with Nextflow and containerized with Apptainer, ensuring environment reproducibility and scalability. Comprehensive documentation is available at https://metafun-doc.readthedocs.io/en/main. The pipeline was validated using a colorectal cancer cohort dataset. By addressing key methodological gaps, metaFun facilitates accessible and reproducible metagenomic analysis for the broader research community.
{"title":"metaFun: An analysis pipeline for metagenomic big data with fast and unified functional searches.","authors":"Hyeon Gwon Lee,Ju Yeon Song,Jaekyung Yoon,Yusook Chung,Soon-Kyeong Kwon,Jihyun F Kim","doi":"10.1080/19490976.2025.2611544","DOIUrl":"https://doi.org/10.1080/19490976.2025.2611544","url":null,"abstract":"Metagenomic approaches offer unprecedented opportunities to characterize microbial community structure and function, yet several challenges remain unresolved. Inconsistent genome quality impairs reliability of metagenome-assembled genomes, lack of unified taxonomic criteria limits cross-study comparability, and multi-step workflows involving numerous programs and parameters hinder reproducibility and accessibility. We benchmarked existing programs and parameters using simulated metagenomic data to identify optimal configurations. metaFun is an open-source, end-to-end pipeline that integrates quality control, taxonomic profiling, functional profiling, de novo assembly, binning, genome assessment, comparative genomic analysis, pangenome annotation, network analysis, and strain-level microdiversity analysis into a unified framework. Interactive modules support standardized data interpretation and exploratory visualization. The pipeline is implemented with Nextflow and containerized with Apptainer, ensuring environment reproducibility and scalability. Comprehensive documentation is available at https://metafun-doc.readthedocs.io/en/main. The pipeline was validated using a colorectal cancer cohort dataset. By addressing key methodological gaps, metaFun facilitates accessible and reproducible metagenomic analysis for the broader research community.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"13 1","pages":"2611544"},"PeriodicalIF":12.2,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145961499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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