Gut Microbes最新文献

{"title":"Systematically-designed mixtures outperform single fibers for gut microbiota support.","authors":"T M Cantu-Jungles, V Agamennone, T J Van den Broek, F H J Schuren, B Hamaker","doi":"10.1080/19490976.2024.2442521","DOIUrl":"https://doi.org/10.1080/19490976.2024.2442521","url":null,"abstract":"<p><p>Dietary fiber interventions to modulate the gut microbiota have largely relied on isolated fibers or specific fiber sources. We hypothesized that fibers systematically blended could promote more health-related bacterial groups. Initially, pooled <i>in vitro</i> fecal fermentations were used to design dietary fiber mixtures to support complementary microbial groups related to health. Then, microbial responses were compared for the designed mixtures versus their single fiber components <i>in vitro</i> using fecal samples from a separate cohort of 10 healthy adults. The designed fiber mixtures outperformed individual fibers in supporting bacterial taxa across donors resulting in superior alpha diversity and unexpected higher SCFA production. Moreover, unique shifts in community structure and specific taxa were observed for fiber mixtures that were not observed for single fibers, suggesting a synergistic effect when certain fibers are put together. Fiber mixture responses were remarkably more consistent than individual fibers across donors in promoting several taxa, especially butyrate producers from the <i>Clostridium</i> cluster XIVa. This is the first demonstration of synergistic fiber interactions for superior support of a diverse group of important beneficial microbes consistent across people, and unexpectedly high SCFA production. Overall, harnessing the synergistic potential of designed fiber mixtures represents a promising and more efficacious avenue for future prebiotic development.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2442521"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863986","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}

{"title":"Genomic island-encoded LmiA regulates acid resistance and biofilm formation in enterohemorrhagic <i>Escherichia coli</i> O157:H7.","authors":"Hongmin Sun, Lingyan Jiang, Jingnan Chen, Chenbo Kang, Jun Yan, Shuai Ma, Mengjie Zhao, Houliang Guo, Bin Yang","doi":"10.1080/19490976.2024.2443107","DOIUrl":"https://doi.org/10.1080/19490976.2024.2443107","url":null,"abstract":"<p><p>Enterohemorrhagic <i>Escherichia coli</i> (EHEC) O157:H7 is an important intestinal pathogen that causes severe foodborne diseases. We previously demonstrated that the genomic island-encoded regulator LmiA activates the locus of enterocyte effacement (LEE) genes to promote EHEC O157:H7 adherence and colonization in the host intestine. However, whether LmiA is involved in the regulation of any other biological processes in EHEC O157:H7 remains largely unexplored. Here, we compared global gene expression differences between the EHEC O157:H7 wild-type strain and an <i>lmiA</i> mutant strain using RNA-seq technology. Genes whose expression was affected by LmiA were identified and classified using the Cluster of Orthologous Groups (COG) database. Specifically, the expression of acid resistance genes (including <i>gadA</i>, <i>gadB</i>, and <i>gadC</i>) was significantly downregulated, whereas the transcript levels of biofilm-related genes (including <i>Z_RS00105</i>, <i>yadN</i>, <i>Z_RS03020</i>, and <i>fdeC</i>) were increased, in the Δ<i>lmiA</i> mutant compared to the EHEC O157:H7 wild-type strain. Further investigation revealed that LmiA enhanced the acid resistance of EHEC O157:H7 by directly activating the transcription of <i>gadA</i> and <i>gadBC</i>. In contrast, LmiA reduced EHEC O157:H7 biofilm formation by indirectly repressing the expression of biofilm-related genes. Furthermore, LmiA-mediated regulation of acid resistance and biofilm formation is highly conserved and widespread among EHEC and enteropathogenic <i>E. coli</i> (EPEC). Our findings provide essential insight into the regulatory function of LmiA in EHEC O157:H7, particularly its role in regulating acid resistance and biofilm formation.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2443107"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846257","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}

{"title":"Gut microbiota and microbial metabolites for osteoporosis.","authors":"Xuan-Qi Zheng, Ding-Ben Wang, Yi-Rong Jiang, Chun-Li Song","doi":"10.1080/19490976.2024.2437247","DOIUrl":"10.1080/19490976.2024.2437247","url":null,"abstract":"<p><p>Osteoporosis is an age-related bone metabolic disease. As an essential endocrine organ, the skeletal system is intricately connected with extraosseous organs. The crosstalk between bones and other organs supports this view. In recent years, the link between the gut microecology and bone metabolism has become an important research topic, both in preclinical studies and in clinical trials. Many studies have shown that skeletal changes are accompanied by changes in the composition and structure of the gut microbiota (GM). At the same time, natural or artificial interventions targeting the GM can subsequently affect bone metabolism. Moreover, microbiome-related metabolites may have important effects on bone metabolism. We aim to review the relationships among the GM, microbial metabolites, and bone metabolism and to summarize the potential mechanisms involved and the theory of the gut‒bone axis. We also describe existing bottlenecks in laboratory studies, as well as existing challenges in clinical settings, and propose possible future research directions.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2437247"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846350","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}

{"title":"T cells regulate intestinal motility and shape enteric neuronal responses to intestinal microbiota.","authors":"Patricia Rodrigues Marques de Souza, Catherine M Keenan, Laurie E Wallace, Yasaman Bahojb Habibyan, Marcela Davoli-Ferreira, Christina Ohland, Fernando A Vicentini, Kathy D McCoy, Keith A Sharkey","doi":"10.1080/19490976.2024.2442528","DOIUrl":"https://doi.org/10.1080/19490976.2024.2442528","url":null,"abstract":"<p><p>How the gut microbiota and immune system maintain intestinal homeostasis in concert with the enteric nervous system (ENS) remains incompletely understood. To address this gap, we assessed small intestinal transit, enteric neuronal density, enteric neurogenesis, intestinal microbiota, immune cell populations and cytokines in wildtype and T-cell deficient germ-free mice colonized with specific pathogen-free (SPF) microbiota, conventionally raised SPF and segmented filamentous bacteria (SFB)-monocolonized mice. SPF microbiota increased small intestinal transit in a T cell-dependent manner. SPF microbiota increased neuronal density in the myenteric and submucosal plexuses of the ileum and colon, similar to conventionally raised SPF mice, independently of T cells. SFB increased neuronal density in the ileum in a T cell-dependent manner, but independently of T cells in the colon. SPF microbiota stimulated enteric neurogenesis (Sox2 expression in enteric neurons) in the ileum in a T cell-dependent manner, but in the colon this effect was T cell-independent. T cells regulated nestin expression in the ENS. SPF colonization increased Th17 cells, RORγT⁺ Treg cells, and IL-1β and IL-17A levels in the ileum and colon. By neutralizing IL-1β and IL-17A, we observed that they control microbiota-mediated enteric neurogenesis but were not involved in the regulation of motility. Together, these findings provide new insights into the microbiota-neuroimmune dialog that regulates intestinal physiology.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2442528"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863988","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}

{"title":"Non-stochastic reassembly of a metabolically cohesive gut consortium shaped by N-acetyl-lactosamine-enriched fibers.","authors":"Madison Moore, Hunter D Whittington, Rebecca Knickmeyer, M Andrea Azcarate-Peril, Jose M Bruno-Bárcena","doi":"10.1080/19490976.2024.2440120","DOIUrl":"https://doi.org/10.1080/19490976.2024.2440120","url":null,"abstract":"<p><p>Diet is one of the main factors shaping the human microbiome, yet our understanding of how specific dietary components influence microbial consortia assembly and subsequent stability in response to press disturbances - such as increasing resource availability (feeding rate) - is still incomplete. This study explores the reproducible re-assembly, metabolic interplay, and compositional stability within microbial consortia derived from pooled stool samples of three healthy infants. Using a single-step packed-bed reactor (PBR) system, we assessed the reassembly and metabolic output of consortia exposed to lactose, glucose, galacto-oligosaccharides (GOS), and humanized GOS (hGOS). Our findings reveal that complex carbohydrates, especially those containing low inclusion (~1.25 gL^-1) components present in human milk, such as N-acetyl-lactosamine (LacNAc), promote taxonomic, and metabolic stability under varying feeding rates, as shown by diversity metrics and network analysis. Targeted metabolomics highlighted distinct metabolic responses to different carbohydrates: GOS was linked to increased lactate, lactose to propionate, sucrose to butyrate, and CO₂, and the introduction of bile salts with GOS or hGOS resulted in butyrate reduction and increased hydrogen production. This study validates the use of single-step PBRs for reliably studying microbial consortium stability and functionality in response to nutritional press disturbances, offering insights into the dietary modulation of microbial consortia and their ecological dynamics.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2440120"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853944","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}

{"title":"The regulatory effect of chitooligosaccharides on islet inflammation in T2D individuals after islet cell transplantation: the mechanism behind <i>Candida albicans</i> abundance and macrophage polarization.","authors":"Yayu Zhang, Xiaoguo Ji, Kunlin Chang, Hao Yin, Mengyao Zhao, Liming Zhao","doi":"10.1080/19490976.2024.2442051","DOIUrl":"https://doi.org/10.1080/19490976.2024.2442051","url":null,"abstract":"<p><p>Islet cell transplantation (ICT) represents a promising therapeutic approach for addressing diabetes mellitus. However, the islet inflammation during transplantation significantly reduces the surgical outcome rate, which is related to the polarization of macrophages. Chitooligosaccharides (COS) was previously reported which could modulate the immune system, alleviate inflammation, regulate gut microecology, and repair the intestinal barrier. Therefore, we hypothesized COS could relieve pancreatic inflammation by regulating macrophage polarization and gut microbiota. First, 18S rDNA gene sequencing was performed on fecal samples from the ICT population, showing abnormally increased amount of <i>Candida albicans</i>, possibly causing pancreatic inflammation. Functional oligosaccharides responsible for regulating macrophage polarization and inhibiting the growth of <i>Candida albicans</i> were screened. Afterwards, human flora-associated T2D (HMA-T2D) mouse models of gut microbiota were established, and the ability of the selected oligosaccharides were validated <i>in vivo</i> to alleviate inflammation and regulate gut microbiota. The results indicated that ICT significantly decreased the alpha diversity of gut fungal, altered fungal community structures, and increased <i>Candida albicans</i> abundance. Moreover, <i>Candida albicans</i> promoted M1 macrophage polarization, leading to islet inflammation. COS inhibited <i>Candida albicans</i> growth, suppressed the MyD88-NF-κB pathway, activated STAT6, inhibited M1, and promoted M2 macrophage polarization. Furthermore, COS-treated HMA-T2D mice displayed lower M1 macrophage differentiation and higher M2 macrophage numbers. Additionally, COS also enhanced <i>ZO-1</i> and <i>Occludin</i> mRNA expression, reduced <i>Candida albicans</i> abundance, and balanced gut microecology. This study illustrated that COS modulated macrophage polarization via the MyD88/NF-κB and STAT6 pathways, repaired the intestinal barrier, and reduced <i>Candida albicans</i> abundance to alleviate islet inflammation.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2442051"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853997","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}

{"title":"Candida tropicalis-derived vitamin B3 exerts protective effects against intestinal inflammation by promoting IL-17A/IL-22-dependent epithelial barrier function","authors":"Ha T Doan, Li-Chieh Cheng, Yi-Ling Chiu, Yuan-Kai Cheng, Cheng-Chih Hsu, Yee-Chun Chen, Hsiu-Jung Lo, Hao-Sen Chiang","doi":"10.1080/19490976.2024.2416922","DOIUrl":"https://doi.org/10.1080/19490976.2024.2416922","url":null,"abstract":"Candida tropicalis-a prevalent gut commensal fungus in healthy individuals – contributes to intestinal health and disease. However, how commensal C. tropicalis influences intestinal homeostasis and...","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"15 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142490765","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}

{"title":"The role and mechanism of gut-lung axis mediated bidirectional communication in the occurrence and development of chronic obstructive pulmonary disease.","authors":"Xiaofan Song,Xina Dou,Jiajing Chang,Xiaonan Zeng,Qinhong Xu,Chunlan Xu","doi":"10.1080/19490976.2024.2414805","DOIUrl":"https://doi.org/10.1080/19490976.2024.2414805","url":null,"abstract":"The current studies have shown that the occurrence and development of chronic obstructive pulmonary disease (COPD) are closely related to the changes in gut health and its microenvironment, and even some gut diseases have significant clinical correlation with COPD. The dysbiosis of gut microbiota observed in COPD patients also suggests a potential bidirectional interaction between the gut and lung. Communication between the gut and lung may occur through circulating inflammatory cells, gut microbial metabolites, and circulating inflammatory mediators, but the mechanism of bidirectional communication between the gut and lung in COPD is still under study. Therefore, more research is still needed in this area. In this review, we summarize recent clinical studies and animal models on the role of the gut-lung axis in the occurrence and development of COPD and its mechanisms, so as to provide ideas for further research in this field. In addition, we also summarized the negative effects of COPD medication on gut microbiota and the gut microbiota risk factors for COPD and proposed the potential prevention and treatment strategies.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"97 1","pages":"2414805"},"PeriodicalIF":12.2,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142489731","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}

{"title":"Morphine-induced intestinal microbial dysbiosis drives TLR-dependent IgA targeting of gram-positive bacteria and upregulation of CD11b and TLR2 on a sub-population of IgA+ B cells.","authors":"Nicolas Vitari,Salma Singh,Junyi Tao,Bridget Truitt,Udhghatri Kolli,Richa Jalodia,Kathryn M LaPorte,Yaa Abu,Danielle Antoine,Umakant Sharma,Sabita Roy","doi":"10.1080/19490976.2024.2417729","DOIUrl":"https://doi.org/10.1080/19490976.2024.2417729","url":null,"abstract":"IgA binding dictates the composition of the intestinal microbiome and reflects dysbiotic states during chronic disease. Both pathogenic and commensal bacteria differentially bind to IgA with varying outcomes. Little is known regarding IgA dynamics immediately following microbial dysbiosis. Recent work shows that morphine treatment rapidly induces microbial dysbiosis within hours of administration. This microbial shift is characterized by the expansion of pathogenic bacteria with a concurrent decrease in commensal bacteria. Because of this rapid microbial shift, a murine model of chronic morphine treatment was used to gain insight on the host IgA response during early microbial disruption. Within 24 h, morphine treatment induces microbial dysbiosis which disrupts IgA-bacterial homeostasis, resulting in an increased concentration of unbound IgA with a corresponding decrease in the frequency of IgA-bound bacteria. Additionally, the increased concentration of unbound IgA is dependent on the microbiome, as microbial depletion abolishes the increase. At 48 h of morphine treatment, the frequency of IgA-bound bacteria increases and IgA-seq reveals increased IgA targeting of gram-positive bacteria. Both a whole-body TLR2 KO and treatment with the TLR inhibitor OxPAPC resulted in abrogation of IgA binding to bacteria, implicating modulation of IgA binding through TLR signaling. Finally, we identify that a sub-population of IgA+ B cells in the intestinal lamina propria has increased CD11b and TLR2 expression at 24 h of morphine treatment which could be a potential source of the observed IgA that targets gram-positive bacteria. Together, we demonstrate for the first time the role of TLR2 in IgA targeting of intestinal bacteria, and this study sheds light on the IgA dynamics during the initial hours of microbial dysbiosis.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"235 1","pages":"2417729"},"PeriodicalIF":12.2,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142488288","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}

{"title":"Fecal samples and rectal swabs adequately reflect the human colonic luminal microbiota.","authors":"Julia Rode,Linnea Brengesjö Johnson,Julia König,Ignacio Rangel,Lars Engstrand,Dirk Repsilber,Robert J Brummer","doi":"10.1080/19490976.2024.2416912","DOIUrl":"https://doi.org/10.1080/19490976.2024.2416912","url":null,"abstract":"The appropriateness of the fecal microbiota to adequately reflect the gut microbiota composition from more difficult to access luminal content at different colonic locations has been debated. Here, in a healthy population, luminal samples were collected from terminal ileum to rectum using an unique sampling technique without the need of prior bowel cleansing/preparation. Rectal swabs were collected immediately prior colonoscopy by an experienced physician, and fecal samples were collected at home by the participants themselves. Microbiota composition was evaluated as relative abundance, α-diversity and Bray-Curtis dissimilarities. Our data suggest that fecal samples and rectal swabs present noninvasive, easily accessible, low-cost sampling tools that are accurate proxies to characterize luminal large intestinal microbiota composition.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"48 1","pages":"2416912"},"PeriodicalIF":12.2,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142488289","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}