Gut Microbes最新文献

{"title":"Microbial extracellular vesicles from min pigs remodel macrophage polarization via STING to sustain intestinal immune homeostasis.","authors":"Zhendong Sun, Zichuan An, Weichen Hong, Chenpeng He, Jiaxin Liu, Yupu Wang, Chenyu Xue, Na Dong","doi":"10.1080/19490976.2026.2620126","DOIUrl":"10.1080/19490976.2026.2620126","url":null,"abstract":"<p><p>Intestinal immune homeostasis is crucial for intestinal function and health. Increasing evidence suggests that certain gut microbiota can enhance the host's intestinal immune regulatory capacity. However, the mechanisms by which the microbiota confers beneficial traits and robust immunity to the host, as well as the cross-species reproducibility of these effects, remain unclear. This study, through multi-omics integration comparison and functional validation, revealed that <i>Streptococcus hyointestinalis</i> from Min pigs regulates macrophage polarization homeostasis by targeting and inhibiting the excessive activation of the STING signaling pathway and its downstream pro-inflammatory cascade reactions through its extracellular vesicles (EVs), thereby shifting them toward the M2 phenotype. This process ensures the integrity of the intestinal barrier and alleviates colitis induced by the combined effects of low temperature and sodium sulfate-induced colitis (DSS). Notably, in <i>Sting</i>^<i>-/-</i> mice, the EV-mediated intestinal protective effect was eliminated, confirming its targeted efficacy. Our data reveal a microbial EV‒STING‒macrophage axis in which symbiotic bacterial exosomes promote reparative macrophage programs by regulating STING signaling and maintaining intestinal integrity under environmental stress. These findings reveal a novel host-microbiota communication pathway with therapeutic potential for the treatment of inflammation-driven intestinal diseases.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2620126"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12851393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146051655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Orchestrating life's first community: molecular assembly by human milk oligosaccharides.","authors":"Ye Zhou, Bo Yang, Jianxin Zhao, Paul Ross, Catherine Stanton, Wei Chen","doi":"10.1080/19490976.2026.2632973","DOIUrl":"10.1080/19490976.2026.2632973","url":null,"abstract":"<p><p>The infant gut microbiota, orchestrated by human milk oligosaccharides (HMOs), forms a critical foundation for lifelong health. Despite their recognized importance, the molecular strategies through which HMOs govern microbial competition and niche establishment remain poorly understood. Moving beyond ecological observations, this review synthesizes current mechanistic evidence on the molecular machinery of HMO metabolism in microbial assembly. We explore the specialized enzymes that confer competitive advantages and the metabolic networks fueled by HMO breakdown. Furthermore, we distinguish substrate-driven effects from the hypothesized signaling roles of intact HMOs in modulating host-microbe interactions, indicating where the evidence is associative versus causal. By integrating these pathways, we provide a blueprint for leveraging HMO biology to develop targeted nutritional interventions for preventing early-life disorders.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2632973"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12928651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146226674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Host metabolism shapes the intestinal microbiota: a top-down paradigm of environmental selection pressure.","authors":"Ziyu Ma, Huairuo Shi, Xinjie Bai, Zixu Wang, Jing Cao, Yulan Dong, Yaoxing Chen","doi":"10.1080/19490976.2026.2667735","DOIUrl":"https://doi.org/10.1080/19490976.2026.2667735","url":null,"abstract":"<p><p>Intestinal homeostasis is not a stochastic microbial assembly but a deterministic outcome orchestrated by host-mediated metabolic gating. Traditional research has prioritized the microbiota's impact on host physiology. However, the consistent expansion of facultative anaerobes, such as <i>Enterobacteriaceae</i>, observed in pathological states like intestinal inflammation, suggests that dysbiosis is fundamentally a consequence of impaired host regulation. Here, we propose a \"top-down\" paradigm of host metabolic regulation, framing the host as an \"ecological engineer\" that actively shapes the microbiome through metabolism. We detail three critical metabolic filters: (1) the maintenance of epithelial hypoxia via mitochondrial <i>β</i>-oxidation to suppress aerobic respiration; (2) the implementation of \"nutritional immunity\" to restrict glucose and inflammation-derived electron acceptors (nitrate and tetrathionate); and (3) the energy-dependent synthesis of the gel-forming mucin 2 (<i>MUC2</i>) mucus layer and antimicrobial peptides (AMPs). We argue that the breakdown of these filters leads to \"niche opening,\" which acts as the fundamental driver of dysbiosis. Finally, we discuss therapeutic strategies aimed at restoring host bioenergetics-including Peroxisome proliferator-activated receptor gamma (<i>PPAR-γ</i>) agonists, melatonin, and ketogenic diets-to rebuild the host's ecological filtration capacity and fundamentally correct dysbiosis.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2667735"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837158","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":"Exploring the gut microbiome and metabolomic interactions of antimetabolite drugs to optimize therapy.","authors":"Jingyang Chen, Yanan Wang, Lei Xu, Xiaona Li, Libo Zhao","doi":"10.1080/19490976.2026.2638009","DOIUrl":"10.1080/19490976.2026.2638009","url":null,"abstract":"<p><p>Antimetabolite drugs are cornerstones in treating various cancers and autoimmune diseases; however, their clinical utility is often hampered by systemic toxicity caused by drug-induced gut microbiota dysbiosis. Predicting patient responses remains a significant challenge. Several studies have highlighted the influence of gut microbiota on antimetabolite treatment outcomes, revealing complex bidirectional interactions between the drugs and microbial communities. This review synthesizes the effects of common antimetabolites (including 5-fluorouracil, methotrexate, gemcitabine, capecitabine, 6-mercaptopurine, and thioguanine) on gut microbial communities and outlines a framework (pharmacokinetics, endogenous metabolite production, immune modulation, and apoptotic pathway modulation) for assessing chemotherapy-microbiota interactions. Additionally, potential microbial biomarkers for predicting treatment responses and strategies for manipulating the gut microbiota to enhance therapeutic efficacy are discussed. Therefore, advances in methodologies such as metagenomics and real-time microbial monitoring will be essential for unraveling these interactions and promoting the precise application of antimetabolite drugs.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2638009"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12959226/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147305083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<b>Responses of intestinal organoids to infection by</b> <i><b>Mycobacterium avium</b></i> <b>resemble symptoms observed in Crohn's disease</b>.","authors":"Wanbin Hu, Adriana Martinez Silgado, Ninouk Akkerman, Ronald W A L Limpens, Roman I Koning, Hans Clevers, Herman P Spaink","doi":"10.1080/19490976.2026.2630483","DOIUrl":"10.1080/19490976.2026.2630483","url":null,"abstract":"<p><p>Crohn's disease (CD) is a chronic inflammatory bowel disease (IBD). <i>Mycobacterium avium</i>, which causes Johne's disease in ruminants, has been suggested as a potential CD trigger due to shared pathology, but early epithelial responses remain unclear. This study established a mouse small intestinal organoid (mSIO) model of <i>M. avium</i> infection to assess CD-related inflammation. Infected mSIOs were examined by confocal microscopy, block-face scanning electron microscopy, and macrophage co-culture to track bacterial localization and immune cell behavior. The data give unprecedent dynamic and super high resolution insights in the responses of gut cells to mycobacterial infection. RNA-seq with GSEA revealed strong induction of inflammatory genes and enrichment of pro-inflammatory pathways. Comparative analysis with CD-humanized mouse data showed overlapping gene expression and enrichment of the IBD signaling pathway. Notably, <i>Mmp7</i>, which can be linked to epithelial remodeling and inflammation, was a common marker in both models. This study presents a robust mSIO model of <i>M. avium</i> infection that recapitulates features of CD-associated inflammation both with high-resolution imaging and transcriptomics and identifies <i>Mmp7</i> as a potential molecular link between infection and CD-like pathology.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2630483"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915785/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146194501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HLA-B27-associated gut microbiota and amino acid perturbations promote ankylosing spondylitis through M1 macrophage activation.","authors":"Tianwen Huang, Hang Yang, Lingshu Zhang, Xiangpeng Wang, Ye Chen, Huanzi Dai, Kenji Hashimoto, Yubin Luo, Yaoyu Pu, Yi Liu","doi":"10.1080/19490976.2026.2630561","DOIUrl":"10.1080/19490976.2026.2630561","url":null,"abstract":"<p><p>Ankylosing spondylitis (AS) is strongly associated with the human leukocyte antigen B27 (HLA-B27), yet how this genetic risk factor interacts with the gut microbiome remains unclear. We integrated fecal gut microbiota analysis, untargeted metabolomics, and clinical phenotyping in 88 participants, including HLA-B27-positive patients with AS (<i>n</i> = 28), HLA-B27-positive healthy controls (<i>n</i> = 30), and HLA-B27-negative healthy controls (<i>n</i> = 30). HLA-B27 positivity, particularly in AS, was associated with marked alterations in gut microbial composition and metabolic profiles, with forty bacterial species showing progressive disease-related shifts across cohorts. Integrated pathway and metabolomic analyses identified three amino acid-related pathways consistently disrupted in AS: tryptophan metabolism, cysteine metabolism, and pyruvate-centered biosynthesis of branched-chain amino acids, ornithine, and lysine. Correlation network analyses linking differential taxa, metabolites, and clinical indices revealed previously unrecognized microbial and metabolic signatures that robustly distinguished AS from both control groups. To explore causality, fecal microbiota transplantation (FMT) from clinical donors into antibiotic-treated mice recapitulated key disease-relevant features, including impaired intestinal barrier function, systemic inflammation, trabecular bone loss, and polarization of macrophages toward a proinflammatory M1 phenotype. Mechanistic validation identified cinnabarinic acid as a critical microbial-derived metabolite that suppresses M1 macrophage polarization via activation of the aryl hydrocarbon receptor (AhR) pathway and confers protection in the FMT model. Together, these findings support a model in which HLA-B27-associated gut dysbiosis and metabolic reprogramming promote AS pathogenesis through macrophage-mediated inflammation and osteocatabolic signaling, highlighting microbial-metabolic pathways as potential therapeutic targets.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2630561"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146206975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The potential immunological mechanisms of gut microbiota dysbiosis caused by antibiotics exacerbate the lethality of influenza viruses.","authors":"Jianing Zhu, Zihang Huang, Ying Lin, Jie Zhu, Rui Min, Zibo Wan, Yuting Chen, Jianwen Zhu, Li Xing, Sheng Li, Chinasa Valerie Olovo, Xiaoquan Wang, Guocai Li, Pinghu Zhang","doi":"10.1080/19490976.2025.2609451","DOIUrl":"10.1080/19490976.2025.2609451","url":null,"abstract":"<p><strong>Background: </strong>Antibiotics are not recommended to treat influenza A virus (IAV). However, antibiotic misuse for IAV persists worldwide. How to scientifically use antibiotics for IAV-infected patients remains a considerable challenge.</p><p><strong>Results: </strong>Here, we investigated the impact of antibiotics on viral pathogenicity, pulmonary-intestinal antiviral immunity, and antiviral drug efficacy. Our findings indicated that antibiotic intervention exacerbated IAV-caused mortality and lung injury in mice, manifested as increased mortality rates, shortened survival time, aggravated pulmonary injury, and excessive inflammatory responses. Furthermore, antibiotic pretreatment significantly diminished the efficacy of antivirals. Metagenomic sequencing revealed that antibiotics reduced the diversity and abundance of beneficial gut microbiota, including <i>Lactobacillus</i> and <i>Bifidobacterium</i>, while promoting the proliferation of pathogenic bacteria such as <i>Klebsiella pneumoniae</i> and <i>Escherichia coli</i>. Mechanistically, antibiotic intervention exacerbated IAV-caused excessive inflammatory responses by the blockage of pulmonary-intestinal antiviral immune pathways, which were caused by the upregulation of PKR, RIG-I, ISG15, and TRIM25 levels while downregulating IPS-1 mRNA levels. However, it is noteworthy that the combination of antibiotics and antiviral drugs effectively offset the adverse effects of antibiotic pretreatment on influenza mortality by upregulating IPS-1 levels and partially restoring pulmonary-intestinal immune homeostasis.</p><p><strong>Conclusions: </strong>Pulmonary-intestinal immune homeostasis imbalance caused by antibiotic misuse can not only markedly exacerbate the lethality of IAV, but also significantly attenuate the efficacy of antiviral drugs. A mechanistic study confirmed that gut microbes dysbiosis caused by antibiotic pretreatment exacerbates the homeostasis imbalance of host antiviral immunity by blocking the RIG/MDA5/IPS-1 antiviral signaling pathway. However, combination therapy with antibiotics and antivirals effectively reversed the fatal outcome exacerbated by antibiotic pretreatment. Collectively, our findings not only provide a scientific explanation from the perspective of antiviral immunity as to why antibiotics should not be arbitrarily used to treat viral infections but also lay the scientific foundation for the rational clinical use of antivirals and antibiotics for treating influenza.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2609451"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12773635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145888308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pre-existing β-lactamase gene diversity is associated with lower risk of ESBL-producing Enterobacterales colonization in patients exposed to ceftriaxone.","authors":"Quentin Le Bastard, Rémi Gschwind, Julie Lao, Marie-Anne Vibet, Eric Batard, Stéphane Corvec, Emmanuel Montassier, Etienne Ruppé","doi":"10.1080/19490976.2026.2627692","DOIUrl":"10.1080/19490976.2026.2627692","url":null,"abstract":"<p><p>Exposure to broad-spectrum antibiotics, particularly to third-generation cephalosporins (3GC), increases the risk of colonization by extended-spectrum beta-lactamase-producing Enterobacterales (ESBL-E). While clinical risk factors for ESBL-E acquisition are well established, the role of the gut microbiome and resistome remains unclear. We conducted a prospective study of patients with suspected bacterial infections receiving ceftriaxone to identify microbiome and resistome features associated with ESBL-E acquisition. Rectal samples collected before antibiotic administration, during treatment, and 30 d after initiation were analyzed by shotgun metagenomic sequencing. Among 80 patients, 12 (15%) acquired ESBL-E colonization by day 30. Ceftriaxone exposure induced a profound and sustained reduction in microbial richness and diversity across all patients. However, no specific taxonomic signature predicted subsequent ESBL-E colonization. In contrast, patients who did not acquire ESBL-E displayed a significantly richer and more diverse repertoire of β-lactamase-encoding genes at baseline, which was independently associated with protection against colonization. Moreover, patients exposed to multiple antibiotics experienced greater and more sustained microbiome disruption compared with those receiving ceftriaxone alone. These findings provide the first real-world evidence that pre-existing β-lactamasome diversity may confer ecological protection against antibiotic-driven colonization by ESBL-E in infected patients, highlighting the importance of functional resistome diversity over taxonomic composition in colonization resistance.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2627692"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12893698/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146156982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered crosstalk of bacterial lipopolysaccharide with immune cells in colorectal cancer compared to paired adjacent intestinal tissue.","authors":"Åsa Walberg, Anna Maria Reuss, Reihane Ziadlou, Céline Mamie, Claudia Gottier, Anna White, Mohammadmilad Ameri, Marie-Charlotte Brüggen, Matthias Turina, Michaela Ramser, Paulina Wawrzyniak, Maria Walker, Luca Truscello, Adriano Aguzzi, Anne Müller, Barbara Hubeli, Yasser Morsy, Michael Scharl","doi":"10.1080/19490976.2026.2665878","DOIUrl":"10.1080/19490976.2026.2665878","url":null,"abstract":"<p><p>Commensal bacteria play a crucial role in modulating human immune responses in the intestine. Under homeostatic conditions, the gut microbiota is tightly regulated by interactions with the mucosal immune system. However, colorectal cancer (CRC) is characterized by an imbalance in bacterial composition and bacterial translocation across the intestinal barrier. The spatial distribution of bacteria and their interactions with immune cells in CRC tumors are poorly understood. By applying 3D light-sheet imaging, spatial transcriptomics, and imaging mass cytometry to patient-derived CRC and adjacent intestinal tissue, bacterial lipopolysaccharide (LPS) can be visualized alongside immune cells and vessels. The results showed regional bacterial LPS accumulation and colocalization with distinct immune cell subsets. In CRC-adjacent tissue, bacterial LPS is mainly associated with CD11c⁺ dendritic cells, CD15⁺ neutrophils, and CD163⁺ macrophages. In matched CRC tissue, the number and LPS colocalization of CD163⁺ macrophages and CD11c⁺ dendritic cells decreased, while CD15⁺ neutrophils and their colocalization with LPS increased. Notably, immune cell composition and immune cell‒bacteria interactions differ between tumors and adjacent tissue, offering insights into host‒microbiota dynamics and mechanistic interactions.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2665878"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13154938/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut microbiota in chronic inflammation: the interplay with lipid mediators.","authors":"Suxia Bao, Chengcan Yao","doi":"10.1080/19490976.2026.2667605","DOIUrl":"10.1080/19490976.2026.2667605","url":null,"abstract":"<p><p>The gut microbiota plays a fundamental role in maintaining host health by regulating immune function, epithelial barrier integrity, and metabolic homeostasis. Disruption of microbial community structure (also known as dysbiosis) and altered host-microbiota interactions can shift microbial composition and metabolite production, promote immune dysregulation, and contribute to the initiation and persistence of chronic inflammation. Eicosanoids, a class of signaling lipid mediators derived from arachidonic acid , are essential modulators of acute and chronic inflammatory responses. Emerging evidence highlights a bidirectional interplay between the microbiota and eicosanoid pathways as a hallmark of chronic inflammation. Microbial taxa and their metabolites regulate arachidonic acid availability, eicosanoid biosynthesis, and receptor signaling in host cells. In turn, host-derived eicosanoids shape the gut environment, influencing the gut microbiota and host health state. This self-reinforcing loop drives key features of chronic inflammatory diseases, including a shift toward pro-inflammatory eicosanoid profiles, a relative deficiency of anti-inflammatory or pro-resolving lipid mediators, and microbiota dysbiosis. In this review, we summarize recent advances in the mechanisms underpinning microbiota-eicosanoid crosstalk, outline its contribution to chronic inflammatory diseases, and discuss the therapeutic potential of targeting this bidirectional axis.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2667605"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13154968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}