ArticleCell communication and signaling : CCS2025
Inhibition of Farnesoid-x-receptor signaling during abdominal sepsis by dysbiosis exacerbates gut barrier dysfunction.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Review
- Metabolic and neuroimmune control of rheumatoid arthritis: therapeutic implications of FXR and α7-nAChR axes.Inflammopharmacology · 2026Review
- Bile Acids and the Gut-X Axis: TCM-Mediated Systemic Protection and Therapeutic Opportunities for Multi-Organ Diseases.Metabolites · 2026Review
- The Gastrointestinal Barrier-Mechanisms of Barrier Dysfunction in Liver Cirrhosis and Spontaneous Bacterial Peritonitis.Biomedicines · 2026Review
- Multi-omics analysis of gut microbiota and metabolome reveals potential biomarkers in pediatric snoring.BMC microbiology · 2026Article
- Lactate and lactylation in sepsis: regulation of immune-metabolic crosstalk and organ injury.Frontiers in immunology · 2026Review
- Article
- Multi-omics profiling reveals microbiota-gut-brain axis dysregulation in an LPS-induced model of sepsis-associated encephalopathy.Frontiers in cellular and infection microbiology · 2026Article
- Progress on the correlation between sepsis and gut microbiota: a narrative review.Frontiers in microbiology · 2026Review
- Gut barrier-microbiota crosstalk in sepsis: from pathogenesis to potential therapies.Frontiers in immunology · 2026Review
- Gut microbiota dysbiosis in sepsis and sepsis-associated organ injury: mechanisms, gut-organ axes, and therapeutic strategies.Frontiers in microbiology · 2026Review
- Bile acid dysregulation in sepsis: mechanisms, clinical implications, and future perspectives.Frontiers in cellular and infection microbiology · 2026Review
- Activation of farnesoid X receptor upregulates binding immunoglobulin protein expression and alleviates diabetic nephropathy.World journal of diabetes · 2025Article
- Targeting the gut-liver axis in cholangiocarcinoma: mechanisms, therapeutic advances, and future directions.Frontiers in oncology · 2025Review
- Lung-gut axis, intestinal microbiota, and pulmonary fibrosis: mechanisms and therapeutic potential.Frontiers in microbiology · 2025Review
- Immunomodulatory role of gut microbial metabolites: mechanistic insights and therapeutic frontiers.Frontiers in microbiology · 2025Review
- Intestinal injury signaling pathway in sepsis.Frontiers in immunology · 2025Review
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12 authors.
Funding
Abstract
BACKGROUND AND
aimsBacterial translocation and intestinal dysbiosis due to gut barrier dysfunction are widely recognized as major causes of the initiation and development of intra-abdominal sepsis. Systemic bacterial translocation and hepatic activation of the myeloid differentiation primary response gene 88 (Myd88) can disturb bile acids (BAs) metabolism, further exacerbating intestinal dysbiosis. The farnesoid X receptor (FXR) and fibroblast growth factor (FGF) 15/19 are well known to be involved in the control of BAs synthesis and enterohepatic circulation. However, the influence of intestinal microbiota on intestinal Myd88 signaling, the FXR/FGF15 axis, as well as gut-liver crosstalk during sepsis remains unclear. The present study aims to decipher the role of intestinal Myd88 in abdominal sepsis, its impact on intestinal FXR signaling and FGF15-mediated gut-liver crosstalk.
methodsExpression levels of FXR and FGF15 in the liver and intestines, alongside assessments of gut barrier function, were evaluated in septic wild-type (WT) mice 24 h post-cecal ligation and puncture (CLP) surgery. Subsequently, the FXR agonist INT-747 was administered to explore the relationship between FXR activation and gut barrier function. Further investigations involved Myd88-deficient mice with specific deletion of Myd88 in intestinal epithelial cells (Myd88
resultsInduction of sepsis via CLP led to hepatic cholestasis, suppressed FXR-FGF15 signaling, altered gut microbiota composition, and compromised gut barrier function. Administration of INT-747 increased intestinal FXR and FGF15 expression, strengthened gut barrier function, and enhanced barrier integrity. Interestingly, Myd88
conclusionsThis study highlights the critical role of Myd88/FXR signaling in intestinal epithelial cells as a pivotal mediator of the detrimental effects induced by sepsis-related intestinal dysbiosis on barrier function and bile acid metabolism. In summary, disordered intestinal flora in septic mice specifically triggers intestinal epithelial Myd88 activation, inhibit the FXR-FGF15 axis, and then worsen intestinal barrier function impairment.
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