Inflammatory bowel disease (IBD), which primarily includes ulcerative colitis (UC) and Crohn’s disease (CD), has seen a rapid rise in incidence in China in recent years. Traditional medications and biologics still face limitations such as limited targeting and a high risk of relapse upon discontinuation. Gut microbiota dysbiosis and the resulting metabolic disturbances are key pathological mechanisms underlying intestinal barrier damage and mucosal immune imbalance in IBD. This article focuses on the microbiota-metabolism axis to elucidate the physiological functions of three core metabolic pathways—short-chain fatty acids, bile acids, and tryptophan—and their pathological alterations in IBD. In addition, the regulatory mechanisms and clinical evidence of typical probiotics such as Clostridium butyricum, Escherichia coli, Faecalibacterium prausnitzii, Bifidobacterium and Limosilactobacillus reuteri on the above pathways were sorted out. Existing studies have shown that probiotics can play an anti-inflammatory role by refilling the exhausted metabolic pathways, repairing the intestinal epithelial barrier and regulating mucosal immunity, which is a safe and good auxiliary intervention for IBD. This article systematically reviews the above evidence to provide a reference for the subsequent mechanism research and clinical application of probiotics in IBD.
No takes yet. Share an insight, caveat, or question.
Xinting Li (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: