The gut microbiome–immune axis in inflammatory bowel disease: Microbial mechanisms and therapeutic implications

Abstract

The human gut microbiome makes up a highly diverse microbial ecosystem that is crucial for host metabolism, immunological modulation, and intestinal barrier integrity. The bacteria phyla Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria dominate the intestinal microbiota, contributing to metabolic processes such as dietary polysaccharide fermentation and the synthesis of bioactive microbial metabolites. Dysbiosis, or disruptions in microbial composition and function, has been linked to the development of autoimmune disorders. Microbial mechanisms that relate dysbiosis to disease include the growth of pro-inflammatory microbial taxa, decreased synthesis of short-chain fatty acids (SCFAs), altered microbial metabolic pathways, and loss of epithelial barrier integrity. Among autoimmune disorders, inflammatory bowel disease (IBD), which encompasses Crohn’s disease and ulcerative colitis, is one of the best-studied cases of microbiome-associated pathology. In this review, we focus on the role of gut microbiome alterations in the pathogenesis of IBD, highlighting microbial dysbiosis, changes in microbial metabolites, and host–microbiome interactions that contribute to intestinal inflammation. This review also examines microbiome-targeted therapeutic strategies, including probiotics, prebiotics, fecal microbiota transplantation, and postbiotics, alongside emerging artificial intelligence–based approaches to personalized treatment, and consider how comorbid systemic conditions may shape microbial homeostasis in IBD patients. Understanding these microbial pathways may open new possibilities for microbiome-based diagnostics and therapeutic approaches in IBD.