Research progress on intestinal probiotics-mediated protection of the intestinal mucosal barrier in ulcerative colitis
TL;DR
Current findings suggest that probiotics can inhibit pathogen adhesion and colonization, enhance the production of beneficial metabolites such as short-chain fatty acids and tryptophan-derived compounds, and promote the expression of tight-junction proteins, as well as mucins such as MUC1 and MUC2.
Abstract
Ulcerative colitis (UC) is a major subtype of inflammatory bowel disease characterized by a chronic, relapsing course. Its pathogenesis involves complex interactions among gut microbial dysbiosis, epithelial barrier disruption, dysregulated immune responses, and oxidative stress. Impairment of the intestinal mucosal barrier facilitates the translocation of luminal antigens, bacteria, and microbial metabolites into the mucosa, thereby aggravating local inflammation. Probiotics may help maintain barrier homeostasis by reshaping the gut microbial community, reinforcing epithelial and mucus barriers, modulating mucosal immunity, and reducing oxidative injury. This review summarizes recent evidence on the protective effects of probiotics, including Lactobacillus spp., Bifidobacterium spp., and Akkermansia muciniphila, on the intestinal mucosal barrier in UC. Current findings suggest that probiotics can inhibit pathogen adhesion and colonization, enhance the production of beneficial metabolites such as short-chain fatty acids and tryptophan-derived compounds, and promote the expression of tight-junction proteins, including ZO-1, occludin, claudin-1, and claudin-4, as well as mucins such as MUC1 and MUC2. These effects may be mediated through the regulation of NF-κB, NLRP3, aryl hydrocarbon receptor (AhR), mitogen-activated protein kinase (MAPK), and related signaling pathways, thereby attenuating inflammation and oxidative stress and promoting epithelial repair. Combination strategies involving probiotics and prebiotics, traditional Chinese medicine-derived components, postbiotics, fecal microbiota transplantation, or novel delivery systems may improve microbial engraftment, enhance colon-targeted delivery, and strengthen microbiota remodeling and barrier repair. Nevertheless, the available evidence remains limited by substantial strain specificity, insufficient clinical validation, and the absence of standardized intervention protocols. Further multi-omics studies and well-designed clinical trials are warranted to clarify the efficacy, mechanisms, optimal dosing, and safety of these interventions in UC.