Microplastics, Gut Dysbiosis, and Inflammatory Pathways in Ulcerative Colitis

Microplastics (MPs) are pervasive environmental pollutants characterized by their widespread distribution. They can enter the human body through multiple routes, including inhalation and dietary intake, accumulate in the gastrointestinal tract, and subsequently disrupt intestinal microecological homeostasis, thereby contributing to digestive diseases. Ulcerative colitis (UC), a chronic inflammatory bowel disease of unclear etiology, has been closely associated with gut microbiota dysbiosis, which is considered one of its central pathogenic mechanisms. This review comprehensively review the fundamental characteristics of MPs and their interactions with the gut microbiota and microbial metabolites. It further elucidates the key mechanisms by which MPs mediate the initiation and progression of UC, with particular emphasis on intestinal mucosal barrier dysfunction and immune dysregulation. Mechanistically, MPs disrupt SCFAs-producing microbial networks and activate epithelial inflammatory pathways, particularly TLR4-NF-κB signaling, thereby amplifying mucosal inflammation in UC. This review is the first to completely connect the regulatory axis of MPs - gut microbiota - metabolites - intestinal barrier - immune inflammation, clarify the core pathological chain of UC induced by MPs, make up for the shortcomings of existing reviews that only conduct single-dimensional analysis and lack integration of complete mechanisms, and provide a new theoretical framework for this field. Additionally, current research limitations are discussed, and future research directions and potential intervention strategies are proposed, aiming to provide novel theoretical insights into the etiology and prevention of UC.