文献类型：期刊文献

英文题名：Microplastics, Gut Dysbiosis, and Inflammatory Pathways in Ulcerative Colitis

作者：Chen, Yalong[1,2];Tian, Xudong[2]

第一作者：Chen, Yalong;陈月玲;陈亚兰

通信作者：Tian, XD[1]

机构：[1]Gansu Univ Tradit Chinese Med, Coll Integrated Tradit Chinese & Western Med, Lanzhou, Gansu, Peoples R China;[2]Gansu Prov Hosp Tradit Chinese Med, Gastrospleen Dis Diag & Treatment Ctr, 418 Guazhou Rd, Lanzhou 730050, Peoples R China

第一机构：甘肃中医药大学中西医结合学院

通信机构：[1]corresponding author), Gansu Prov Hosp Tradit Chinese Med, Gastrospleen Dis Diag & Treatment Ctr, 418 Guazhou Rd, Lanzhou 730050, Peoples R China.

年份：2026

卷号：19

外文期刊名：JOURNAL OF INFLAMMATION RESEARCH

收录：;Scopus(收录号：2-s2.0-105044212984);WOS:【SCI-EXPANDED(收录号:WOS:001826696500001)】；

基金：This work was supported by the National Natural Science Foundation of China (82560887), the Major Project of Gansu Provincial Joint Research Fund (24JRRA897), the Gansu Provincial Science and Technology Plan Funding-Youth Science and Technology Fund Project (23JRRA1728). The authors gratefully acknowledge the sponsorship of these funds.

语种：英文

外文关键词：gut microbiota; immunity; inflammatory; microplastics; ulcerative colitis

摘要：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-kappa B 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.