关键词: 旋毛虫副肌球蛋白, 免疫机制, 慢性结肠炎, CD103⁺耐受性树突状细胞

Abstract: Objective  This investigation seeks to discern the effect of Trichinella spiralis paramyosin (TsPmy) in modulating chronic colitis. Methods  We commenced with the preparation of TsPmy, followed by the induction of chronic colitis in Rag1 KO mice via naïve T cells. The subjects Rag1 KO mice were systematically allocated into three groups by random number table: a treatment group receiving CD4⁺Foxp3^－CD45RB^hi T cells with TsPmy, a control group receiving CD4⁺Foxp3^－CD45RB^hi T cells with PBS, and a baseline group consisting of untreated Rag1 KO mice. Mice diagnosed with chronic colitis received intraperitoneal TsPmy injections. Subsequent evaluations included assessments of clinical manifestations, colon shortening, and histological examination of colonic inflammation using hematoxylin-eosin (HE) staining. Flow cytometry facilitated the quantitative analysis of T helper 1 cell （Th1） and T helper 17 cell (Th17) cell populations in the colonic lamina propria, alongside the enumeration of gut-specific CD103⁺ regulatory dendritic cells (DCs). Results  Administering TsPmy conferred a significant attenuation of the weight loss, disease activity index, and pathological damage of colon tissue in mice. Key findings included a marked decrement in the proportions of pro-inflammatory Th1 and Th17 cells and an enhanced presence of immunomodulatory CD103⁺DCs within the colonic lamina propria. Conclusions  TsPmy has a mitigating influence on chronic colitis in murine models through the expansion of CD103⁺ DCs and the concurrent reduction of Th1 and Th17 cell populations. These insights pave the way for further investigation into helminth-derived paramyosins as a novel therapeutic strategy for chronic colitis.

Key words: Trichinella spiralis paramyosin (TsPmy), immune mechanism, chronic colitis, CD103⁺ tolerogenic dendritic cells