岩藻糖通过FUT2抑制肠道巨噬细胞焦亡在肠道炎症中的作用

维持肠道黏膜免疫稳态是临床治疗溃疡性结肠炎的重要措施。我们前期研究发现岩藻糖可以改善肠黏膜免疫失调，但机制尚不清楚。已有的基础证实调控肠道黏膜巨噬细胞焦亡水平可以维持肠黏膜免疫稳态，因此对结肠巨噬细胞焦亡水平的调控可能是维持肠道免疫稳态的关键手段。本课题以肠道免疫失衡为切入点，以岩藻糖为干预手段，拟构建特异性敲除肠巨噬细胞FUT2基因小鼠敲除小鼠，通过岩藻糖-FUT2-经典与非经典炎症小体通路抑制探讨岩藻糖与肠道巨噬细胞焦亡的关系，这对深入了解肠道免疫功能的调控，为溃疡性结肠炎的治疗提供理论依据。

Maintaining intestinal mucosal immune homeostasis plays a key role in the treatment of ulcerative colitis. Our results demonstrated that L-fucose can improve intestinal mucosal immune disorders, but the mechanism is still unclear.Previous studies has proved that mucosal immune homeostasis can be maintained by the regulation of macrophage pyroptosis. Therefore, regulation of macrophage pyroptosis in colon may be a key target to maintain intestinal immune homeostasis. Our study takes the intestinal immune function as a target, using L-fucose for tool to discuss the effect and mechanism between L-fucose and pyroptosis. By building a specific knock out of macrophages FUT2 genes in mice, we will discuss the relationship between the L-fucose and macrophage pyroptosis through the fucose-FUT2-canonical and non-canonical inflammasome pathway inhibition. A better understanding of the intestinal immune function would potentially provide theoretical basis for the treatment of ulcerative colitis.