新近研究表明，具核梭杆菌(Fn)与炎症性肠病（IBD）、结直肠癌的发生密切相关；自噬作为机体自我保护机制，在IBD的发生发展中起重要作用。我们前期研究发现：Fn感染引起的炎症反应中，宿主细胞miRNA表达谱失衡，let-7f表达上调，自噬体不能成熟为自噬溶酶体，但具体机制不清楚。生物信息学分析显示：Atg16L1作为自噬发生的关键信号分子，可作为let-7f的靶蛋白。因此，我们推测：Fn感染可能通过诱导let-7f表达，抑制Atg16L1，从而阻碍自噬体向自噬溶酶体成熟，减弱了自噬对该菌的清除，导致该菌持续感染和IBD的发生。本项目拟在Fn感染的细胞和动物模型上，检测具核梭杆菌感染引起的肠上皮细胞自噬的变化以及炎症情况，研究let-7f在Fn诱导的肠上皮细胞自噬调节与持续性感染发生的作用机制，为寻找IBD新的有效的治疗手段提供线索和理论依据。

In recent years,the researches of “Fusobacterium nucleatum (Fn),inflammatory bowel disease (IBD) and colorectal cancer” are of great concern. Autophagy, which acts as a highly conservative mechanism of self-protection, plays crucial roles in the development of IBD. The infection of F. nucleatum in intestinal epithelial cells can inhibit the autophagy, leading to inflammatory bowel disease (IBD). Our previous study showed that miRNA expression was disrupted in the inflammatory response by the Fn infection, and the expression of let-7f was up-regulation, which could inhibit autophagy. However, the exact mechanism is unclear. The analysis of bioinformatics indicated that Atg16L1, which plays the key role in autophagy pathway, is the target protein of let-7f. Therefore, we hypothesize: F. nucleatum infection induces the expression of let-7f, which inhibits Atg16L1, leading to persistent infection of bacteria and the occurrence of IBD. In thisstudy, through over-expression and down-expression of let-7f in intestinal epithelial cells induced by F. nucleatum, we intend to clarify the mechanism of autophagy inhibited by F. nucleatum, and provide theoretical guidance for the treatment of F. nucleatum infection.