维持肠道黏膜屏障功能是临床防治危重疾病的重要措施。我们前期研究发现岩藻糖可以改善肠黏膜屏障功能，但其机制尚不清楚。已有的基础证实调节肠上皮细胞自噬水平可以修复肠黏膜屏障，因此对肠上皮细胞自噬水平的调控可能是维持黏膜屏障功能的关键手段。本课题以肠道黏膜屏障为切入点，以岩藻糖为干预手段，拟构建特异性敲除肠上皮细胞FUT2基因小鼠以及I型干扰素受体IFN-a/βR小鼠模型，通过岩藻糖-PI3K/AKT/mTOR直接途径以及岩藻糖-干扰素-PI3K/AKT/mTOR间接途径探讨岩藻糖与肠上皮细胞自噬水平的关系，这对深入了解肠道黏膜屏障功能的调控，为肠道炎性疾病及其它危重症的治疗提供新思路。

Increasing intestinal mucosa barrier function plays a key role in the prevention and treatment of severe illness. Our results demonstrated that fucose could improve the function of intestinal mucosal barrier, but its mechanism is not clear. Further study showed that intestinal mucosal barrier could be repaired by regulating the autophagy level of intestinal epithelial cells. Therefore, regulation of autophagy level of intestinal epithelial cells may be a key target to maintain the function of mucosal barrier. Our study takes the intestinal mucosa barrier function as a target, using fucose for tool to discuss the effect and mechanism between fucose and autophagy. By building a specific knock out of intestinal epithelial cells FUT2 genes and type I interferon receptor IFN - a/β mouse model in mice, we will discuss the relationship bwtween the fucose and intestinal epithelial cell autophagy level through the fucose-PI3K/AKT/mTOR direct pathway and fucose-interferon-PI3K/AKT/mTOR indirect way. A better understanding of intestinal mucosa barrier function would potentially provide important insights into pathogenesis and may generate new therapeutic approaches.