肠道共生菌与固有淋巴细胞ILC3间的相互作用不仅影响溃疡性结肠炎(UC)的发生发展，还在UC黏膜愈合中发挥重要作用。树突状细胞(DC)分泌的视黄酸(RA)是肠道共生菌调控ILC3/IL-22通路的重要分子，但共生菌是否依赖RA促进黏膜修复仍未阐明。前期我们发现Akkermansia muciniphila(A. muciniphila)促进小鼠实验性肠炎黏膜修复，且上调肠道ILC3比例和DC中RA关键酶RALDH2表达。我们推测A. muciniphila通过上调DC中RA表达，进而激活ILC3/IL-22通路，介导肠上皮增殖修复，最终促进UC肠黏膜愈合。本项目拟构建小鼠肠炎模型，结合临床样本、转基因动物和体外实验，深入探讨共生菌与免疫细胞间互作进而影响肠黏膜愈合的调控模式和作用机制。本项目将为共生菌促进UC黏膜愈合提供新理论依据及A. muciniphila防治UC的临床应用奠定基础。

The interaction between intestinal commensal bacteria and type 3 innate lymphoid cells (ILC3s) determines the progression of ulcerative colitis (UC) and plays an important role in mucosal healing. Retinoic acid (RA) secreted by dendritic cells holds an important position in ILC3/IL-22 axis meditated by the gut commensals. However, whether there is any relationship between the therapitic effect of gut commensals and beneficial effect of RA remains unclear. In our previous research, we found that Akkermansia muciniphila (A. muciniphila) can promote the mucosal healing in mouse colitis model induced by DSS and increase intestinal ILC3 percentage and RALDH2 expression in lamina propria dendritic cells, which is a key synthase of RA. We hypothesized that A. muciniphila may exert its therapeutic function by upregulating the expression of RA in dendritic cells, which contributes to the proliferation and healing of gut mucosa by up-regulating ILC3/IL-22 axis. In this project, we plan to construct the mouse model of UC combined with clinical samples, transgenic animals and in vitro experiments, to unveil the regulation pattern and mechanism by which the process of intestinal mucosal healing is affected by the interaction between symbiotic bacteria and intestinal immune cells. This research will provide a fresh theoretical basis for symbiotic bacteria-mediated UC mucosal healing, and prepare for the clinical application of A. muciniphila in the treatment of UC.