肠成纤维细胞与肠上皮细胞（IEC）间的对话可能在肠粘膜屏障功能调节中起重要作用，但对其调控机制尚缺乏深入了解。肠成纤维细胞来源的EGF可明显促进IEC的增殖、分化，促进肠粘膜屏障功能，我们推测IEC来源的内源性抗菌肽LL-37则可能通过其受体P2X7途径调节肠成纤维细胞表达EGF。因此，本研究拟通过体外肠成纤维细胞-IEC共培养模型及肠粘膜功能损伤动物模型，利用RNA干扰等技术，观察LL-37是否是通过激活P2X7促进肠成纤维细胞中EGF的表达，验证LL-37-EGF通路的存在，并进一步评价LL-37-EGF通路在生理及病理条件下对维持肠粘膜屏障功能的重要意义，为阐明肠成纤维细胞在维持肠粘膜屏障功能中的重要作用提供理论依据，为肠粘膜屏障功能障碍防治研究提供新思路。

The crosstalk between the intestinal fibroblasts and intestinal epithelial cells (IEC) plays an important role in the regulation of intestinal epithelial barrier. However, the mechanism is still unclear. Intestinal fibroblasts derived EGF can stimulate proliferation and differentiation of IEC, meanwhile maintain the intestinal barrier. We hypothesize that endogenous antimicrobial peptide LL-37，which derived from IEC, may activate the receptor P2X7 to stimulate EGF expression derived from intestinal fibroblasts. Fibroblast-IEC co-cultured model and mouse mucosal injury model will be established, RNA interference will be used to investigate if LL-37 via P2X7 activation to stimulate the expression of EGF in intestinal fibroblasts. furthermore to investigate the role of LL-37-EGF pathway in the maintenance of intestinal epithelial barrier function under physiological and pathological conditions, then provide a theoretical basis to clarify the important role of the intestinal fibroblast cells in the maintenance of the intestinal mucosal barrier function and provide new ideas for the research of prevention and treatment about intestinal mucosal barrier dysfunction.