幽门螺杆菌（H.pylori）感染引起的炎性微环境在胃癌的发生发展中有重要作用，而肿瘤相关成纤维细胞(CAFs)构成了肿瘤微环境中主要的细胞群体。前期研究发现H.pylori能主动黏附CAFs，而CAFs能促进胃癌细胞的克隆性生长，用H.pylori诱导的胃癌沙鼠模型伴有进行性大量淋巴细胞的侵润。因此，我们推测H.pylori感染引起的炎性反应，通过直接和间接方式活化成纤维细胞为CAFs， 活化的CAFs分泌各种因子，募集淋巴细胞建立炎性微环境，与上皮细胞相互作用，促进胃癌细胞的发生、生长、侵袭和转移。本项目用三维培养和Transwell小室，构建CAFs与胃癌细胞直接和间接的互作模型，用H.pylori感染，在体内、体外研究炎性环境下CAFs的活化、募集淋巴细胞的机制、CAFs与胃癌细胞的互作、以及促进胃癌细胞生长和转移的分子机制，从炎性微环境的角度揭示H.pylori引起胃癌的分子机制

Inflammatory microenvironment induced by Helicobacter pylori (H.pylori) plays an important role in the development and progression of gastric cancer. Cancer-associated fibroblasts (CAFs) constitute the major cell population in tumor microenvironment. We found that H.pylori can actively adhere to CAFs, and CAFs can promote the clonal growth of gastric cancer cells. The gerbil model of gastric cancer induced by H.pylori is accompanied by a lot of lymphocyte infiltration. Therefore, we speculate that the inflammatory response to H.pylori can directly and indirectly activate fibroblasts to CAFs. The activated CAFs secret many kinds of factors to establish inflammatory microenvironment by the recruitment of lymphocytes. CAFs interacts with epithelial cells to promote the occurrence, growth, invasion and metastasis of gastric cancer cells. In this study, the direct and indirect interaction between CAFs and gastric cancer cells is constructed by three-dimensional cell culture and Transwell. H.pylori is used to infect the both cells to study, in vivo and in vitro, the activation of CAFs, the mechanism of lymphocyte recruitment, the interaction between CAFs and gastric cancer cells and the molecular mechanism of gastric cancer cell growth and metastasis in inflammatory environment. This study will reveal the molecular mechanism of inflammatory microenvironment in gastric cancer induced by H.pylori.