幽门螺杆菌感染重塑胃黏膜细胞间的通讯，阐明其诱发胃上皮病变的机制具有重要意义。前期研究发现，高致病性幽门螺杆菌(CagA+H.pylori)感染胃上皮细胞后抑制线粒体自噬，促进线粒体蛋白HSPD1经外泌体释放，而外泌体HSPD1可能通过增强氧化磷酸化促进巨噬细胞向M2型分化。因此，我们推断:CagA+H.pylori感染胃上皮细胞并抑制胃上皮线粒体自噬，造成线粒体蛋白HSPD1经由外泌体释放；外泌体HSPD1蛋白通过促进巨噬细胞自（旁）分泌IL-10抑制mTOR途径促进巨噬细胞氧化磷酸化，促进M2分化及抑制性免疫微环境，最终促进慢性胃炎进展。本项目拟从细胞、动物及临床标本，多角度聚焦于外泌体HSPD1蛋白调控巨噬细胞氧化磷酸化及M2定向分化的具体机制，找寻CagA+H.pylori感染导致慢性胃炎进展的潜在治疗靶点，为预防幽门螺杆菌感染所致慢性胃炎及胃癌奠定基础。

Helicobacter pylori (H.pylori) infection reshapes the communication between gastric mucosal cells, and it is of great significance to illustrate its mechanism of inducing gastric epithelial lesions. Pre-experiments have found that highly pathogenic CagA+H.pylori inhibits mitochondrial autophagy, and promotes the release of mitochondrial protein HSPD1 via exosomes in CagA+H.pylori infected gastric epithelial cells. While exosomal HSPD1 may promote the differentiation of macrophages to M2 type through oxidative phosphorylation pathway. Therefore, we conclude that CagA+H.pylori infects gastric epithelial cells and inhibits gastric epithelial mitochondrial autophagy, resulting in the release of mitochondrial protein HSPD1 via exosomes. Exosomal HSPD1 protein promotes M2 differentiation, suppresses the immune microenvironment and facilitates chronic gastritis by promoting macrophages to secrete IL-10 and inhibit the mTOR pathway and by promoting oxidative phosphorylation of macrophages. This project intends to focus on the specific mechanism of exosomal HSPD1 protein regulating the oxidative phosphorylation and M2 type directional differentiation of macrophages to find potential therapeutic targets for chronic gastritis progression caused by CagA+H.pylori infection from cell, animal and clinical specimens. This project will lay the foundation for the prevention of chronic gastritis and gastric cancer caused by H.pylori infection.