Helicobacter pylori (H. pylori) is one of the most important pathogenic bacteria associated with various gastrointestinal diseases. At present, its apoptotic or antiapoptotic mechanism on gastric epithelial cells remains unknown and needs further illustrated. In this study, acute infection model (H. pylori and GES-1 cells were co-cultured for 24 h at a multiplicity of infection MOI of 100:1) and chronic infection model (GES-1 cells were infected repeatedly every 24 h at a multiplicity of infection MOI of 100:1 for approximately 8 weeks) were established, respectively. the chronic H. pylori infected GES-1 cells underwent a typically morphological change and Western Blot results showed that there was slight decrease in expression of E-cadherin, and obvious increase in expression of Vimentin. Apoptosis of these two models were analyzed by flow cytometry compared with the control cells, meanwhile, apoptosis associated markers (Bcl-xL, Bcl-2, Bax, etc) were detected by Western blot, additional in clinical H. pylori-positive gastric cancer tissues. Results showed that compared with the control cells, acute infection of H. pylori significantly accelerated the apoptosis of GES-1, increased the expression of Bax and Cleaved caspase-3, down-regulated expression of Bcl-xL and Bcl-2. Moreover, an opposite result was found in chronic infection of model and clinical gastric cancer tissues, and enhanced expression of NF–κB p65. Taken together, these findings suggest that H. pylori infection plays differential effects on apoptosis of gastric epithelial cells.

幽门螺杆菌（H. pylori）是与各种胃肠道疾病相关的最重要的致病菌之一。目前，其对胃上皮细胞的凋亡或抗凋亡机制仍然未知，需要进一步说明。在这项研究中，急性感染模型（幽门螺杆菌和GES-1细胞在感染复数MOI为100：1的条件下共培养24小时）和慢性感染模型（GES-1细胞在24h时每24 h重复感染一次）分别建立了大约8周的100：1的感染复数MOI）。慢性幽门螺杆菌被感染的GES-1细胞通常发生形态学改变，Western Blot结果显示，E-钙粘蛋白的表达略有下降，而波形蛋白的表达则明显增加。通过流式细胞术与对照细胞比较，分析了这两种模型的凋亡，同时，通过蛋白质印迹法检测了凋亡相关标志物（Bcl-xL，Bcl-2，Bax等），另外在临床幽门螺杆菌阳性胃癌中组织。结果表明，与对照细胞相比，幽门螺杆菌的急性感染显着促进GES-1的凋亡，增加Bax和Cleaved caspase-3的表达，下调Bcl-xL和Bcl-2的表达。此外，在模型和临床胃癌组织的慢性感染中发现相反的结果，并且NF-κBp65的表达增强。综上所述，这些发现表明幽门螺杆菌感染对胃上皮细胞凋亡具有不同的作用。