Endoplasmic reticulum stress is involved in H. Pylori associated gastritis

幽门螺杆菌空泡毒素(VacA)诱导的胃上皮细胞凋亡在Hp诱导的胃上皮细胞凋亡中起重要作用。然而，VacA细胞凋亡的确切机制尚不清楚。我们的目的是检测内质网应激和促凋亡的BH3蛋白在人幽门螺杆菌感染和VacA处理的细胞中的参与。幽门螺杆菌感染的胃粘膜组织中Gadd34和GRP78mRNA表达显著增加。免疫组织化学显示CRP78在胃上皮细胞中表达。AZ521经VacA处理后，细胞凋亡诱导ER应激标记物CHOP显著升高，并参与细胞凋亡。据我们所知，本研究是最早将内质网应激与人幽门螺杆菌感染及其凋亡诱导毒素VacA联系起来的研究之一。

Apoptosis by H. pylori vactuolating cytotoxin(VacA) plays a role in H. Pylori induced apoptosis in gastric epitherial cells. However, precise mechanism of VacA apoptosis is not understood. Our aim was to examine involvement of ER stress and pro-apoptotic BH3 only proteins in human H. Pylori infection and in VacA treated cells. GADD34 mRNA and GRP 78 mRNA were significantly increased in H. Pylori infected gastric mucosa. Immunohistochemistry showed CRP78 staining in gastric epitherial cells. Apoptosis inducing ER stress marker CHOP was significantly elevated in AZ521 treated with VacA, and was contributing to apoptosis. The present study is, to our knowledge, among the first to implicate the association of ER stress with human H. Pylori infection and its apoptosis inducing toxin, VacA.