NF-KB and Bcl-2 in Helicobacter pylori induced apoptosis in gastric epithelial cells

Helicobacter pylori (H. pylori) has been considered as an important pathogen. of gastroduodenal inflammation and gastric carcinogenesis. However,the pathogenic mechanisms including H. pylori-induced apoptosis and subsequent molecular mechanisms have not been clarified yet. The present study examined the role of Bcl-2 and its relation to NF-kappaB in H. pylori-induced apoptosis in human gastric epithelial AGS cells. AGS cells were cultured in the presence of H. pylori, at a bacterium/cell ratio of 300:1, for the determination of apoptosis, NF-kappaB activation with IkappaBalpha degradation, and Bcl-2 level. AGS cells were transfected with a control vector (pCMV cells) or a full-length human Bcl-2 expression vector (Bcl-2 cells). H. pylori-induced apoptosis and NFkappaB activation were compared in the wild-type cells and the transfected cells. As a result, H. pylori increased apoptotic cells with chromatin condensation and reduced Bcl-2 levels, which were accompanied with NF-kappaB activation. H. pylori induced sixfold increase in the number of apoptotic cells in wild-type cells and pCMV cells. H. pylori-induced increment of apoptotic cells were relatively lower in Bcl-2 cells than pCMV cells. H. pylori-induced NF-kappaB activation and IkappaBalpha degradation were not different in the wild-type cells, pCMV cells, and Bcl-2 cells. In conclusion, the reduced gastric Bcl-2 level may be the main pathogenic mechanism of H. pylori-induced apoptosis in gastric epithelial cells.