Regulation of β1-integrin in autophagy and apoptosis of gastric epithelial cells infected with Helicobacter pylori

Helicobacter pylori infection is an essential factor in the development of human gastric diseases, but its pathogenic mechanism is still unclear. In this work we have showed that, the LC3II levels were increased and beta 1-integrin levels were decreased in H. pylori-positive human gastric tissue samples and H. pylori co-cultured GES-1 cells. There was significant upregulation of LC3II levels and downregulation of P62 levels in GES-1 cells after beta 1-integrin knockdown co-cultured with H. pylori. This indicated that beta 1-integrin downregulation promoted autophagy in GES-1 cells after H. pylori infection. The cell apoptosis rate and poly ADP-ribose polymerase (PARP) and caspase-3 activities were increased in GES-1 cells pretreated with 3-methyladenine (3-MA ) after H. pylori infection. Furthermore, there was a significant decrease in apoptosis of beta 1-integrin knockdown GES-1 cells co-cultured with H. pylori; apoptosis was also downregulated in beta 1-integrin knockdown- and 3-MA-treated GES-1 cells co-cultured with H. pylori. Correspondingly, PARP and caspase-3 activities were decreased in beta 1-integrin knockdown cells co-cultured with H. pylori and beta 1-integrin knockdown-3-MA-treated-1 cells with H. pylori infection. Thus, beta 1-integrin is a novel autophagy and apoptosis regulator during H. pylori infection. However, inhibition of autophagy did not reverse the decrease in apoptosis caused by downregulation of beta 1-integrin.