Abstract
BACKGROUND AND OBJECTIVES: Studies have indicated that Helicobacter pylori (H. pylori) infection could correlate with autophagy dysregulation. This research was undertaken to investigate whether H. pylori can dysregulate the expression of genes related to autophagy in human gastric adenocarcinoma (AGS) cells. MATERIALS AND METHODS: Ten H. pylori clinical isolates recovered from peptic ulcer disease (PUD) and chronic gastritis (CG) patients were used for cell infection assays. AGS cells infected with H. pylori strains at a multiplicity of infection (MOI) of 100 were incubated at 37°C for 12 h. The expression of autophagy-related genes (atg5, atg12, atg16L1, LC3B, and beclin-1) was determined in AGS cells by RT-qPCR. ELISA was applied to measure IL-8 production. RESULTS: The gene expression of atg5, atg12, atg16L1, LC3B was upregulated by both CG and PUD strains. The overexpression was more pronounced in PUD than CG strains. On the contrary, beclin-1 gene was downregulated in all H. pylori-infected AGS cells. In addition, H. pylori strains could significantly produce IL-8 in AGS cells. CONCLUSION: Our in vitro study demonstrates that H. pylori could alter the expression of autophagy-related genes. Further investigation could precisely uncover the mechanism whereby H. pylori dysregulates host autophagy.