Helicobacter pylori dysregulates the expression of autophagy-related genes in human gastric adenocarcinoma cell line in vitro

Marzieh  Esmaeilzadeh; Farshid  Kafilzadeh; Mohammad  Kargar; Hamid Asadzadeh  Aghdaei; Abbas  Yadegar

doi:10.18502/ijm.v17i5.19879

Marzieh Esmaeilzadeh Department of Microbiology, Jahrom Branch, Islamic Azad University, Jahrom, Iran
Farshid Kafilzadeh Department of Microbiology, Jahrom Branch, Islamic Azad University, Jahrom, Iran
Mohammad Kargar Department of Microbiology, Zand Institute of Higher Education, Shiraz, Iran
Hamid Asadzadeh Aghdaei Basic and Molecular Epidemiology of Gastrointestinal Disorders Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Abbas Yadegar Foodborne and Waterborne Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran

DOI: https://doi.org/10.18502/ijm.v17i5.19879

Keywords: Autophagy; Helicobacter pylori; Interleukin-8; Peptic ulcer; Gene expression

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 overexpres- sion was more pronounced in PUD than CG strains. On the contrary, beclin-1 gene was downregulated in all H. pylori-in- fected 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.