Role of autophagy associated with Helicobacter pylori CagA and VacA toxins in gastric cancer

Helicobacter pylori (H. pylori) is a gram-negative microaerophilic bacterium that has been introduced as a cause of mucosal inflammation and gastric cancer. The most important pathogenic factors are VacA and CagA, which are associated with increased disease severity in clinical strains. Autophagy is a protected lysosomal degradation pathway degrading cytoplasmic content and is important in host cell defense, survival, differentiation and development. It can have a tumor suppressor activity or cancer progression and plays an important role in host safety and homeostatic. H. pylori can affect host pathogenic pathway through VacA and CagA virulence factors and carcinogenesis. Increasing autophagy in tumor cells prevents the accumulation of non-functional mitochondria that can disrupt tumorigenicity. The ability of H. pylori to manipulate host pathogenesis pathway is considered as one of the important aspects of its pathogenesis. Several studies have shown that infection with H. pylori causes autophagy in both gastric epithelial cells and phagocytes. In the epithelial cells of the stomach, VacA is a necessary factor in autophagy. While CagA is a negative regulator of the phenomenon, the elimination of this gene from H. pylori has increased autophagy and the production of inflammatory cytokines is reduced.