Modulation of autophagy by Helicobacter pylori and its role in gastric carcinogenesis

• Helicobacter pylori infection is strongly associated with gastric cancer.
• H. pylori can manipulate the autophagy pathway of its host through the VacA virulence factor.
• Altered autophagy can influence intracellular survival and persistence of H. pylori.
• H. pylori-disrupted autophagy may promote an environment favoring gastric carcinogenesis.

Helicobacter pylori infection represents the strongest known risk factor for the development of gastric cancer. The vacuolating cytotoxin (VacA) plays a key role in disease pathogenesis by exerting pleiotrophic effects on the host. One effect of acute VacA exposure is the induction of autophagy. However, prolonged exposure to the toxin disrupts autophagy by preventing maturation of the autolysosome. Novel insights into the mechanism and consequences of this phenomenon have emerged, but many aspects remain largely unknown. Current evidence supports a scenario in which H. pylori-suppressed autophagy facilitates intracellular survival and persistence of the pathogen, while also generating an environment favoring carcinogenesis.