Functional analysis of H. pylorivirulence factors for gastric disease induction through its endocytosis inhibition

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Helicobacter pylori is a common pathogen that causes chronic gastritis and gastric cancer. Epidemiologic evidence suggests that H. pylori with both highly active vacuolating cytotoxin A (VacA) and cytotoxin-associated gene A (CagA), the major virulence factors, have an advantage in adapting to the host environment. However, the mechanistic relationship between VacA and CagA remains obscure. We report that CagA suppresses pinocytic endocytosis and the cytotoxicity of VacA in gastric epithelial cells. Our data suggest that H. pylori secretes VacA to attack distant host cells while injecting CagA into the gastric epithelial cells to which the bacteria are directly attached, thereby protecting these attached host cells from the cytotoxicity of VacA and creating a local ecological niche. This mechanism may allow H. pylorito balance damage to one population of host cells with the preservation of another, allowing for persistent infection.