Helicobacter pylori infection and oxidative stress.

Abstract

Helicobacter pylori (H. pylori) infection promotes the migration of polymorphonuclear leukocytes from the gastric mucosal microcirculation through chemokine induction, leading to the excessive production of ROS. Like eukaryotes, H. pylori possesses superoxide dismutase and catalase, and is resistant to ROS from host polymorphonuclear leukocytes. Oxidants such as monochloramine produced by ROS cause chronic inflammation in the gastric mucosa. H. pylori-derived virulence factor m1-type VacA induces intracellular ROS accumulation and autophagy, which degrades the H. pylori-derived oncoprotein, CagA. In CD44v9-positive gastric cancer stem-like cells, reduced-type glutathione levels increase within the cell because of the cystine transporter on the cell surface, wherein oxidative stress-induced autophagy no longer occurs. As a result, the oncoprotein CagA accumulates in the cells, thus becoming tumorigenic.