Peroxiredoxin I protects gastric mucosa from oxidative injury induced by H. pylori infection

Abstract

Background and aim: Helicobacter pylori (H. pylori) infection enhances the production of reactive oxygen species and peroxynitrite, thereby resulting in oxidative tissue damage. In this study, we examined the role of peroxiredoxin I (Prx I), a stress-induced antioxidant enzyme, in protecting gastric mucosa from H. pylori-induced gastric mucosal injury.

Methods: Wild type (Prx I(+/+)) and Prx I-deficient type (Prx I(-/-)) mice were maintained for 2 to 12 months with or without infection of H. pylori, Sydney strain-1. Gastric mucosal expression of Prx I was assessed by immunoblot analysis and immunohistochemistry. The degree of gastritis was evaluated by the updated Sydney system and by mucosal levels of inflammatory cytokines (MIP-2, IL-1beta, and TNF-alpha). Oxidative DNA injury and apoptosis were analyzed by mucosal level of 8-hydroxy-2'-deoxyguanosine, and the number of apoptotic cells stained with a single-stranded DNA antibody, respectively.

Results: H. pylori infection upregulated gastric mucosal Prx I expression in the Prx I(+/+) but not the Prx I(-/-) mice. H. pylori infection also induced more severe gastritis and a more prominent increase in MIP level, more marked oxidative DNA injury, and apoptosis in the Prx I(-/-) than the Prx I(+/+) mice. In the absence of H. pylori infection, no changes were demonstrated in gastric mucosa in either the Prx I(+/+) or the Prx I(-/-) mice.

Conclusion: These data suggest that H. pylori infection upregulates gastric mucosal Prx I expression, and further, that Prx I plays an important role in gastric mucosal protection against oxidative injury induced by H. pylori infection.