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


CONCLUSIONS
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.
Sato
Daisuke
D
Department of Gastroenterology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
Yanaka
Akinori
A
Shibahara
Takeshi
T
Matsui
Hirofumi
H
Nakahara
Akira
A
Yanagawa
Toru
T
Warabi
Eiji
E
Ishii
Tetsuro
T
Hyodo
Ichinosuke
I
D000818:Animals; D005753:Gastric Mucosa / Q000382:microbiology*; D016481:Helicobacter Infections / Q000378:metabolism* / Q000517:prevention & control; D016480:Helicobacter pylori; D051379:Mice; D018384:Oxidative Stress; D054464:Peroxiredoxins / Q000502:physiology*
D054464:Peroxiredoxins