Helicobacter pylori: a ROS-inducing bacterial species in the stomach

被引：165

作者：

Handa, Osamu ^{[1
]}

Naito, Yuji ^{[1
]}

Yoshikawa, Toshikazu ^{[1
]}

机构：

[1] Kyoto Prefectural Univ Med, Dept Mol Gastroenterol & Hepatol, Kamigyo Ku, Kyoto 6028566, Japan

来源：

INFLAMMATION RESEARCH | 2010年 / 59卷 / 12期

基金：

日本学术振兴会; 日本科学技术振兴机构;

关键词：

Oxidative stress; Leucocytes; Infection; NO; NITRIC-OXIDE SYNTHASE; NEUTROPHIL CHEMOATTRACTANT-1 CINC-1; NECROSIS-FACTOR-ALPHA; GASTRIC-CANCER; MONGOLIAN GERBILS; REACTIVE OXYGEN; ANTIOXIDANT PROPERTIES; COCCOID FORM; IN-VITRO; CELLS;

D O I：

10.1007/s00011-010-0245-x

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) have been reported to impact gastric inflammation and carcinogenesis. However, the precise mechanism by which Helicobacter pylori induces gastric carcinogenesis is presently unclear. This review focuses on H. pylori-induced ROS/RNS production in the host stomach, and its relationship with gastric carcinogenesis. Activated neutrophils are the main source of ROS/RNS production in the H. pylori-infected stomach, but H. pylori itself also produces ROS. In addition, extensive recent studies have revealed that H. pylori-induced ROS production in gastric epithelial cells might affect gastric epithelial cell signal transduction, resulting in gastric carcinogenesis. Excessive ROS/RNS production in the stomach can damage DNA in gastric epithelial cells, implying its involvement in gastric carcinogenesis. Understanding the molecular mechanism behind H. pylori-induced ROS, and its involvement in gastric carcinogenesis, is important for developing new strategies for gastric cancer chemoprevention.

引用

页码：997 / 1003

页数：7

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