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Am J Physiol Gastrointest Liver Physiol 286: G148-G156, 2004. First published September 4, 2003; doi:10.1152/ajpgi.00137.2003
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INFLAMMATION/IMMUNITY/MEDIATORS

Anti-inflammatory effect of two isoforms of COX in H. pylori-induced gastritis in mice: possible involvement of PGE2

Tetsuya Tanigawa, Toshio Watanabe, Masaki Hamaguchi, Eiji Sasaki, Kazunari Tominaga, Yasuhiro Fujiwara, Nobuhide Oshitani, Takayuki Matsumoto, Kazuhide Higuchi, and Tetsuo Arakawa

Department of Gastroenterology, Osaka City University Graduate School of Medicine, Osaka 545-8585, Japan

Submitted 24 March 2003 ; accepted in final form 28 August 2003

Neutrophil infiltration mediated by TNF-{alpha} is associated with various types of gastric injury, whereas PGs play a crucial role in gastric defense. We examined roles of two isoforms of cyclooxygenase (COX) and PGE2 in Helicobacter pylori-induced gastritis in mice. Mice infected with H. pylori were given selective COX-1 inhibitor SC-560 (10 mg/kg), selective COX-2 inhibitor NS-398 (10 mg/kg), or nonselective COX inhibitor indomethacin (2 mg/kg) with or without 16,16-dimethyl PGE2 for 1 wk. H. pylori infection increased levels of mRNA for COX-1 and -2 in gastric tissue by 1.2-fold and 3.3-fold, respectively, accompanied by a significant increase in PGE2 production by gastric tissue. H. pylori infection significantly elevated MPO activity, a marker of neutrophil infiltration, and epithelial cell apoptosis in the stomach. SC-560 augmented MPO activity and epithelial cell apoptosis with associated reduction in PGE2 production, whereas NS-398 had the same effects without affecting PGE2 production. Inhibition of both COX-1 and -2 by indomethacin or concurrent treatment with SC-560 and NS-398 resulted in a stronger increase in MPO activity and apoptosis than inhibition of either COX-1 or -2 alone. H. pylori infection elevated TNF-{alpha} mRNA expression in the stomach, which was further increased by indomethacin. Effects of COX inhibitors on neutrophil infiltration, apoptosis, and TNF-{alpha} expression in H. pylori-infected mice were abolished by exogenous 16,16-dimethyl PGE2. In conclusion, PGE2 derived from either COX-1 or -2 is involved in regulation of gastric mucosal inflammation and contributes to maintenance of mucosal integrity during H. pylori infection via inhibition of TNF-{alpha} expression.

neutrophil; tumor necrosis factor-{alpha}; gastric mucosal integrity


Address for reprint requests and other correspondence: T. Watanabe, Dept. of Gastroenterology, Osaka City Univ. Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka 545-8585, Japan (E-mail: watanabet{at}med.osaka-cu.ac.jp).




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