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Am J Physiol Gastrointest Liver Physiol 279: G791-G798, 2000;
0193-1857/00 $5.00
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Vol. 279, Issue 4, G791-G798, October 2000

Role of cyclooxygenase-2 in Helicobacter pylori- induced gastritis in Mongolian gerbils

Satoru Takahashi1,2, Takuya Fujita2, and Akira Yamamoto2

Departments of 1 Applied Pharmacology and 2 Biopharmaceutics, Kyoto Pharmaceutical University, Kyoto 607-8414, Japan

Cyclooxygenase (COX)-2 expression is induced in the gastric mucosa of Helicobacter pylori-infected patients, but its role remains unclear. We examined the effects of NS-398 and indomethacin on gastric pathology in H. pylori-infected Mongolian gerbils. COX-1 was detected in both normal and H. pylori-infected mucosa, whereas COX-2 was expressed only in the infected mucosa. PGE2 production was elevated by H. pylori infection, and the increased production was reduced by NS-398, which did not affect PGE2 production in normal mucosa. Indomethacin inhibited PGE2 production in both normal and infected mucosa. Hemorrhagic erosions, neutrophil infiltration, lymphoid follicles, and epithelium damage were induced by H. pylori infection. NS-398 and indomethacin aggravated these pathological changes but did not increase viable H. pylori number. H. pylori-increased production of neutrophil chemokine and interferon-gamma was potentiated by NS-398 and indomethacin. Neither NS-398 nor indomethacin caused any pathological changes or cytokine production in normal animals. These results indicate that COX-2 as well as COX-1 might play anti-inflammatory roles in H. pylori-induced gastritis.

prostaglandin; nonsteroidal anti-inflammatory drug; infection


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