Background: It is still a point of controversy whether Helicobacter pylori-infected patients are more likely to develop mucosal damage while taking NSAIDs. Selective cyclooxygenase (COX-2) inhibitors may be associated with less severe gastric mucosal damage than conventional NSAIDs, but this association is undefined in H. pylori-induced gastritis. The aim of this study was to evaluate the effects of selective COX-2 and nonselective NSAIDs on H. pylori-induced gastritis.
Methods: After intragastric administration of indomethacin, NS-398 or vehicle alone, once daily for 5 days in H. pylori-infected and uninfected Mongolian gerbils, we evaluated gastric mucosal damage, inflammatory cell infiltration and prostaglandin E2 (PGE2) concentration. We investigated whether H. pylori infection induced the COX-2 expression.
Results: In H. pylori-uninfected groups, the indomethacin-treated group showed the highest mucosal damage score and the lowest PGE2 concentration. There was no difference in mucosal damage scores and PGE2 concentration between NS-398 and vehicle-alone treated group. In H. pylori-infected groups, there was no difference in mucosal damage scores, irrespective of the type of drugs administered. The indomethacin-treated group showed the lowest PGE2 concentration, similar to that of the NS-398 and vehicle-alone treated groups, both without H. pylori infection. Gastric neutrophil and monocyte infiltration scores were higher in H. pylori-infected groups than in uninfected groups. However, there was no difference in these scores according to the type of drugs administered, within H. pylori-infected or uninfected groups. COX-2 protein expression was observed in H. pylori-infected Mongolian gerbils but not in uninfected ones.
Conclusions: Our animal study showed that H. pylori infection induced COX-2 expression and increased prostaglandin concentration. Administration of NSAIDs decreased the prostaglandin concentration, but did not increase mucosal damage in H. pylori-induced gastritis. Selective COX-2 inhibitors, instead of conventional NSAIDs, had no beneficial effect on preventing mucosal damage in H. pylori-induced gastritis.