Cyclooxygenase-2 expression in gastric antral mucosa before and after eradication of Helicobacter pylori infection

OBJECTIVE: Helicobacter pylori (H. pylori) causes chronic gastritis. The in ducible prostaglandin synthetase cyclooxygenase 2 (COX-2) plays an importan t role in inflammatory conditions. We hypothesized that Ii pylori-associate d chronic gastritis would express COX-2 protein. Our aim was to evaluate th e effect of eradication of Ii. pylori infection on COX-2 expression in the antral mucosa of patients before and after antibiotic therapy. METHODS: Tissues were obtained from patients with nonulcer dyspepia undergo ing Ii. pylori eradication. Ten patients with proven Ii pylori infection an d subsequent successful eradication were studied. Three biopsies of antral mucosa were evaluated before and after Ii pylori eradication. The amount of acute and chronic inflammation was quantitated. Immunohistochemical staini ng for COX-2 was expressed as a percentage of the total number of cells and correlated with the degree of chronic inflammation. RESULTS: Specific immunostaining for COX-2 was observed in antral mucosa of patients infected with Ii pylori. Patchy cytoplasmic staining was seen in surface epithelial cells and strong cytoplasmic staining for COX-2 was seen in parietal cells. Spotty cytoplasmic staining for COX-2 was also seen in lamina- propria plasma cells, as well as there being macrophages present in the germinal centers of lymphoid aggregates. COX-2 expression could be det ected both before and after eradication of Ii. pylori. The mean percentage of cells staining for COX-2 was significantly higher in H. pylori-infected mucosa, compared with mucosa after successful Ii pylori eradication (33.4% +/- 5.4 vs 18.9% +/- 3.3, p = 0.038). COX-2 immunostaining correlated best with the chronic inflammation score (r(2) = 0.78, p < 0.001). There was a s trong correlation for those subjects who were H. pylori infected, as well a s for those who had successful Ii pylori eradication. CONCLUSIONS: Ii. pylori associated acute and chronic antral inflammation wa s associated with immunohistochemical detection of COX-2 protein in epithel ial cells, in addition to associated mononuclear cells and parietal cells. Expression was reduced, but not eliminated, in the epithelium after success ful eradication of Ii, pylori. Despite the reduction in COX-2 expression af ter H. pylori eradication, expression of COX-2 in epithelial cells remained and strongly correlated with the extent of the chronic inflammatory cell i nfiltrate. The clinical implications of Ii pylori-associated induction of C OX-2 expression for patients on selective COX-2 inhibitors, in addition to the role of COX-2 in gastric carcinogenesis, deserve further study. (C) 199 9 by Am. Cell. of Gastroenterology.