IL-10、COX-2在幽门螺杆菌相关性胃炎组织中的表达及相关性研究

Objective To investigate the correlation and expression of Interleukin-10 (IL-10) and cyclooxygenase-2 (COX-2) in Helicobacter pylori (H. pylori)-infected gastritis, provide the clinical and experimental basis of immunotherapy of H. pylori-infected gastritis and preventing gastric cancer. Methods Endoscopic biopsies were obtained from gastric antrum at endoscopy from 110 patients with gastritis. Three biopsy specimens were obtained from each patient. Rapid urease testing, Warthin-Starry staining and HE staining were used. The samples of 74 patients fulfilled the criteria of H. pylori scientific study. Fifty-nine patients were H. pylori positive and 15 patients were H. pylori negative. The expression of IL-10 and COX-2 were detected by immunohistothemistry. Results The expression of IL-10 and COX-2 in H. pylori positive gastritis were 49.15% and 59.32%, which were significantly higher than those in H. pylori negative gastritis (13.33% vs 20.00%) (P＜0.05). In H. pylori positive group, the expression of IL-10 in active gastritis (32.26%) was significantly lower than that in inactive gastritis (67.86%) (P＜0.02). The expression of COX-2 in active gastritis (74.19%) was significantly higher than that in inactive gastritis (42.86%) (P＜0.03). In H. pylori positive group, the expression of IL-10 and COX-2 were 64.00% and 44.00% in chronic superficial gastritis, 38.10% and 61.90% in chronic atrophic gastritis, 38.46% and 84.62% in intestinal metaplasia and dysplasia group, respectively. This difference was not statistically significant in the expression of IL-10 (P＞0.05). The expression of COX-2 tended to increase gradually. The expression of COX-2 was higher in intestinal metaplasia and dysplasia than that in superficial gastritis group (P＜0.05). In H. pylori positive group, there was a negative correlation between IL-10 and COX-2 (r=-0.566, P＜0.001). Conclusion The expression of IL-10 and COX-2 are associated with H. pylori infection. IL-10 may have a protective action by inhibiting the overexpression of COX-2, which has correlation with gastritis and gastric cancer.