Poster Round 5.1: Inflammation and Host Response

Abstract

Background Helicobacter pylori-induced corpus-predominant gastritis appears to carry the highest risk for developing gastric cancer. The alteration of arachidonic acid metabolism, especially via the cyclooxygenase-2 (COX-2) pathway, was shown to play an important role in gastric carcinogenesis. Whether the 5-lipoxygenase (5-LOX) pathway is also involved in gastric carcinogenesis is not known. Aim To evaluate the effects of H. pylori eradication in subjects with corpus-predominant gastritis with respect to histology and the expression of 5-lipoxygenase and leukotriene receptors. Methods Patients with H. pylori-induced corpus-predominant gastritis received triple therapy for H. pylori eradication. Five years later, esophagogastroduodenoscopy with biopsies was repeated. The expression of 5-LOX, leukotriene B4 receptor (BLT)1, and cysteinyl-leukotriene receptor (CysLT)1 was analyzed by immunohistochemistry. COX-2 expression was assessed as internal control. Results Twelve patients were found to have a persistent H. pylori infection 5 years after the eradication therapy and were matched for age and sex to those with successful eradication in a 1 : 1 ratio. None of the study participants developed intraepithelial neoplasia or gastric cancer. Gastritis improved only in patients with successful eradication therapy. The expression of CysLT1 was decreased, and that of BLT1 was increased in patients with successful eradication (p < .05), but not in those with persistent H. pylori infection. The expression of 5-LOX was unchanged in both patients with successful eradication and those with eradication failure. COX-2 was significantly down-regulated only in subjects with successful H. pylori eradication (p < .05). Conclusions H. pylori eradication led to a resolution of corpus-predominant gastritis, and restored the expression of the enzymes/receptors involved in the COX/5-LOX pathway. In this way, the risk for developing gastric cancer may be reduced.