[Role of ammonia-monochloramine system in Helicobacter pylori--induced gastric mucosal injury]

Abstract

Monochloramine is a reactive oxidant which is yielded by the reaction of neutrophil-derived hypochlorous acid and ammonia. Luminol-dependent chemiluminescence assay reveals that H. pylori directly elicits a respiratory burst of neutrophils. This activation is also observed by adding the bacterial supernatant of cultured or sonicated H. pylori, suggesting that H. pylori-derived soluble factor may be responsible for the release of chlorinated oxidants. In vitro cytotoxicity assay indicates that cultured rabbit gastric mucosal cells are significantly damaged by neutrophils which are stimulated by H. pylori. This injury is attenuated by urease inhibitor, antioxidants, and taurine (monochloramine scavenger). These data support the concept that ammonia-monochloramine system plays an important role in H. pylori-associated gastric mucosal injury. Omeprazole and rebamipide significantly inhibit not only H. pylori-induced respiratory burst of neutrophils but also H. pylori-associated urease activity. This evidence emphasizes the advantageous effect of these anti-ulcer compounds on H. pylori-positive gastric lesion and postulates a new strategy for anti-H. pylori treatment.