Helicobacter pylori elicits gastric mucosal cell damage associated with neutrophil-derived toxic oxidants

Purpose: To investigate Helicobacter pylori-dependent neutrophil activation and the in vitro effects of neutrophil-derived toxic oxidants on gastric mucosal cell injury. Methods and results: The luminol-dependent chemiluminescence activity of human neutrophils increased significantly after H. pylori was added, indicating that the oxidative burst of neutrophils was actually conducted by H pylori. The cytotoxicity of cultured gastric mucosal cells was assessed by the release of 2,7-bis-carboxyethyl-5(6)-carboxyfluorescein fluorescence from cellular cytoplasm. Neither H. pylori nor neutrophils alone produced significant epithelial cell injury but considerable damage was inflicted by H. pylori-activated neutrophils. Moreover, the epithelial cell injury was aggravated by ammonia (1 mmol/l) and inhibited by scavengers of reactive oxygen metabolites (catalase, taurine). Conclusions: These observations suggest that gastric mucosal damage may be elicited by H. pylori-activated neutrophils, which is, in part, regulated by reactive oxygen metabolites. It also appears that the ammonia-dependent oxidant, monochloramine, plays a unique part in this mucosal injury.