Activation of human phagocyte oxidative metabolism by Helicobacter pylori.

A characteristic feature of chronic antral gastritis is the abundant inflammatory response in close association with Helicobacter pylori, but the immunopathological mechanisms of tissue damage are unknown. Because reactive oxygen radicals have been implicated in the tissue damage of other chronic inflammatory disorders, we investigated the potential ability of H. pylori sonicate to influence the oxidative burst responsiveness of human polymorphonuclear leukocytes and monocytes. For both cell types, a dose-dependent stimulation in a chemiluminescence system was observed. Furthermore, preincubation in sonicate caused a marked priming of the cells to subsequent stimulation with the oligopeptide N-f-methionyl-leucyl-phenylalanine and phorbol-myristate-acetate. The sonicate activity was nondialysable, completely destroyed by proteinase and resistant to heat treatment. However, dialysis of boiled sonicate significantly reduced the activity, suggesting the breakdown of a larger molecule(s) to smaller fragments still biologically active. Preliminary experiments suggest that the activity is 25-35 kilodaltons. The demonstration of a protein with stimulatory activity for production of reactive oxygen radicals by human phagocytes may contribute to the understanding of the immunopathology associated with H. pylori infection.