Helicobacter pylori induces but survives the extracellular release of oxygen radicals from professional phagocytes using its catalase activity

Helicobacter pylori can colonize the gastric epithelium of humans, leading to the induction of an intense inflammatory response with the infiltration of mainly polymorphonuclear leucocytes (PMNs) and monocytes. These professi onal phagocytes appear to be a primary cause of the damage to surface epith elial layers, and probably contribute to the pathogenesis associated with p ersistent H. pylori infections. We have shown previously that H, pylori adh eres to professional phagocytes, but is not engulfed efficiently, suggestin g an antiphagocytic escape mechanism that is dependent on the pathogen's ty pe IV secretion system. Here, we show that H. pylori induces the generation and extracellular release of oxygen metabolites as a consequence of its at tachment to phagocytic cells, but is capable of surviving this response. Th e catalase activity of H. pylori is apparently essential for survival at th e phagocytes' cell surface. Opsonization of H. pylori leads to an increased burst, and the inhibition of bacterial protein synthesis to a decreased on e. Ca2+ concentration, cytoskeleton rearrangement and protein kinase C (PKC ) are involved in the H. pylori-induced oxidative burst in both monocytes a nd PMNs. This survival phenomenon has important implications for both the p ersistence of this important pathogen and the host tissue damage that accom panies persistent H. pylori infection.