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

Abstract

SummaryHelicobacter 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 professional phagocytes appear to be a primary cause of the damage to surface epithelial layers, and probably contribute to the pathogenesis associated with persistent H. pylori infections. We have shown previously that H. pylori adheres to professional phagocytes, but is not engulfed efficiently, suggesting an antiphagocytic escape mechanism that is dependent on the pathogen's type IV secretion system. Here, we show that H. pylori induces the generation and extracellular release of oxygen metabolites as a consequence of its attachment to phagocytic cells, but is capable of surviving this response. The catalase activity of H. pylori is apparently essential for survival at the phagocytes' cell surface. Opsonization of H. pylori leads to an increased burst, and the inhibition of bacterial protein synthesis to a decreased one. Ca 21 concentration, cytoskeleton rearrangement and protein kinase C (PKC) are involved in the H. pyloriinduced oxidative burst in both monocytes and PMNs. This survival phenomenon has important implications for both the persistence of this important pathogen and the host tissue damage that accompanies persistent H. pylori infection.

Catalase (KatA) and KatA-associated protein (KapA) are essential to persistent colonization in the Helicobacter pylori SS1 mouse model

“…We have proposed that catalase is a crucial component in the evasion of the host immune response (Hazell et al, 2001). This theory was supported by the findings of Ramarao et al (2000) that H. pylori induces the release of ROS upon adherence to professional phagocytes in vitro, and catalase-deficient mutants did not survive the respiratory burst. These data are supported by our study showing that catalase facilitates survival of H. pylori upon exposure to high (~100 mM) concentrations of hydrogen peroxide (Harris et al, 2002).…”

Mutation of cytotoxin-associated gene A affects expressions of antioxidant proteins of Helicobacter pylori

“…Therefore, proteins (enzymes) involved in oxidative stress resistance are the important factors for bacterial colonization and pathogenesis [28] . Microaero philic organisms, such as H pylori, are particularly vulnerable to the detrimental effects of oxygen and oxidative stress.…”

Identification of Surface Proteins of Helicobacter pylori by Selective Biotinylation, Affinity Purification, and Two-dimensional Gel Electrophoresis

“…Cag16 is a member of the Cag pathogenicity island that is known to enhance inflammatory responses to H. pylori. Cag16 is essential for the expression of the VirB7 homologue HP0532, which is supposedly a structural component of the type IV secretion system (42,43 (49). Information about a potential role for HtrA in H. pylori virulence is lacking.…”