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

Authors

  • Nalini Ramarao,

    1. Max Planck Institute for Biology, Department of Infection Biology, Spemannstr. 34, 72076 Tübingen, Germany.
    2. Max Planck Institute for Infection Biology, Department of Molecular Biology, Monbijoustr. 2, 10117 Berlin, Germany.
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  • Scott D. Gray-Owen,

    1. Max Planck Institute for Biology, Department of Infection Biology, Spemannstr. 34, 72076 Tübingen, Germany.
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  • Thomas F. Meyer

    Corresponding author
    1. Max Planck Institute for Biology, Department of Infection Biology, Spemannstr. 34, 72076 Tübingen, Germany.
    2. Max Planck Institute for Infection Biology, Department of Molecular Biology, Monbijoustr. 2, 10117 Berlin, Germany.
    • †Present address: Department of Medical Genetics and Microbiology, University of Toronto, 1 King's College Circle, M5S 1A8, Toronto, Canada. *For correspondence. E-mail meyer@mpiib-berlin.mpg.de; Tel. (+49) 30 28 46 04 02; Fax (+49) 30 28 46 04 01.

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Abstract

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 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. Ca2+ concentration, cytoskeleton rearrangement and protein kinase C (PKC) are involved in the H. pylori-induced 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.

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