4.5 Editorial Material

How does the oxidative burst of macrophages kill bacteria? Still an open question

Journal

MOLECULAR MICROBIOLOGY
Volume 80, Issue 3, Pages 580-583

Publisher

WILEY-BLACKWELL
DOI: 10.1111/j.1365-2958.2011.07612.x

Keywords

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Funding

  1. NIAID NIH HHS [R01 AI080705-01A1, AI080705, R01 AI063230, R01 AI063230-05, R01 AI080705] Funding Source: Medline

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P>Reactive oxygen species (ROS) are critical components of the antimicrobial repertoire of macrophages, yet the mechanisms by which ROS damage bacteria in the phagosome are unclear. The NADH-dependent phagocytic oxidase produces superoxide, which dismutes to form H(2)O(2). The Barras and Meresse labs use a GFP fusion to an OxyR regulated gene to show that phagocyte-derived H(2)O(2) is gaining access to the Salmonella cytoplasm. However, they have also shown previously that Salmonella has redundant systems to detoxify this H(2)O(2). Although Salmonella propagate in a unique vacuole, their data suggest that ROS are not diminished in this modified phagosome. These recent results are put into the context of our overall understanding of potential oxidative bacterial damage occurring in macrophages.

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