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How does the oxidative burst of macrophages kill bacteria? Still an open question
Author(s) -
Slauch James M.
Publication year - 2011
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2011.07612.x
Subject(s) - phagosome , phagocyte , biology , nadph oxidase , respiratory burst , context (archaeology) , salmonella , microbiology and biotechnology , reactive oxygen species , oxidative phosphorylation , bacteria , vacuole , superoxide , cytoplasm , phagocytosis , biochemistry , genetics , paleontology , enzyme
Summary 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 Méresse 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.