Abstract
The small Rho guanosine triphosphatases (GTPases) Rac1 and Rac2 have distinct roles in regulating neutrophil chemotaxis; however, little is known about their possible unique roles in mediating bacterial killing. To elucidate the relative roles of Rac1 and Rac2 in regulating neutrophil-mediated bacterial killing, we utilized the previously described mice model in which mouse neutrophils are deficient in either Rac1, Rac2, or both isoforms. We demonstrate here that while both Rac isoforms are required for normal neutrophil chemotaxis and bacterial killing, they have non-overlapping roles in bacterial phagocytosis and NADPH oxidase function.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Chemotaxis, Leukocyte
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Escherichia coli / cytology
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Escherichia coli / immunology*
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Mice
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Mice, Knockout
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Neutrophils / cytology
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Neutrophils / immunology*
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Neutrophils / microbiology
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Peroxidase / metabolism
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Phagocytosis*
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Protein Isoforms / deficiency
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Protein Isoforms / genetics
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Protein Isoforms / metabolism
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RAC2 GTP-Binding Protein
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rac GTP-Binding Proteins / deficiency
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rac GTP-Binding Proteins / genetics
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rac GTP-Binding Proteins / metabolism*
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rac1 GTP-Binding Protein / deficiency
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rac1 GTP-Binding Protein / genetics
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rac1 GTP-Binding Protein / metabolism*
Substances
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Protein Isoforms
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Peroxidase
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rac GTP-Binding Proteins
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rac1 GTP-Binding Protein