Abstract
A type III protein secretion system encoded by Salmonella pathogenicity island 2 (SPI2) has been found to be required for virulence and survival within macrophages. Here, SPI2 was shown to allow Salmonella typhimurium to avoid NADPH oxidase-dependent killing by macrophages. The ability of SPI2-mutant bacteria to survive in macrophages and to cause lethal infection in mice was restored by abrogation of the NADPH oxidase-dependent respiratory burst. Ultrastructural and immunofluorescence microscopy demonstrated efficient localization of the NADPH oxidase in the proximity of vacuoles containing SPI2-mutant but not wild-type bacteria, suggesting that SPI2 interferes with trafficking of oxidase-containing vesicles to the phagosome.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Bacterial Proteins / genetics
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Bacterial Proteins / physiology
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Cerium / analysis
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Genes, Bacterial
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Hydroxides*
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Macrophages, Peritoneal / enzymology*
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Macrophages, Peritoneal / microbiology*
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Macrophages, Peritoneal / ultrastructure
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Microscopy, Electron
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Microscopy, Fluorescence
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NADPH Oxidases / metabolism*
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Peroxides / analysis
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Phagosomes / microbiology
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Respiratory Burst
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Salmonella Infections, Animal / microbiology
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Salmonella typhimurium / genetics*
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Salmonella typhimurium / pathogenicity*
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Salmonella typhimurium / physiology
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Superoxides / metabolism
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Tetradecanoylphorbol Acetate / pharmacology
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Vacuoles / enzymology
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Vacuoles / microbiology
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Virulence
Substances
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Bacterial Proteins
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Hydroxides
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Peroxides
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Superoxides
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Cerium
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cerium hydroxide
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NADPH Oxidases
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Tetradecanoylphorbol Acetate