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Salmonella pathogenicity island 2-dependent evasion of the phagocyte NADPH oxidase.

TitleSalmonella pathogenicity island 2-dependent evasion of the phagocyte NADPH oxidase.
Publication TypeJournal Article
Year of Publication2000
AuthorsVazquez-Torres, A, Xu, Y, Jones-Carson, J, Holden, DW, Lucia, SM, Dinauer, MC, Mastroeni, P, Fang, FC
JournalScience
Volume287
Issue5458
Pagination1655-8
Date Published2000 Mar 3
ISSN0036-8075
KeywordsAnimals, Bacterial Proteins, Cerium, Genes, Bacterial, Hydroxides, Macrophages, Peritoneal, Mice, Mice, Inbred C57BL, Mice, Knockout, Microscopy, Electron, Microscopy, Fluorescence, NADPH Oxidase, Peroxides, Phagosomes, Respiratory Burst, Salmonella Infections, Animal, Salmonella typhimurium, Superoxides, Tetradecanoylphorbol Acetate, Vacuoles, Virulence
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.

Alternate JournalScience
PubMed ID10698741
Grant ListAI39557 / AI / NIAID NIH HHS / United States
AI44486 / AI / NIAID NIH HHS / United States