Salmonella Pathogenicity Island 2-Dependent Evasion of the Phagocyte NADPH Oxidase

Author:

Vazquez-Torres Andrés1,Xu Yisheng1,Jones-Carson Jessica1,Holden David W.2,Lucia Scott M.1,Dinauer Mary C.3,Mastroeni Pietro4,Fang Ferric C.1

Affiliation:

1. Departments of Medicine, Pathology, and Microbiology, University of Colorado Health Sciences Center, Denver, CO 80262, USA.

2. Department of Infectious Diseases, Imperial College School of Medicine, London W12 ONN, UK.

3. Indiana University School of Medicine, Indianapolis, IN 46202, USA.

4. Department of Biochemistry, Imperial College of Medicine and Technology, London SW7 2BZ, UK.

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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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