title: Salmonella selectively stops traffic.
abstract: The intracellular pathogen Salmonella replicates in infected host cells within a specialized vacuole referred to as the Salmonella-containing vacuole (SCV). Effector molecules encoded by the Salmonella pathogenicity island 2 (SPI-2) type III secretion system (TTSS) are essential for Salmonella to survive in the intracellular environment. It was previously shown that SPI-2 allows Salmonella to inhibit the recruitment of NADPH phagocyte oxidase-containing vesicles to SCVs. New research has now revealed that SPI-2 effectors also interfere with the colocalization of inducible nitric oxide synthase (iNOS) to SCVs, thus protecting the pathogen from the antimicrobial actions of reactive nitrogen species.
authors.affiliation: Depts of Laboratory Medicine and Microbiology, University of Washington School of Medicine, Seattle, WA 98195-7242, USA. fcfang@washington.edu
authors.forename: Ferric
authors.initials: F
authors.lastname: Fang
authors.forename: Andrés
authors.initials: A
authors.lastname: Vazquez-Torres
mesh_terms: D001426:Bacterial Proteins / Q000378:metabolism*; D008565:Membrane Proteins / Q000378:metabolism*; D019255:NADPH Oxidases / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II; D010586:Phagocytes / Q000378:metabolism; D012475:Salmonella / Q000378:metabolism*
chemical_list: D001426:Bacterial Proteins; D008565:Membrane Proteins; C440638:SPI-2 protein, Salmonella; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D019255:NADPH Oxidases