Intracellular pathogens such as Salmonella enterica are confronted with several antimicrobial effector mechanisms when they enter the eukaryotic host. For successful proliferation inside host cells, pathogens must not only counteract these defence mechanisms, but also make use of other host functions to maintain their privileged intracellular niche and a continuous supply of nutrient. Previous observations indicated that intracellular Salmonella avoid delivery of NADPH oxidase to Salmonella-containing vacuoles (SCVs). In addition, we observed that wild-type Salmonella can prevent colocalization of inducible nitric oxide synthase (iNOS) to the SCV and the subsequent damage of intracellular bacteria by peroxynitrite, a highly antimicrobial compoundgenerated by reaction of reactive nitrogen intermediates with reactive oxygen intermediates. However, isogenic strains deficient in the type III secretion system (TTSS) encoded by Salmonella pathogenicity island 2 (SPI-2) were targeted by peroxynitrite and reduced intracellular proliferation of the mutant strains was observed.
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