ArticleThe Journal of experimental medicine2002
Salmonella pathogenicity island 2 mediates protection of intracellular Salmonella from reactive nitrogen intermediates.
Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers.
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143 citing papers in PubMed, 347 citations in OpenAlex.
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- The role of tissue resident memory CD4 T cells in Salmonella infection: Implications for future vaccines.Vaccine · 2023Review
- Salmonella T3SS effector SseK1 arginine-glycosylates the two-component response regulator OmpR to alter bile salt resistance.Scientific reports · 2023Article
- Nitric oxide is a host cue for Salmonella Typhimurium systemic infection in mice.Communications biology · 2023Article
- Single molecule analyses reveal dynamics of Salmonella translocated effector proteins in host cell endomembranes.Nature communications · 2023Article
- Lysosomal trafficking regulator restricts intracellular growth ofFrontiers in cellular and infection microbiology · 2023Article
- Salmonella Typhimurium outer membrane protein A (OmpA) renders protection from nitrosative stress of macrophages by maintaining the stability of bacterial outer membrane.PLoS pathogens · 2022Article
- Copper microenvironments in the human body define patterns of copper adaptation in pathogenic bacteria.PLoS pathogens · 2022Review
- Nitrate Utilization Promotes Systemic Infection ofInternational journal of molecular sciences · 2022Article
83 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Salmonella typhimurium causes an invasive disease in mice that has similarities to human typhoid. A type III protein secretion system encoded by Salmonella pathogenicity island 2 (SPI2) is essential for virulence in mice, as well as survival and multiplication within macrophages. Reactive nitrogen intermediates (RNI) synthesized by inducible nitric oxide synthase (iNOS) are involved in the control of intracellular pathogens, including S. typhimurium. We studied the effect of Salmonella infection on iNOS activity in macrophages. Immunofluorescence microscopy demonstrated efficient colocalization of iNOS with bacteria deficient in SPI2 but not wild-type Salmonella, and suggests that the SPI2 system interferes with the localization of iNOS and Salmonella. Furthermore, localization of nitrotyrosine residues in the proximity was observed for SPI2 mutant strains but not wild-type Salmonella, indicating that peroxynitrite, a potent antimicrobial compound, is excluded from Salmonella-containing vacuoles by action of SPI2. Altered colocalization of iNOS with intracellular Salmonella required the function of the SPI2-encoded type III secretion system, but not of an individual "Salmonella translocated effector." Inhibition of iNOS increased intracellular proliferation of SPI2 mutant bacteria and, to a lesser extent, of wild-type Salmonella. The defect in systemic infection of a SPI2 mutant strain was partially restored in iNOS(-/-) mice. In addition to various strategies to detoxify RNI or repair damage due to RNI, avoidance of colocalization with RNI is important in adaptation of a pathogen to an intracellular life style.
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