ArticleThe Journal of experimental medicine2005
Repression of SPI2 transcription by nitric oxide-producing, IFNgamma-activated macrophages promotes maturation of Salmonella phagosomes.
Article in The Journal of experimental medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 66 citations in OpenAlex.
- Host-microbiota-pathogen interactions drive Salmonella enterica serovar Typhimurium pathogenesis.Nature reviews. Microbiology · 2026Review
- DksA inhibitors against intracellular and persistentScience advances · 2026Article
- Cell-specific expression ofHaematologica · 2021Article
- Glycolytic reprograming in Salmonella counters NOX2-mediated dissipation of ΔpH.Nature communications · 2020Article
- SpoT Induces IntracellularmBio · 2020Article
- Replication ofFrontiers in cellular and infection microbiology · 2020Article
- Controversy Surrounding the Function of SpiC Protein inFrontiers in microbiology · 2019Review
- Intestinal Acid Sphingomyelinase Protects From Severe Pathogen-Driven Colitis.Frontiers in immunology · 2019Article
- Zinc-dependent substrate-level phosphorylation powers Salmonella growth under nitrosative stress of the innate host response.PLoS pathogens · 2018Article
- Guanosine tetraphosphate relieves the negative regulation of Salmonella pathogenicity island-2 gene transcription exerted by the AT-rich ssrA discriminator region.Scientific reports · 2018Article
- Article
- Magnesium homeostasis protects Salmonella against nitrooxidative stress.Scientific reports · 2017Article
- Nitric Oxide Accumulation: The Evolutionary Trigger for Phytopathogenesis.Frontiers in microbiology · 2017Article
- Iron at the interface of immunity and infection.Frontiers in pharmacology · 2014Review
- Ferric uptake regulator-dependent antinitrosative defenses in Salmonella enterica serovar Typhimurium pathogenesis.Infection and immunity · 2014Article
- Low-molecular-weight thiol-dependent antioxidant and antinitrosative defences in Salmonella pathogenesis.Molecular microbiology · 2013Article
- DksA-dependent resistance of Salmonella enterica serovar Typhimurium against the antimicrobial activity of inducible nitric oxide synthase.Infection and immunity · 2012Article
- The Fur regulon in anaerobically grown Salmonella enterica sv. Typhimurium: identification of new Fur targets.BMC microbiology · 2011Article
- Article
- Nitric oxide and salmonella pathogenesis.Frontiers in microbiology · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
By remodeling the phagosomal membrane, the type III secretion system encoded within the Salmonella pathogenicity island-2 (SPI2) helps Salmonella thrive within professional phagocytes. We report here that nitric oxide (NO) generated by IFNgamma-activated macrophages abrogates the intracellular survival advantage associated with a functional SPI2 type III secretion system. NO congeners inhibit overall expression of SPI2 effectors encoded both inside and outside the SPI2 gene cluster, reflecting a reduced transcript level of the sensor kinase SsrA that governs overall SPI2 transcription. Down-regulation of SPI2 expression in IFNgamma-treated macrophages does not seem to be the result of global NO cytotoxicity, because transcription of the housekeeping rpoD sigma factor remains unchanged, whereas the expression of the hmpA-encoded, NO-metabolizing flavohemoprotein is stimulated. Because of the reduced SPI2 expression, Salmonella-containing vacuoles interact more efficiently with compartments of the late endosomal/lysosomal system in NO-producing, IFNgamma-treated macrophages. These findings demonstrate that inhibition of intracellular SPI2 transcription by NO promotes the interaction of Salmonella phagosomes with the degradative compartments required for enhanced antimicrobial activity. Transcriptional repression of a type III secretion system that blocks phagolysosome biogenesis represents a novel mechanism by which NO mediates resistance of IFNgamma-activated phagocytes to an intracellular pathogen.
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