<i>Salmonella</i>
            Pathogenicity Island 2-Dependent Evasion of the Phagocyte NADPH Oxidase

Vázquez‐Torres, Andrés; Xu, Yisheng; Jones-Carson, Jessica; Holden, David W.; Lucia, Scott; Dinauer, Mary C.; Mastroeni, Pietro; Fang, Ferric C.

doi:10.1126/science.287.5458.1655

Cited by 519 publications

(446 citation statements)

References 43 publications

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“…In macrophages, Salmonella inhibit the fusion of SCV with endosomes and lysosomes 128 and prevent the localization of NADPH oxidase 129,130 and Nos2 131 with SCVs, thereby protecting the bacteria from the microbicidal effect of ROI and RNI.…”

Section: Nadph Oxidase and Nos2mentioning

confidence: 99%

Genetic regulation of host responses to Salmonella infection in mice

Malo

2002

Genes Immun

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Salmonella spp are Gram-negative bacteria capable of infecting a wide range of host species, including humans, domesticated and wild mammals, reptiles, birds and insects. The outcome of an encounter between Salmonella and its host is dependent upon multiple factors including the host genetic background. To facilitate the study of the genetic factors involved in resistance to this pathogen, mouse models of Salmonella infection have been developed and studied for years, allowing identification of several genes and pathways that may influence the disease outcome. In this review, we will cover some of the genes involved in mouse resistance to Salmonella that were identified through the study of congenic mouse strains, cloning of spontaneous mouse mutations, use of site-directed mutagenesis or quantitative trait loci analysis. In parallel, the relevant information pertaining to genes involved in resistance to Salmonella in humans will be discussed.

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Section: Nadph Oxidase and Nos2mentioning

confidence: 99%

Genetic regulation of host responses to Salmonella infection in mice

Malo

2002

Genes Immun

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“…In vitro studies, using different host cell types, have shown that S. typhimurium replicates intracellularly within Salmonella-containing vacuoles (SCVs) apparently protected from host cell antimicrobial activities (Buchmeier and Heffron, 1991;Rathman et al, 1997;Vazquez-Torres et al, 2000). Genetic studies have led to the identification of a large number of genes necessary for intracellular survival.…”

Section: Introductionmentioning

confidence: 99%

Intracellular replication ofSalmonella typhimuriumstrains in specific subsets of splenic macrophagesin vivo

Salcedo

Noursadeghi

Cohen

et al. 2001

Cellular Microbiology

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210

183

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SummaryWe used flow cytometry and confocal immunofluorescence microscopy to study the localization of Salmonella typhimurium in spleens of infected mice. Animals were inoculated intragastrically or intraperitoneally with S. typhimurium strains, constitutively expressing green fluorescent protein. Independently of the route of inoculation, most bacteria were found in intracellular locations 3 days after inoculation. Using a panel of antibodies that bound to cells of different lineages, including mononuclear phagocyte subsets, we have shown that the vast majority of S. typhimurium bacteria reside within macrophages. Bacteria were located in red pulp and marginal zone macrophages, but very few were found in the marginal metallophilic macrophage population. We have demonstrated that the Salmonella SPI-2 type III secretion system is required for replication within splenic macrophages, and that sifA 2 mutant bacteria are found within the cytosol of these cells. These results confirm that SifA and SPI-2 are involved in maintenance of the vacuolar membrane and intracellular replication in vivo.

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“…For example, Neisseria gonorrhoeae does not prevent O 2 Ϫ generation but prevents extracellular release of O 2 Ϫ , thus allowing extracellular neisseriae to survive (16). On the other hand, Salmonella enterica serovar Typhimurium does not prevent O 2 Ϫ generation but blocks release of O 2 Ϫ in salmonella-containing vacuoles, so that intracellular salmonellae can survive (23). Luminol is a small membrane-permeable molecule that can be used to measure total (intra-and extracellular) O 2 Ϫ production (8).…”

Section: Upon Exposure To Neutrophils the Hge Agent Did Not In-mentioning

confidence: 99%

Human Granulocytic Ehrlichiosis Agent Inhibits Superoxide Anion Generation by Human Neutrophils

Mott

Rikihisa

2000

Infect Immun

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The human granulocytic ehrlichiosis (HGE) agent, which replicates in neutrophils, was found not to induce superoxide anion (O 2 ؊ ) generation or extracellular release by human peripheral blood neutrophils, as measured by a luminol-dependent chemiluminescence assay or a cytochrome c reduction assay, respectively. Furthermore, the HGE agent completely prevented O 2 ؊ release by neutrophils upon stimulation with phorbol myristate acetate (PMA), formylmethionyl-leucyl-phenylalanine, or Escherichia coli. The inhibition was HGE agent dose dependent, required ehrlichial contact with the host cells, and was reversible upon removal of the extracellular HGE agent bound to the host cells prior to PMA stimulation. Structural integrity of or new protein synthesis by the HGE agent was not required for the inhibition; carbohydrate but not surface protein of the HGE agent was required. The HGE agent did not prevent O 2 ؊ generation in human peripheral blood monocytes derived from the same individual. This neutrophil-specific prevention of O 2 ؊ generation by the HGE agent would be critical in survival of the HGE agent. This is the first demonstration of the rapid inhibition of preexisting NADPH oxidase in human neutrophils by the HGE agent.An emerging tick-borne zoonosis caused by the human granulocytic ehrlichiosis (HGE) agent was first described in 1994 (5) and has been increasingly recognized in the United States and several European countries. HGE is a disease characterized by systemic illness such as fever, chills, headache, malaise, and/or myalgia. Laboratory tests may reveal thrombocytopenia, leukopenia, elevated C-reactive protein levels, and elevated liver enzyme activities. The HGE agent is a unique obligatory intracellular bacterium that replicates in neutrophils. Neutrophils have a strong ability to kill invading microorganisms through activation of the NADPH oxidase, which rapidly generates superoxide anion (O 2 Ϫ ) and subsequent formation of other bactericidal reactive oxygen intermediates (hydrogen peroxide, myeloperoxide, hypochlorous acid, hydroxyl radical, or longer-lived N-chloroamines) (1, 7, 9). Recently Banerjee et al. (4) reported that after 5 days of infection with the HGE agent, HL-60 cells (a human promyelocytic leukemia cell line) exhibited a lack of luminol-dependent chemiluminescence (LDCL) response to phorbol myristate acetate (PMA) and down regulation of mRNA of gp91 phox , one component of the NADPH complex. However, for the HGE agent to survive in neutrophils, this inhibition must occur immediately rather than 5 days after establishment of infection. Although use of neutrophils is more difficult than use of cell lines, we determined whether human peripheral blood neutrophils produce O 2 Ϫ upon exposure to the HGE agent. Since we found that the HGE agent does not induce O 2 Ϫ generation, we determined whether this is a generalized and/or active inhibition and whether both intracellular and extracellular O 2 Ϫ generation is prevented. We further examined what type of ehrlichial factors and inter...

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

Cited by 519 publications

References 43 publications

Genetic regulation of host responses to Salmonella infection in mice

Genetic regulation of host responses to Salmonella infection in mice

Intracellular replication ofSalmonella typhimuriumstrains in specific subsets of splenic macrophagesin vivo

Human Granulocytic Ehrlichiosis Agent Inhibits Superoxide Anion Generation by Human Neutrophils

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