Статті в журналах: "Salmonella Pathogenicity Island 2"

1

Hensel, Michael. "Salmonella Pathogenicity Island 2." Molecular Microbiology 36, no. 5 (June 2000): 1015–23. http://dx.doi.org/10.1046/j.1365-2958.2000.01935.x.

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2

BAYOUMI, MOHAMED A., and MANSEL W. GRIFFITHS. "Probiotics Down-Regulate Genes in Salmonella enterica Serovar Typhimurium Pathogenicity Islands 1 and 2." Journal of Food Protection 73, no. 3 (March 1, 2010): 452–60. http://dx.doi.org/10.4315/0362-028x-73.3.452.

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Salmonella Typhimurium pathogenesis relies mainly on the expression of genes of two pathogenicity islands, Salmonella pathogenicity islands 1 and 2 (SPI1 and SPI2). Each island has its own pattern of expression and regulation. Success in suppression of the responsible key activator of each island would be an effective way of controlling Salmonella, especially with the emerging problem of antibiotic-resistant strains. Probiotics have been shown to inhibit several foodborne pathogens, and their mode of action may partly involve down-regulation of virulence genes. To investigate whether probiotics played a role in the regulation of the pathogenicity islands SPI1 and SPI2 in Salmonella, two reporter strains were constructed in which the general regulator of SPI1, hilA, and the response regulator of SPI2, ssrB, were fused with luxCDABE genes. These constructs were used to screen the effect of probiotics on the expression of each gene. Molecules secreted by Bifidobacterium bifidum were able to down-regulate both genes.

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3

Fass, Ephraim, and Eduardo A. Groisman. "Control of Salmonella pathogenicity island-2 gene expression." Current Opinion in Microbiology 12, no. 2 (April 2009): 199–204. http://dx.doi.org/10.1016/j.mib.2009.01.004.

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4

Garai, Preeti, Sandhya Marathe, and Dipshikha Chakravortty. "Effectors of Salmonella Pathogenicity Island 2: An Island crucial to the life of Salmonella." Virulence 2, no. 3 (May 2011): 177–80. http://dx.doi.org/10.4161/viru.2.3.16578.

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5

Pawelek, John M., Stefano Sodi, Ashok K. Chakraborty, James T. Platt, Samuel Miller, David W. Holden, Michael Hensel, and K. Brooks Low. "Salmonella pathogenicity island-2 and anticancer activity in mice." Cancer Gene Therapy 9, no. 10 (September 11, 2002): 813–18. http://dx.doi.org/10.1038/sj.cgt.7700501.

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6

Deiwick, Jorg, Thomas Nikolaus, Sezgin Erdogan, and Michael Hensel. "Environmental regulation of Salmonella pathogenicity island 2 gene expression." Molecular Microbiology 31, no. 6 (April 1999): 1759–73. http://dx.doi.org/10.1046/j.1365-2958.1999.01312.x.

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7

Chakravortty, Dipshikha, Imke Hansen-Wester, and Michael Hensel. "Salmonella Pathogenicity Island 2 Mediates Protection of Intracellular Salmonella from Reactive Nitrogen Intermediates." Journal of Experimental Medicine 195, no. 9 (April 29, 2002): 1155–66. http://dx.doi.org/10.1084/jem.20011547.

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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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8

Hansen-Wester, Imke, Bärbel Stecher, and Michael Hensel. "Analyses of the Evolutionary Distribution of Salmonella Translocated Effectors." Infection and Immunity 70, no. 3 (March 2002): 1619–22. http://dx.doi.org/10.1128/iai.70.3.1619-1622.2002.

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ABSTRACT The type III secretion system encoded by Salmonella pathogenicity island 2 (SPI2) translocates Salmonella translocated effectors (STE) into host cells. STE are encoded by genes outside of SPI2. The distribution of STE loci within the salmonellae was investigated. In contrast to the SPI2 locus that is conserved within Salmonella enterica, STE loci show a variable distribution. In addition to other virulence determinants, the possession of various sets of STE loci may contribute to the different host ranges and pathogenic potentials of S. enterica serovars.

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9

Jones, Michael A., Paul Wigley, Kerrie L. Page, Scott D. Hulme, and Paul A. Barrow. "Salmonella enterica Serovar Gallinarum Requires the Salmonella Pathogenicity Island 2 Type III Secretion System but Not the Salmonella Pathogenicity Island 1 Type III Secretion System for Virulence in Chickens." Infection and Immunity 69, no. 9 (September 1, 2001): 5471–76. http://dx.doi.org/10.1128/iai.69.9.5471-5476.2001.

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ABSTRACT Salmonella enterica serovar Gallinarum is a host-specific serotype that causes the severe systemic disease fowl typhoid in domestic poultry and a narrow range of other avian species but rarely causes disease in mammalian hosts. Specificity of the disease is primarily at the level of the reticuloendothelial system, but few virulence factors have been described other than the requirement for an 85-kb virulence plasmid. In this work, by making functional mutations in the type III secretion systems (TTSS) encoded by Salmonella pathogenicity island 1 (SPI-1) and SPI-2, we investigated the role of these pathogenicity islands in interactions between Salmonella serovar Gallinarum and avian cells in vitro and the role of these pathogenicity islands in virulence in chickens. The SPI-1 mutant showed decreased invasiveness into avian cells in vitro but was unaffected in its ability to persist within chicken macrophages. In contrast the SPI-2 mutant was fully invasive in nonphagocytic cells but failed to persist in macrophages. In chicken infections the SPI-2 mutant was attenuated while the SPI-1 mutant showed full virulence. In oral infections the SPI-2 mutant was not observed in the spleen or liver, and following intravenous inoculation it was cleared rapidly from these sites. SPI-2 function is required by Salmonella serovar Gallinarum for virulence, primarily through promoting survival within macrophages allowing multiplication within the reticuloendothelial system, but this does not preclude the involvement of SPI-2 in uptake from the gut to the spleen and liver. SPI-1 appears to have little effect on virulence and survival of Salmonella serovar Gallinarum in the host.

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10

Osborne, Suzanne E., and Brian K. Coombes. "Transcriptional Priming of Salmonella Pathogenicity Island-2 Precedes Cellular Invasion." PLoS ONE 6, no. 6 (June 28, 2011): e21648. http://dx.doi.org/10.1371/journal.pone.0021648.

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11

Hansen-Wester, Imke, Dipshikha Chakravortty, and Michael Hensel. "Functional Transfer of Salmonella Pathogenicity Island 2 to Salmonella bongori and Escherichia coli." Infection and Immunity 72, no. 5 (May 2004): 2879–88. http://dx.doi.org/10.1128/iai.72.5.2879-2888.2004.

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ABSTRACT The type III secretion system (T3SS) encoded by the Salmonella pathogenicity island 2 (SPI2) has a central role in systemic infections by Salmonella enterica and for the intracellular phenotype. Intracellular S. enterica uses the SPI2-encoded T3SS to translocate a set of effector proteins into the host cell, which modify host cell functions, enabling intracellular survival and replication of the bacteria. We sought to determine whether specific functions of the SPI2-encoded T3SS can be transferred to heterologous hosts Salmonella bongori and Escherichia coli Mutaflor, species that lack the SPI2 locus and loci encoding effector proteins. The SPI2 virulence locus was cloned and functionally expressed in S. bongori and E. coli. Here, we demonstrate that S. bongori harboring the SPI2 locus is capable of secretion of SPI2 substrate proteins under culture conditions, as well as of translocation of effector proteins under intracellular conditions. An SPI2-mediated cellular phenotype was induced by S. bongori harboring the SPI2 if the sifA locus was cotransferred. An interference with the host cell microtubule cytoskeleton, a novel SPI2-dependent phenotype, was observed in epithelial cells infected with S. bongori harboring SPI2 without additional effector genes. S. bongori harboring SPI2 showed increased intracellular persistence in a cell culture model, but SPI2 transfer was not sufficient to confer to S. bongori systemic pathogenicity in a murine model. Transfer of SPI2 to heterologous hosts offers a new tool for the study of SPI2 functions and the phenotypes of individual effectors.

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12

Uchiya, Kei-ichi, and Toshiaki Nikai. "Salmonella enterica Serovar Typhimurium Infection Induces Cyclooxygenase 2 Expression in Macrophages: Involvement of Salmonella Pathogenicity Island 2." Infection and Immunity 72, no. 12 (December 2004): 6860–69. http://dx.doi.org/10.1128/iai.72.12.6860-6869.2004.

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ABSTRACT Salmonella pathogenicity island 2 (SPI-2) is required for intramacrophage survival and systemic infection in mice. We have recently reported that Salmonella enterica causes activation of the protein kinase A (PKA) signaling pathway in a manner dependent on SPI-2, resulting in the upregulation of interleukin-10 expression in macrophages (K. Uchiya et al., Infect. Immun. 72:1964-1973, 2004). We show in the present study the involvement of SPI-2 in a signal transduction pathway that induces the expression of cyclooxygenase 2 (COX-2), an inducible enzyme involved in the synthesis of prostanoids. High levels of prostaglandin E2 (PGE2) and prostacyclin (PGI2), which are known to activate the PKA signaling pathway via their receptors, were induced in J774 macrophages infected with wild-type Salmonella compared to a strain carrying a mutation in the spiC gene, located within SPI-2. The increased production of both prostanoids was dependent on COX-2. COX-2 expression was dose dependently blocked by treatment with a specific inhibitor of the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway, and the phosphorylation level of ERK1/2 was higher in macrophages infected with wild-type Salmonella compared to the spiC mutant. Taken together, these results indicate that Salmonella causes an SPI-2-dependent ERK1/2 activation that leads to increased COX-2 expression, resulting in the upregulation of PGE2 and PGI2 production in macrophages. A COX-2 inhibitor inhibited not only Salmonella-induced activation of the PKA signaling pathway but also growth of wild-type Salmonella within macrophages, suggesting that Salmonella utilizes the COX-2 pathway to survive within macrophages and that the mechanism involves activation of the PKA signaling pathway.

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13

Chakraborty, Sangeeta, Debalina Chaudhuri, Arjun Balakrishnan, and Dipshikha Chakravortty. "Salmonella methylglyoxal detoxification by STM3117-encoded lactoylglutathione lyase affects virulence in coordination with Salmonella pathogenicity island 2 and phagosomal acidification." Microbiology 160, no. 9 (September 1, 2014): 1999–2017. http://dx.doi.org/10.1099/mic.0.078998-0.

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Intracellular pathogens such as Salmonella enterica serovar Typhimurium (S. Typhimurium) manipulate their host cells through the interplay of various virulence factors. A multitude of such virulence factors are encoded on the genome of S. Typhimurium and are usually organized in pathogenicity islands. The virulence-associated genomic stretch of STM3117–3120 has structural features of pathogenicity islands and is present exclusively in non-typhoidal serovars of Salmonella. It encodes metabolic enzymes predicted to be involved in methylglyoxal metabolism. STM3117-encoded lactoylglutathione lyase significantly impacts the proliferation of intracellular Salmonella. The deletion mutant of STM3117 (Δlgl) fails to grow in epithelial cells but hyper-replicates in macrophages. This difference in proliferation outcome was the consequence of failure to detoxify methylglyoxal by Δlgl, which was also reflected in the form of oxidative DNA damage and upregulation of kefB in the mutant. Within macrophages, the toxicity of methylglyoxal adducts elicits the potassium efflux channel (KefB) in the mutant which subsequently modulates the acidification of mutant-containing vacuoles (MCVs). The perturbation in the pH of the MCV milieu and bacterial cytosol enhances the Salmonella pathogenicity island 2 translocation in Δlgl, increasing its net growth within macrophages. In epithelial cells, however, the maturation of Δlgl-containing vacuoles were affected as these non-phagocytic cells maintain less acidic vacuoles compared to those in macrophages. Remarkably, ectopic expression of Toll-like receptors 2 and 4 on epithelial cells partially restored the survival of Δlgl. This study identified a novel metabolic enzyme in S. Typhimurium whose activity during intracellular infection within a given host cell type differentially affected the virulence of the bacteria.

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14

Tsai, Caressa N., and Brian K. Coombes. "High-Throughput Chemical Screening for Inhibitors of Salmonella Pathogenicity Island 2." STAR Protocols 1, no. 2 (September 2020): 100057. http://dx.doi.org/10.1016/j.xpro.2020.100057.

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15

Löber, Stefanie, Daniela Jäckel, Nina Kaiser, and Michael Hensel. "Regulation of Salmonella pathogenicity island 2 genes by independent environmental signals." International Journal of Medical Microbiology 296, no. 7 (November 14, 2006): 435–47. http://dx.doi.org/10.1016/j.ijmm.2006.05.001.

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16

Brown, Nat F., Bruce A. Vallance, Brian K. Coombes, Yanet Valdez, Bryan A. Coburn, and B. Brett Finlay. "Salmonella Pathogenicity Island 2 Is Expressed Prior to Penetrating the Intestine." PLoS Pathogens 1, no. 3 (November 18, 2005): e32. http://dx.doi.org/10.1371/journal.ppat.0010032.

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17

Vazquez-Torres, A. "Salmonella Pathogenicity Island 2-Dependent Evasion of the Phagocyte NADPH Oxidase." Science 287, no. 5458 (March 3, 2000): 1655–58. http://dx.doi.org/10.1126/science.287.5458.1655.

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18

Linehan, Sheena A., Anne Rytkönen, Xiu-Jun Yu, Mei Liu, and David W. Holden. "SlyA Regulates Function of Salmonella Pathogenicity Island 2 (SPI-2) and Expression of SPI-2-Associated Genes." Infection and Immunity 73, no. 7 (July 2005): 4354–62. http://dx.doi.org/10.1128/iai.73.7.4354-4362.2005.

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ABSTRACT During the systemic phase of murine infection with Salmonella enterica serovar Typhimurium, bacterial virulence is correlated with the ability to grow and survive within host macrophages. Salmonella pathogenicity island 2 (SPI-2), encoding a type three secretion system, has emerged as an important contributor to Salmonella intracellular growth. SPI-2 mutants have been proposed to be more accessible than wild-type Salmonella to oxyradicals generated by the NADPH phagocyte oxidase. We performed mixed infections of mice to investigate the relationship between SPI-2 and SlyA, a transcriptional regulator that confers resistance to oxyradicals. In mixed-infection experiments, the SPI-2 null mutant was severely attenuated in virulence, whereas slyA mutants were only mildly attenuated. Surprisingly, further experiments indicated that the function of SPI-2 was partially dependent on slyA. The intracellular behavior of a slyA mutant in infected cells was consistent with inefficient SPI-2 expression, as formation of Salmonella-induced filaments and the intracellular F-actin meshwork, features that depend on SPI-2, were present at abnormally low frequencies. Furthermore, the translocated levels of the SPI-2 effector SseJ were severely reduced in a strain carrying a mutation in slyA. We used flow cytometry to investigate the role of SlyA in expression of green fluorescent protein (GFP) from transcriptional fusions with promoters of either of two other SPI-2 effector genes, sifB and sifA. The slyA mutant exhibited reduced GFP expression from both promoters. Combining mutations in slyA and other regulators of SPI-2 indicated that SlyA acts through the SsrAB two-component regulatory system. SlyA exhibits partial functional redundancy with OmpR-EnvZ and contributes to the transcriptional response to low osmolarity and the absence of calcium, two environmental stimuli that promote SPI-2 gene expression.

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19

Uchiya, Kei-ichi, and Toshiaki Nikai. "Salmonella Pathogenicity Island 2-Dependent Expression of Suppressor of Cytokine Signaling 3 in Macrophages." Infection and Immunity 73, no. 9 (September 2005): 5587–94. http://dx.doi.org/10.1128/iai.73.9.5587-5594.2005.

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ABSTRACT Salmonella pathogenicity island 2 (SPI-2), which is located at centisome 30.7 on the chromosome of Salmonella enterica serovar Typhimurium, is required for growth within macrophages and systemic infection in mice. We recently reported that the infection of macrophages with Salmonella induces the expression of cyclooxygenase-2 in a manner dependent on SPI-2 (K. Uchiya and T. Nikai, Infect. Immun. 72:6860-6869, 2004). In the present study, gene expression analysis using a cDNA array further showed the involvement of SPI-2 in the expression of suppressor of cytokine signaling 3 (SOCS-3), which is involved in the inhibition of cytokine signaling via the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway. A high level of SOCS-3 expression was induced in J774 macrophages infected with wild-type Salmonella compared to that in macrophages infected with a strain carrying a mutation in the spiC gene within SPI-2. Other members of the SOCS family were not detected in Salmonella-infected macrophages. The SPI-2-induced up-regulation of SOCS-3 expression was dependent on activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway. Furthermore, the inhibition of gamma-interferon-induced STAT-1 and interleukin-6-induced STAT-3 tyrosine phosphorylation correlated with the expression of SOCS-3. Taken together, these results indicate that Salmonella causes SPI-2-dependent activation of ERK1/2, leading to SOCS-3 expression, which in turn inhibits cytokine signaling via the JAK/STAT pathway.

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20

Suvarnapunya, Akamol E., and Murry A. Stein. "DNA base excision repair potentiates the protective effect of Salmonella Pathogenicity Island 2 within macrophages." Microbiology 151, no. 2 (February 1, 2005): 557–67. http://dx.doi.org/10.1099/mic.0.27555-0.

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Reactive oxidants are a primary weapon of the macrophage antibacterial arsenal. The ability of virulent Salmonella to repair oxidative DNA lesions via the base-excision repair system (BER) enables its survival and replication within the macrophage, but is not required for extracellular growth. Salmonella also inhibits the targeting of oxidant generators to the Salmonella-containing vacuole (SCV) via Salmonella Pathogenicity Island 2 (SPI2). Accordingly, the relative contributions of these two discrete systems to Salmonella resistance to both oxidative mutagenesis and lethality within RAW 264.7 macrophages were investigated. A mutant unable to initiate BER was constructed by deleting all three BER bifunctional glycosylases (Δfpg/nth/nei), and was significantly impaired for early intramacrophage survival. Mutations in various SPI2 effector (sifA and sseEFG) and structural (ssaV) genes were then analysed in the BER mutant background. Loss of SPI2 function alone appeared to increase macrophage-induced mutation. Statistical analyses of the reduced intramacrophage survival of SPI2 mutants and the corresponding SPI2/BER mutants indicated a synergistic interaction between BER and SPI2, suggesting that SPI2 promotes intramacrophage survival by protecting Salmonella DNA from exposure to macrophage oxidants. Furthermore, this protection may involve the SseF and SseG effectors. In contrast, the SifA effector did not seem to play a major role in oxidant protection. It is speculated that Salmonella initially stalls oxidative killing by preserving its genomic integrity through the function of BER, until it can upregulate SPI2 to limit its exposure to macrophage oxidants.

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21

Lee, Anthea K., Corrella S. Detweiler, and Stanley Falkow. "OmpR Regulates the Two-Component System SsrA-SsrB in Salmonella Pathogenicity Island 2." Journal of Bacteriology 182, no. 3 (February 1, 2000): 771–81. http://dx.doi.org/10.1128/jb.182.3.771-781.2000.

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ABSTRACT Salmonella pathogenicity island 2 (SPI-2) encodes a putative, two-component regulatory system, SsrA-SsrB, which regulates a type III secretion system needed for replication inside macrophages and systemic infection in mice. The sensor and regulator homologs,ssrAB (spiR), and genes within the secretion system, including the structural gene ssaH, are transcribed after Salmonella enters host cells. We have studied the transcriptional regulation of ssrAB and the secretion system by using gfp fusions to the ssrA andssaH promoters. We found that early transcription ofssrA, after entry into macrophages, is most efficient in the presence of OmpR. An ompR mutant strain does not exhibit replication within cultured macrophages. Furthermore, footprint analysis shows that purified OmpR protein binds directly to thessrA promoter region. We also show that minimal medium, pH 4.5, induces SPI-2 gene expression in wild-type but notompR mutant strains. We conclude that the type III secretion system of SPI-2 is regulated by OmpR, which activates expression of ssrA soon after Salmonella enters the macrophage.

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22

Kuhle, Volker, Garth L. Abrahams, and Michael Hensel. "Intracellular Salmonella enterica Redirect Exocytic Transport Processes in a Salmonella Pathogenicity Island 2-Dependent Manner." Traffic 7, no. 6 (April 21, 2006): 716–30. http://dx.doi.org/10.1111/j.1600-0854.2006.00422.x.

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23

Uchiya, Kei-ichi, Eduardo A. Groisman, and Toshiaki Nikai. "Involvement of Salmonella Pathogenicity Island 2 in the Up-Regulation of Interleukin-10 Expression in Macrophages: Role of Protein Kinase A Signal Pathway." Infection and Immunity 72, no. 4 (April 2004): 1964–73. http://dx.doi.org/10.1128/iai.72.4.1964-1973.2004.

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ABSTRACT Salmonellae are facultative intracellular bacteria capable of surviving within macrophages. Salmonella pathogenicity island 2 (SPI-2) is required for growth within macrophages and for virulence in mice. In this study, we show the involvement of SPI-2 in a signal transduction pathway that induces cytokine expression in Salmonella-infected macrophages. High levels of interleukin-10 (IL-10) mRNA were induced in macrophages by infection with wild-type salmonellae compared to a strain carrying a mutation in the spiC gene, which is encoded within SPI-2. The two strains had the same effect on the expression of proinflammatory cytokines such as IL-1α, IL-6, and tumor necrosis factor alpha. IL-10 expression was dose dependently blocked by treatment of infected macrophages with the protein kinase A (PKA) inhibitor H-89, while IL-10 expression was increased by the PKA activator dibutyryl cyclic AMP. Cyclic AMP-dependent PKA activity was higher in macrophages infected with wild-type salmonellae compared to the spiC mutant, and Ser132 phosphorylation of cyclic AMP response element-binding protein (CREB), which is an important mediator of PKA activation, correlated with the levels of PKA activity. Taken together, these results indicate that salmonellae cause an SPI-2-dependent increase in PKA activity that leads to CREB phosphorylation, resulting in up-regulation of IL-10 expression in Salmonella-infected macrophages. Suppression of IL-10 expression by an antisense oligonucleotide did not affect the growth of wild-type salmonellae within macrophages, whereas growth was dose dependently inhibited by H-89, suggesting that the PKA signaling pathway plays a significant role in intramacrophage Salmonella survival.

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24

Bleasdale, Benjamin, Penelope J. Lott, Aparna Jagannathan, Mark P. Stevens, Richard J. Birtles, and Paul Wigley. "The Salmonella Pathogenicity Island 2-Encoded Type III Secretion System Is Essential for the Survival of Salmonella enterica Serovar Typhimurium in Free-Living Amoebae." Applied and Environmental Microbiology 75, no. 6 (January 23, 2009): 1793–95. http://dx.doi.org/10.1128/aem.02033-08.

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ABSTRACT Free-living amoebae represent a potential reservoir and predator of Salmonella enterica. Through the use of type III secretion system (T3SS) mutants and analysis of transcription of selected T3SS genes, we demonstrated that the Salmonella pathogenicity island 2 is highly induced during S. enterica serovar Typhimurium infection of Acanthamoeba polyphaga and is essential for survival within amoebae.

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25

Husseiny, Mohamed I., Florian Wartha, and Michael Hensel. "Recombinant vaccines based on translocated effector proteins of Salmonella Pathogenicity Island 2." Vaccine 25, no. 1 (January 2007): 185–93. http://dx.doi.org/10.1016/j.vaccine.2005.11.020.

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26

McCollister, B. D., T. J. Bourret, J. Jones-Carson та A. Vazquez-Torres. "INTERFERON-γ INHIBITS INTRACELLULAR SALMONELLA PATHOGENICITY ISLAND-2 TRANSCRIPTION VIA NITRIC OXIDE." Journal of Investigative Medicine 52 (січень 2004): S129. http://dx.doi.org/10.1097/00042871-200401001-00284.

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27

Chakravortty, Dipshikha, Manfred Rohde, Lorenz Jäger, Jörg Deiwick, and Michael Hensel. "Formation of a novel surface structure encoded by Salmonella Pathogenicity Island 2." EMBO Journal 24, no. 11 (May 12, 2005): 2043–52. http://dx.doi.org/10.1038/sj.emboj.7600676.

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28

Nanton, Minelva, Shaikh Atif, Seung-Joo Lee, Justin Taylor, Sean-Paul Nuccio, Sing Sing Way, and Stephen McSorley. "Inhibition of B and T cell responses by Salmonella Pathogenicity Island II (P3124)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 186.9. http://dx.doi.org/10.4049/jimmunol.190.supp.186.9.

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Abstract New vaccines against NTS and typhoid are urgently required and human and mouse infection models indicate a critical role for CD4+ T cells and B cells in protective immunity. Previous studies also suggest that live Salmonella can actively inhibit host protective immunity, but the mechanism remains poorly defined. Here, we utilized a novel OVA-B cell tetramer approach to examine the antigen-specific B cell response to live Salmonella-OVA vaccination. OVA-B cell expansion and germinal center formation were delayed until 45 days in vaccinated mice, suggesting active inhibition by bacteria. The Salmonella Pathogenicity Island II locus has been implicated in culling CD4+T cell responses during live vaccination. Thus, we examined the effect of the SPI2 locus on B cell responses by concurrently infecting mice with a ΔSPI2 mutant, immunizing with OVA protein and measuring the expansion and germinal center formation of OVA-B cells. Wildtype, and not ΔSPI2, Salmonella inhibited expansion of OVA-specific B cells 7 days after immunization. The results of this work suggest two dilemmas for Salmonella vaccination. 1. SPI2 effectors cause a sub-optimal Salmonella-specific B and T cell response during live vaccination. 2. Subunit vaccination in conjunction with active Salmonella infection, may elicit a weaker immune response to the administered vaccine. Studies are underway to identify the SPI2 effector protein responsible for dampening Salmonella-specific adaptive immune responses.

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29

Figueira, Rita, and David W. Holden. "Functions of the Salmonella pathogenicity island 2 (SPI-2) type III secretion system effectors." Microbiology 158, no. 5 (May 1, 2012): 1147–61. http://dx.doi.org/10.1099/mic.0.058115-0.

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30

Boichenko, M. N., E. V. Budanova, E. O. Kravtsova, E. V. Volchkova, and O. F. Belaya. "Some molecular mechanisms of development typhoid fever persistence infection." Infekcionnye bolezni 18, no. 2 (2020): 84–87. http://dx.doi.org/10.20953/1729-9225-2020-2-84-87.

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The overview presents data on the development of typhoid fever persistence infection associated with the expression of genes specific for S. Typhi pathogenicity island 7 (OSP7). Development of is linked with expression of Salmonella pathogenicity island 7 (SPI7), which is specific for S. Typhi. Expression of the gene tviA from SPI7 promotes S. Typhi to escape recognition by immune system. Other 4 genes of SPI7 are linked with synthesis and secretion of typhoid genotoxin, which by inducing demage of immune cells DNA, is putative cause development of persistence infection. Key words: S. Typhi, SPI7, gene tviA, typhoid genotoxin, chronic infection

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31

Choi, J., D. Shin, H. Yoon, J. Kim, C. R. Lee, M. Kim, Y. J. Seok, and S. Ryu. "Salmonella pathogenicity island 2 expression negatively controlled by EIIANtr-SsrB interaction is required for Salmonella virulence." Proceedings of the National Academy of Sciences 107, no. 47 (November 8, 2010): 20506–11. http://dx.doi.org/10.1073/pnas.1000759107.

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32

Yin, Junlei, Zhao Cheng, Yuchen Wu, Qunli He, Jingjing Zhang, Zhanfeng Yang, Shuming Ding, Jizong Li, and Dongguang Guo. "Characterization and protective efficacy of a Salmonella pathogenicity island 2 (SPI2) mutant of Salmonella Paratyphi A." Microbial Pathogenesis 137 (December 2019): 103795. http://dx.doi.org/10.1016/j.micpath.2019.103795.

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33

Pfeifer, Cheryl G., Sandra L. Marcus, Olivia Steele-Mortimer, Leigh A. Knodler, and B. Brett Finlay. "Salmonella typhimurium Virulence Genes Are Induced upon Bacterial Invasion into Phagocytic and Nonphagocytic Cells." Infection and Immunity 67, no. 11 (November 1, 1999): 5690–98. http://dx.doi.org/10.1128/iai.67.11.5690-5698.1999.

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ABSTRACT Survival and growth of salmonellae within host cells are important aspects of bacterial virulence. We have developed an assay to identifySalmonella typhimurium genes that are induced insideSalmonella-containing vacuoles within macrophage and epithelial cells. A promoterless luciferase gene cassette was inserted randomly into the Salmonella chromosome, and the resulting mutants were screened for genes upregulated in intracellular bacteria compared to extracellular bacteria. We identified four genes inS. typhimurium that were upregulated upon bacterial invasion of both phagocytic and nonphagocytic cells. Expression of these genes was not induced by factors secreted by host cells or media alone. All four genes were induced at early time points (2 to 4 h) postinvasion and continued to be upregulated within host cells at later times (5 to 7 h). One mutant contained an insertion in thessaR gene, within Salmonella pathogenicity island 2 (SPI-2), which abolished bacterial virulence in a murine typhoid model. Two other mutants contained insertions within SPI-5, one in the sopB/sigD gene and the other in a downstream gene,pipB. The insertions within SPI-5 resulted in the attenuation of S. typhimurium in the mouse model. The fourth mutant contained an insertion within a previously undescribed region of the S. typhimurium chromosome, iicA(induced intracellularly A). We detected no effect on virulence as a result of this insertion. In conclusion, all but one of the genes identified in this study were virulence factors within pathogenicity islands, illustrating the requirement for specific gene expression inside mammalian cells and indicating the key role that virulence factor regulation plays in Salmonella pathogenesis.

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34

Bispham, J., B. N. Tripathi, P. R. Watson, and T. S. Wallis. "Salmonella Pathogenicity Island 2 Influences Both Systemic Salmonellosis andSalmonella-Induced Enteritis in Calves." Infection and Immunity 69, no. 1 (January 1, 2001): 367–77. http://dx.doi.org/10.1128/iai.69.1.367-377.2001.

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ABSTRACT We have used signature-tagged mutagenesis to identify mutants of the host-specific Salmonella enterica serotype Dublin which were avirulent in calves and/or BALB/c mice. A mutant with a transposon insertion in the sseD gene ofSalmonella pathogenicity island 2 (SPI-2), which encodes a putative secreted effector protein, was identified. This mutant was recovered from the bovine host but not from the murine host following infection with a pool of serotype Dublin mutants. However, a pure inoculum of the sseD mutant was subsequently shown to be attenuated in calves following infection either by the intravenous route or by the oral route. The sseD mutant was fully invasive for bovine intestinal mucosa but was subsequently unable to proliferate to the same numbers as the parental strain in vivo. Both the sseD mutant and a second SPI-2 mutant, with a transposon insertion in the ssaT gene, induced significantly weaker secretory and inflammatory responses in bovine ligated ileal loops than did the parental strain. These results demonstrate that SPI-2 is required by serotype Dublin for the induction of both systemic and enteric salmonellosis in calves.

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35

McCollister, B. D., T. J. Bourret, J. Jones-Carson та A. Vazquez-Torres. "284 INTERFERON-γ INHIBITS INTRACELLULAR SALMONELLA PATHOGENICITY ISLAND-2 TRANSCRIPTION VIA NITRIC OXIDE." Journal of Investigative Medicine 52, Suppl 1 (1 січня 2004): S129.2—S129. http://dx.doi.org/10.1136/jim-52-suppl1-284.

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36

Waterman, Scott R., and David W. Holden. "Functions and effectors of the Salmonella pathogenicity island 2 type III secretion system." Cellular Microbiology 5, no. 8 (August 2003): 501–11. http://dx.doi.org/10.1046/j.1462-5822.2003.00294.x.

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37

Hensel, Michael, Thomas Nikolaus, and Christine Egelseer. "Molecular and functional analysis indicates a mosaic structure of Salmonella pathogenicity island 2." Molecular Microbiology 31, no. 2 (January 1999): 489–98. http://dx.doi.org/10.1046/j.1365-2958.1999.01190.x.

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38

Suvarnapunya, Akamol E., Daniel V. Zurawski, Rebecca L. Guy, and Murry A. Stein. "Molecular Characterization of the Prototrophic Salmonella Mutants Defective for Intraepithelial Replication." Infection and Immunity 71, no. 4 (April 2003): 2247–52. http://dx.doi.org/10.1128/iai.71.4.2247-2252.2003.

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ABSTRACT Three MudJ prototrophs demonstrated that intracellular replication is a Salmonella virulence trait (K. Y. Leung and B. B. Finlay, Proc. Natl. Acad. Sci. USA, 88:11470-11474, 1991). mutS and mutH are disrupted in mutants 3-11 and 12-23, and ssaQ is disrupted in mutant 17-21. Further analysis revealed that loss of Salmonella pathogenicity island 2 function underlies the intracellular replication defect of 3-11 and 17-21.

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39

Bruce, Hayley L., Paul A. Barrow, and Andrew N. Rycroft. "Zoonotic potential of Salmonella enterica carried by pet tortoises." Veterinary Record 182, no. 5 (December 7, 2017): 141. http://dx.doi.org/10.1136/vr.104457.

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The prevalence of Salmonella in chelonians is not known in the UK and it is not clear whether such Salmonella strains would be pathogenic for human beings. Some strains, such as members of the Arizonae subgroup, may be unable to cause anything more than very mild disease. To determine the carriage of Salmonella in pet tortoises, cloacal swabs were taken for culture. Salmonella enterica Group D was isolated from 5 of the 89 samples. All five were from the same household of seven tortoises. Salmonella isolates were shown by PCR to carry the invA and spiC genes associated with pathogenicity islands 1 and 2. Each isolate carried both genes indicating they had the genetic basis for disease and enterocyte invasion in human beings. The study indicates a low rate of asymptomatic carriage among the general population of pet tortoises. However, it does suggest that those Salmonella strains colonising the tortoise can carry Salmonellapathogenicity island (SPI)-1 and SPI-2 conferring the potential to cause disease in human beings and other animals.

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40

Núñez-Hernández, Cristina, Ana Alonso, M. Graciela Pucciarelli, Josep Casadesús, and Francisco García-del Portillo. "Dormant Intracellular Salmonella enterica Serovar Typhimurium Discriminates among Salmonella Pathogenicity Island 2 Effectors To Persist inside Fibroblasts." Infection and Immunity 82, no. 1 (October 21, 2013): 221–32. http://dx.doi.org/10.1128/iai.01304-13.

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ABSTRACTSalmonella entericauses effector proteins delivered by type III secretion systems (TTSS) to colonize eukaryotic cells. Recentin vivostudies have shown that intracellular bacteria activate the TTSS encoded bySalmonellapathogenicity island-2 (SPI-2) to restrain growth inside phagocytes. Growth attenuation is also observedin vivoin bacteria colonizing nonphagocytic stromal cells of the intestinal lamina propria and in cultured fibroblasts. SPI-2 is required for survival of nongrowing bacteria persisting inside fibroblasts, but its induction mode and the effectors involved remain unknown. Here, we show that nongrowing dormant intracellular bacteria use the two-component system OmpR-EnvZ to induce SPI-2 expression and the PhoP-PhoQ system to regulate the time at which induction takes place, 2 h postentry. Dormant bacteria were shown to discriminate the usage of SPI-2 effectors. Among the effectors tested, SseF, SseG, and SseJ were required for survival, while others, such as SifA and SifB, were not. SifA and SifB dispensability correlated with the inability of intracellular bacteria to secrete these effectors even when overexpressed. Conversely, SseJ overproduction resulted in augmented secretion and exacerbated bacterial growth. Dormant bacteria produced other effectors, such as PipB and PipB2, that, unlike what was reported for epithelial cells, did not to traffic outside the phagosomal compartment. Therefore, permissiveness for secreting only a subset of SPI-2 effectors may be instrumental for dormancy. We propose that theS. entericaserovar Typhimurium nonproliferative intracellular lifestyle is sustained by selection of SPI-2 effectors that are produced in tightly defined amounts and delivered to phagosome-confined locations.

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41

Noster, Janina, Tzu-Chiao Chao, Nathalie Sander, Marc Schulte, Tatjana Reuter, Nicole Hansmeier, and Michael Hensel. "Proteomics of intracellular Salmonella enterica reveals roles of Salmonella pathogenicity island 2 in metabolism and antioxidant defense." PLOS Pathogens 15, no. 4 (April 22, 2019): e1007741. http://dx.doi.org/10.1371/journal.ppat.1007741.

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42

Silphaduang, Umaporn, Mariola Mascarenhas, Mohamed Karmali, and Brian K. Coombes. "Repression of Intracellular Virulence Factors in Salmonella by the Hha and YdgT Nucleoid-Associated Proteins." Journal of Bacteriology 189, no. 9 (February 16, 2007): 3669–73. http://dx.doi.org/10.1128/jb.00002-07.

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ABSTRACT The Hha/YmoA family of nucleoid-associated proteins is involved in gene regulation in enterobacteria. In Salmonella enterica serovar Typhimurium, virulence genes required for intracellular growth are induced following host cell invasion but the proteins responsible for repressing these genes prior to host cell entry have not been fully identified. We demonstrate here that Hha is the major repressor responsible for silencing virulence genes carried in Salmonella pathogenicity island 2 prior to bacteria sensing an intracellular environmental cue.

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43

Vikram, Amit, Guddadarangavvanahally K. Jayaprakasha, Palmy R. Jesudhasan, Suresh D. Pillai, and Bhimanagouda S. Patil. "Obacunone Represses Salmonella Pathogenicity Islands 1 and 2 in anenvZ-Dependent Fashion." Applied and Environmental Microbiology 78, no. 19 (July 27, 2012): 7012–22. http://dx.doi.org/10.1128/aem.01326-12.

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ABSTRACTObacunone belongs to a class of unique triterpenoids called limonoids, present inCitrusspecies. Previous studies from our laboratory suggested that obacunone possesses antivirulence activity and demonstrates inhibition of cell-cell signaling inVibrio harveyiandEscherichia coliO157:H7. The present work sought to determine the effect of obacunone on the food-borne pathogenSalmonella entericaserovar Typhimurium LT2 by using a cDNA microarray. Transcriptomic studies indicated that obacunone repressesSalmonellapathogenicity island 1 (SPI1), the maltose transporter, and the hydrogenase operon. Furthermore, phenotypic data for the Caco-2 infection assay and maltose utilization were in agreement with microarray data suggesting repression of SPI1 and maltose transport. Further studies demonstrated that repression of SPI1 was plausibly mediated throughhilA. Additionally, obacunone seems to repress SPI2 under SPI2-inducing conditions as well as in Caco-2 infection models. Furthermore, obacunone seems to represshilAin an EnvZ-dependent fashion. Altogether, the results of the study seems to suggest that obacunone exerts an antivirulence effect onS.Typhimurium and may serve as a lead compound for development of antivirulence strategies forS.Typhimurium.

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44

Kim, Charles C., and Stanley Falkow. "Delineation of Upstream Signaling Events in the Salmonella Pathogenicity Island 2 Transcriptional Activation Pathway." Journal of Bacteriology 186, no. 14 (July 15, 2004): 4694–704. http://dx.doi.org/10.1128/jb.186.14.4694-4704.2004.

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ABSTRACT Survival and replication in the intracellular environment are critical components of the ability of Salmonella enterica serovar Typhimurium to establish systemic infection in the murine host. Intracellular survival is mediated by a number of genetic loci, including Salmonella pathogenicity island 2 (SPI2). SPI2 is a 40-kb locus encoding a type III secretion system that secretes effector molecules, which permits bacterial survival and replication in the intracellular environment of host cells. A two-component regulatory system, ssrAB, is also encoded in SPI2 and controls expression of the secretion system and effectors. While the environmental signals to which SPI2 responds in vivo are not known, activation of expression is dependent on OmpR and can be stimulated in vitro by chelation of cations or by a shift from rich to acidic minimal medium. In this work, we demonstrated that SPI2 activation is associated with OmpR in the phosphorylated form (OmpR-P). Mutations in envZ and ackA-pta, which disrupted two distinct sources of OmpR phosphorylation, indicated that SPI2 activation by chelators or a shift from rich to acidic minimal medium is largely dependent on functional EnvZ. In contrast, the PhoPQ pathway is not required for SPI2 activation in the presence of OmpR-P. As in the case of in vitro stimulation, SPI2 expression in macrophages correlates with the presence of OmpR-P. Additionally, EnvZ, but not acetyl phosphate, is required for maximal expression of SPI2 in the intracellular environment, suggesting that the in vitro SPI2 activation pathway is the same as that used in vivo.

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45

Wisner, Amanda L. S., Taseen S. Desin, Po-King S. Lam, Emil Berberov, Claudia S. Mickael, Hugh G. Townsend, Andrew A. Potter, and Wolfgang Köster. "Immunization of chickens with Salmonella enterica subspecies enterica serovar Enteritidis pathogenicity island-2 proteins." Veterinary Microbiology 153, no. 3-4 (December 2011): 274–84. http://dx.doi.org/10.1016/j.vetmic.2011.05.041.

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46

Coombes, Brian K., Nat F. Brown, Sonya Kujat-Choy, Bruce A. Vallance, and B. Brett Finlay. "SseA is required for translocation of Salmonella pathogenicity island-2 effectors into host cells." Microbes and Infection 5, no. 7 (June 2003): 561–70. http://dx.doi.org/10.1016/s1286-4579(03)00094-7.

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47

Deekshit, Vijaya Kumar, Ballamoole Krishna Kumar, Praveen Rai, Anusha Rohit, and Indrani Karunasagar. "Simultaneous detection of Salmonella pathogenicity island 2 and its antibiotic resistance genes from seafood." Journal of Microbiological Methods 93, no. 3 (June 2013): 233–38. http://dx.doi.org/10.1016/j.mimet.2013.03.015.

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48

McCollister, B. D., T. J. Bourret, J. Jones-Carson та A. Vazquez-Torres. "Interferon-γ Inhibits Intracellular Salmonella Pathogenicity Island-2 Transcription Via Nitric Oxide". Journal of Investigative Medicine 52, № 1_suppl_part_2 (січень 2001): 129. http://dx.doi.org/10.1177/108155890105201s284.

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49

Forest, Chantal G., Elyse Ferraro, Sébastien C. Sabbagh, and France Daigle. "Intracellular survival of Salmonella enterica serovar Typhi in human macrophages is independent of Salmonella pathogenicity island (SPI)-2." Microbiology 156, no. 12 (December 1, 2010): 3689–98. http://dx.doi.org/10.1099/mic.0.041624-0.

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For successful infection, Salmonella enterica secretes and injects effector proteins into host cells by two distinct type three secretion systems (T3SSs) located on Salmonella pathogenicity islands (SPIs)-1 and -2. The SPI-2 T3SS is involved in intracellular survival of S. enterica serovar Typhimurium and systemic disease. As little is known regarding the function of the SPI-2 T3SS from S. enterica serovar Typhi, the aetiological agent of typhoid fever, we investigated its role for survival in human macrophages. Mutations in the translocon (sseB), basal secretion apparatus (ssaR) and regulator (ssrB) did not result in any reduction in survival under many of the conditions tested. Similar results were obtained with another S. Typhi strain or by using human primary cells. Results were corroborated based on complete deletion of the SPI-2 T3SS. Surprisingly, the data suggest that the SPI-2 T3SS of S. Typhi is not required for survival in human macrophages.

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50

Ho, Theresa D., Nara Figueroa-Bossi, Minhua Wang, Sergio Uzzau, Lionello Bossi, and James M. Slauch. "Identification of GtgE, a Novel Virulence Factor Encoded on the Gifsy-2 Bacteriophage of Salmonella enterica Serovar Typhimurium." Journal of Bacteriology 184, no. 19 (October 1, 2002): 5234–39. http://dx.doi.org/10.1128/jb.184.19.5234-5239.2002.

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ABSTRACT The Gifsy-2 temperate bacteriophage of Salmonella enterica serovar Typhimurium contributes significantly to the pathogenicity of strains that carry it as a prophage. Previous studies have shown that Gifsy-2 encodes SodCI, a periplasmic Cu/Zn superoxide dismutase, and at least one additional virulence factor. Gifsy-2 encodes a Salmonella pathogenicity island 2 type III secreted effector protein. Sequence analysis of the Gifsy-2 genome also identifies several open reading frames with homology to those of known virulence genes. However, we found that null mutations in these genes did not individually have a significant effect on the ability of S. enterica serovar Typhimurium to establish a systemic infection in mice. Using deletion analysis, we have identified a gene, gtgE, which is necessary for the full virulence of S. enterica serovar Typhimurium Gifsy-2 lysogens. Together, GtgE and SodCI account for the contribution of Gifsy-2 to S. enterica serovar Typhimurium virulence in the murine model.

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