scholarly journals Coordinate Regulation of Salmonella Pathogenicity Island 1 (SPI1) and SPI4 in Salmonella enterica Serovar Typhimurium

2007 ◽  
Vol 76 (3) ◽  
pp. 1024-1035 ◽  
Author(s):  
Kara L. Main-Hester ◽  
Katherine M. Colpitts ◽  
Gracie A. Thomas ◽  
Ferric C. Fang ◽  
Stephen J. Libby
Keyword(s):  
Mutant Strain ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Pathogenicity Island ◽  
Open Reading Frames ◽  
Type I ◽  
Coordinate Regulation ◽  
Serovar Typhimurium ◽  
Epithelial Invasion ◽  
Secretory System

ABSTRACT Salmonella enterica serovar Typhimurium harbors five pathogenicity islands (SPI) required for infection in vertebrate hosts. Although the role of SPI1 in promoting epithelial invasion and proinflammatory cell death has been amply documented, SPI4 has only more recently been implicated in Salmonella virulence. SPI4 is a 24-kb pathogenicity island containing six open reading frames, siiA to siiF. Secretion of the 595-kDa SiiE protein requires a type I secretory system encoded by siiC, siiD, and siiF. An operon polarity suppressor (ops) sequence within the 5′ untranslated region upstream of siiA is required for optimal SPI4 expression and predicted to bind the antiterminator RfaH. SiiE concentrations are decreased in a SPI1 mutant strain, suggesting that SPI1 and SPI4 may have common regulatory inputs. SPI1 gene expression is positively regulated by the transcriptional activators HilA, HilC, and HilD, encoded within SPI1, and negatively regulated by the regulators HilE and PhoP. Here, we show that mutations in hilA, hilC, or hilD similarly reduce expression of siiE, and mutations in hilE or phoP enhance siiE expression. Individual overexpression of HilA, HilC, or HilD in the absence of SPI1 cannot activate siiE expression, suggesting that these transcriptional regulators act in concert or in combination with additional SPI1-encoded regulatory loci to activate SPI4. HilA is no longer required for siiE expression in an hns mutant strain, suggesting that HilA promotes SPI4 expression by antagonizing the global transcriptional silencer H-NS. Coordinate regulation suggests that SPI1 and SPI4 play complementary roles in the interaction of S. enterica serovar Typhimurium with the host intestinal mucosa.

scholarly journals SiiE Is Secreted by the Salmonella enterica Serovar Typhimurium Pathogenicity Island 4-Encoded Secretion System and Contributes to Intestinal Colonization in Cattle

2007 ◽  
Vol 75 (3) ◽  
pp. 1524-1533 ◽  
Author(s):  
Eirwen Morgan ◽  
Alison J. Bowen ◽  
Sonya C. Carnell ◽  
Timothy S. Wallis ◽  
Mark P. Stevens
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Pathogenicity Island ◽  
Secretion System ◽  
Type I ◽  
Intestinal Colonization ◽  
Serovar Typhimurium

ABSTRACT Here we report that Salmonella enterica serovar Typhimurium pathogenicity island 4 carries a type I secretion system (siiCDF) which secretes an ∼600-kDa protein (encoded by siiE). SiiE is surface expressed, and its production is regulated by HilA. SiiE and SiiF influence colonization in cattle and the invasion of bovine enterocytes.

scholarly journals Type I interferon induces necroptosis in macrophages during infection with Salmonella enterica serovar Typhimurium

2012 ◽  
Vol 13 (10) ◽  
pp. 954-962 ◽  
Author(s):  
Nirmal Robinson ◽  
Scott McComb ◽  
Rebecca Mulligan ◽  
Renu Dudani ◽  
Lakshmi Krishnan ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Type I Interferon ◽  
Type I ◽  
Serovar Typhimurium

scholarly journals Early Epithelial Invasion by Salmonella enterica Serovar Typhimurium DT104 in the Swine Ileum

2002 ◽  
Vol 39 (6) ◽  
pp. 712-720 ◽  
Author(s):  
D. K. Meyerholz ◽  
T. J. Stabel ◽  
M. R. Ackermann ◽  
S. A. Carlson ◽  
B. D. Jones ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Bacterial Invasion ◽  
M Cells ◽  
Cellular Invasion ◽  
Sem And Tem ◽  
Serovar Typhimurium ◽  
Specific Affinity ◽  
Epithelial Invasion ◽  
Cell Extrusion

Salmonella enterica serovar Typhimurium is an important intestinal pathogen in swine. This study was performed to document the early cellular invasion of Salmonella serovar Typhimurium in swine ileum. Ileal gut-loops were surgically prepared in ten 4- to 5-week-old mixed-breed pigs and inoculated for 0-60 minutes. Loops were harvested and prepared for both scanning and transmission electron microscopy (SEM and TEM, respectively). Preferential bacterial adherence to microfold cells (M cells) was seen within 5 minutes, and by 10 minutes bacterial invasion of the apical membrane was seen in M cells, goblet cells, and enterocytes. This multicellular invasion was observed throughout the course of infection. In addition, SEM revealed a specific affinity of Salmonella serovar Typhimurium to sites of cell extrusion. Using TEM, bacteria in these areas were focused in the crevices formed by the extruding cell and the adjacent cells and in the cytoplasm immediately beneath the extruding cell. Our results suggest that early cellular invasion by Salmonella serovar Typhimurium is nonspecific and rapid in swine. Furthermore, the combination of SEM and TEM data suggests that Salmonella serovar Typhimurium may use sites of cell extrusion as an additional mechanism for early invasion.

scholarly journals Identification of GtgE, a Novel Virulence Factor Encoded on the Gifsy-2 Bacteriophage of Salmonella enterica Serovar Typhimurium

2002 ◽  
Vol 184 (19) ◽  
pp. 5234-5239 ◽  
Author(s):  
Theresa D. Ho ◽  
Nara Figueroa-Bossi ◽  
Minhua Wang ◽  
Sergio Uzzau ◽  
Lionello Bossi ◽  
...  
Keyword(s):  
Virulence Factor ◽  
Salmonella Enterica ◽  
Virulence Genes ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Systemic Infection ◽  
Open Reading Frames ◽  
Effector Protein ◽  
Protein Sequence Analysis ◽  
Serovar Typhimurium ◽  
Reading Frames

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.

scholarly journals Transcriptional Organization and Function of Invasion Genes within Salmonella enterica Serovar Typhimurium Pathogenicity Island 1, Including the prgH,prgI, prgJ, prgK, orgA,orgB, and orgC Genes

2000 ◽  
Vol 68 (6) ◽  
pp. 3368-3376 ◽  
Author(s):  
Joanna R. Klein ◽  
Thomas F. Fahlen ◽  
Bradley D. Jones
Keyword(s):  
Epithelial Cells ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Pathogenicity Island ◽  
Pcr Analysis ◽  
Intestinal Epithelial ◽  
Reading Frame ◽  
Bacterial Proteins ◽  
Serovar Typhimurium ◽  
And Function

ABSTRACT Salmonella enterica serovar Typhimurium initiates infection of a host by inducing its own uptake into specialized M cells which reside within the epithelium overlaying Peyer's patches. Entry of Salmonella into intestinal epithelial cells is dependent upon invasion genes that are clustered together inSalmonella pathogenicity island 1 (SPI-1). Upon contact between serovar Typhimurium and epithelial cells targeted for bacterial internalization, bacterial proteins are injected into the host cell through a type III secretion system that leads to internalization of the bacteria. Previous work has established that the prgH, -I, -J, and -K and orgAgenes reside in SPI-1, and the products of these genes are predicted to be components of the invasion secretion apparatus. We report that an error in the published orgA DNA sequence has been identified so that this region encodes two small genes rather than a single large open reading frame. These genes have been designatedorgA and orgB. Additionally, an opening reading frame downstream of orgB, which we have designatedorgC, has been identified and partially characterized. Previously published work has indicated that the prgH, -I, -J, and -K genes are transcribed from a promoter distinct from that used by the gene immediately downstream, orgA. Here, we present experiments indicating that orgA expression is driven by theprgH promoter. In addition, using reverse transcriptase PCR analysis, we have found that this polycistronic message extends downstream of prgH to include a total of 10 genes. To more fully characterize this invasion operon, we demonstrate that theprgH, prgI, prgJ, prgK,orgA, and orgB genes are each required for invasion and secretion, while orgC is not essential for the invasive phenotype.

scholarly journals HilE Interacts with HilD and Negatively Regulates hilA Transcription and Expression of the Salmonella enterica Serovar Typhimurium Invasive Phenotype

2003 ◽  
Vol 71 (3) ◽  
pp. 1295-1305 ◽  
Author(s):  
M. Aaron Baxter ◽  
Thomas F. Fahlen ◽  
Rebecca L. Wilson ◽  
Bradley D. Jones
Keyword(s):  
Gene Expression ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Gastrointestinal Disease ◽  
Pathogenicity Island ◽  
Specific Gene ◽  
Negative Effects ◽  
Invasive Phenotype ◽  
Serovar Typhimurium ◽  
Two Hybrid

ABSTRACT The ability of Salmonella enterica serovar Typhimurium to traverse the intestinal mucosa of a host is an important step in its ability to initiate gastrointestinal disease. The majority of the genes required for this invasive characteristic are encoded on Salmonella pathogenicity island 1 (SPI1), and their expression is controlled by the transcriptional activator HilA, a member of the OmpR/ToxR family of proteins. A variety of genes (hilC, hilD, fis, sirA/barA, csrAB, phoB, fadD, envZ/ompR, fliZ, hilE, ams, lon, pag, and hha) have been identified that exert positive or negative effects on hilA expression, although the mechanisms by which these gene products function remain relatively unclear. Recent work indicates that the small DNA-binding protein, Hha, has a significant role in repressing hilA transcription and the invasive phenotype, particularly in response to osmolarity signals. We have characterized the Salmonella-specific gene, hilE, and found that it plays an important regulatory role in hilA transcription and invasion gene expression. Mutation of hilE causes derepression of hilA transcription, and overexpression of hilE superrepresses hilA expression and the invasive phenotype. Bacterial two-hybrid experiments indicate that the HilE protein interacts with HilD, suggesting a possible mechanism for HilE negative regulation of hilA gene expression and the Salmonella invasive phenotype. Finally, we have found that the hilE gene resides on a region of the serovar Typhimurium chromosome that has many characteristics of a pathogenicity island.

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