Salmonella enterica serovar Dublin strains which are Vi antigen-positive use type IVB pili for bacterial self-association and human intestinal cell entry

2003 ◽  
Vol 35 (6) ◽  
pp. 279-284 ◽  
Author(s):  
Christina Morris ◽  
Connie K.P Tam ◽  
Timothy S Wallis ◽  
Philip W Jones ◽  
Jim Hackett
Keyword(s):  
Salmonella Enterica ◽  
Cell Entry ◽  
Intestinal Cell ◽  
Self Association ◽  
Salmonella Enterica Serovar Dublin ◽  
Vi Antigen

scholarly journals Whole-Genome Sequences of Two Salmonella enterica Serovar Dublin Strains That Harbor the viaA, viaB, and ompB Loci of the Vi Antigen

2019 ◽  
Vol 8 (14) ◽  
Author(s):  
Manal Mohammed ◽  
Marie-Leone Vignaud ◽  
Sabrina Cadel-Six
Keyword(s):  
Salmonella Enterica ◽  
Capsular Polysaccharide ◽  
Raw Milk ◽  
Genome Sequences ◽  
Polysaccharide Antigen ◽  
Content Type ◽  
Vi Capsular Polysaccharide ◽  
Raw Milk Cheese ◽  
Salmonella Enterica Serovar Dublin ◽  
Vi Antigen

Here, we report the genome sequences of two Salmonella enterica serovar Dublin strains, 03EB8736SAL and 03EB8994SAL, isolated from raw-milk cheese and milk filtrate, respectively. Analysis of the draft genomes of the two isolates reveals the presence of the viaA, viaB, and ompB loci of the Vi capsular polysaccharide antigen (Vi antigen).

scholarly journals Vi Antigen Expression in Salmonella enterica Serovar Typhi Clinical Isolates from Pakistan

2005 ◽  
Vol 43 (3) ◽  
pp. 1158-1165 ◽  
Author(s):  
J. Wain ◽  
D. House ◽  
A. Zafar ◽  
S. Baker ◽  
S. Nair ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Antigen Expression ◽  
Clinical Isolates ◽  
Salmonella Enterica Serovar Typhi ◽  
Vi Antigen

scholarly journals Precise Excision of the Large Pathogenicity Island, SPI7, in Salmonella enterica Serovar Typhi

2004 ◽  
Vol 186 (10) ◽  
pp. 3202-3213 ◽  
Author(s):  
Susan M. Bueno ◽  
Carlos A. Santiviago ◽  
Alejandro A. Murillo ◽  
Juan A. Fuentes ◽  
A. Nicole Trombert ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Pathogenicity Island ◽  
Open Reading Frames ◽  
Epithelial Cell Line ◽  
Direct Repeats ◽  
Salmonella Enterica Serovar Typhi ◽  
Precise Excision ◽  
Join Point ◽  
Reading Frames ◽  
Vi Antigen

ABSTRACT The large pathogenicity island (SPI7) of Salmonella enterica serovar Typhi is a 133,477-bp segment of DNA flanked by two 52-bp direct repeats overlapping the pheU (phenylalanyl-tRNA) gene, contains 151 potential open reading frames, and includes the viaB operon involved in the synthesis of Vi antigen. Some clinical isolates of S. enterica serovar Typhi are missing the entire SPI7, due to its precise excision; these strains have lost the ability to produce Vi antigen, are resistant to phage Vi-II, and invade a human epithelial cell line more rapidly. Excision of SPI7 occurs spontaneously in a clinical isolate of S. enterica serovar Typhi when it is grown in the laboratory, leaves an intact copy of the pheU gene at its novel join point, and results in the same three phenotypic consequences. SPI7 is an unstable genetic element, probably an intermediate in the pathway of lateral transfer of such pathogenicity islands among enteric gram-negative bacteria.

scholarly journals Nature and consequences of interactions between Salmonella enterica serovar Dublin and host cells in cattle

2019 ◽  
Vol 50 (1) ◽  
Author(s):  
Prerna Vohra ◽  
Christina Vrettou ◽  
Jayne C. Hope ◽  
John Hopkins ◽  
Mark P. Stevens
Keyword(s):  
Lymph Nodes ◽  
Salmonella Enterica ◽  
Fluorescent Protein ◽  
Host Cells ◽  
Large Animal ◽  
Ileal Mucosa ◽  
Zoonotic Infections ◽  
Infected Cells ◽  
Green Fluorescent ◽  
Salmonella Enterica Serovar Dublin

AbstractSalmonella enterica is a veterinary and zoonotic pathogen of global importance. While murine and cell-based models of infection have provided considerable knowledge about the molecular basis of virulence of Salmonella, relatively little is known about salmonellosis in naturally-affected large animal hosts such as cattle, which are a reservoir of human salmonellosis. As in humans, Salmonella causes bovine disease ranging from self-limiting enteritis to systemic typhoid-like disease and exerts significant economic and welfare costs. Understanding the nature and consequences of Salmonella interactions with bovine cells will inform the design of effective vaccines and interventions to control animal and zoonotic infections. In calves challenged orally with S. Dublin expressing green fluorescent protein (GFP) we observed that the bacteria were predominantly extracellular in the distal ileal mucosa and within gut-associated lymph nodes 48 h post-infection. Intracellular bacteria, identified by flow cytometry using the GFP signal, were predominantly within MHCII+ macrophage-like cells. In contrast to observations from murine models, these S. Dublin-infected cells had elevated levels of MHCII and CD40 compared to both uninfected cells from the same tissue and cells from the cognate tissue of uninfected animals. Moreover, no gross changes of the architecture of infected lymph nodes were observed as was described previously in a mouse model. In order to further investigate Salmonella-macrophage interactions, net replication of S. enterica serovars that differ in virulence in cattle was measured in bovine blood-derived macrophages by enumeration of gentamicin-protected bacteria and fluorescence dilution, but did not correlate with host-specificity.

scholarly journals Identification of Salmonella enterica Serovar Dublin-Specific Sequences by Subtractive Hybridization and Analysis of Their Role in Intestinal Colonization and Systemic Translocation in Cattle

2008 ◽  
Vol 76 (11) ◽  
pp. 5310-5321 ◽  
Author(s):  
Gillian D. Pullinger ◽  
Francis Dziva ◽  
Bryan Charleston ◽  
Timothy S. Wallis ◽  
Mark P. Stevens
Keyword(s):  
Salmonella Enterica ◽  
Mobile Element ◽  
Subtractive Hybridization ◽  
Pcr Analysis ◽  
Ileal Mucosa ◽  
Significant Attenuation ◽  
Salmonella Enterica Serovar Dublin ◽  
Specific Sequences

ABSTRACTSalmonella entericaserovar Dublin is a host-restricted serovar associated with typhoidal disease in cattle. In contrast, the fowl-associated serovarS. entericaserovar Gallinarum is avirulent in calves, yet it invades ileal mucosa and induces enteritis at levels comparable to those induced byS. entericaserovar Dublin. Suppression subtractive hybridization was employed to identifyS. entericaserovar Dublin strain SD3246 genes absent fromS. entericaserovar Gallinarum strain SG9. Forty-oneS. entericaserovar Dublin fragments were cloned and sequenced. Among these, 24 mobile-element-associated genes were identified, and 12 clones exhibited similarity with sequences of known or predicted function in other serovars. ThreeS. entericaserovar Dublin-specific regions were homologous to regions from the genome ofEnterobactersp. strain 638. Sequencing of fragments adjacent to these three sequences revealed the presence of a 21-kb genomic island, designatedS. entericaserovar Dublin island 1 (SDI-1). PCR analysis and Southern blotting showed that SDI-1 is highly conserved withinS. entericaserovar Dublin isolates but rarely found in other serovars. To probe the role of genes identified by subtractive hybridization in vivo, 24 signature-taggedS. entericaserovar Dublin SD3246 mutants lacking loci not present inSalmonellaserovar Gallinarum SG9 were created and screened by oral challenge of cattle. Though attenuation of tagged SG9 and SD3246Salmonellapathogenicity island-1 (SPI-1) and SPI-2 mutant strains was detected, no obvious defects of these 24 mutants were detected. Subsequently, a ΔSDI-1 mutant was found to exhibit weak but significant attenuation compared with the parent strain in coinfection of calves. SDI-1 mutation did not impair invasion, intramacrophage survival, or virulence in mice, implying that SDI-1 does not influence fitness per se and may act in a host-specific manner.

scholarly journals Genome Sequences of Multidrug-Resistant Salmonella enterica Serovar Dublin Isolates

2019 ◽  
Vol 8 (31) ◽  
Author(s):  
Baha Abdalhamid ◽  
Emily L. Mccutchen ◽  
Kacie D. Flaherty ◽  
Steven H. Hinrichs ◽  
Peter C. Iwen
Keyword(s):  
Antimicrobial Resistance ◽  
Salmonella Enterica ◽  
Draft Genome ◽  
Multidrug Resistant ◽  
Genome Sequences ◽  
Content Type ◽  
Resistance Determinants ◽  
Human Samples ◽  
Systemic Infections ◽  
Salmonella Enterica Serovar Dublin

Salmonella enterica serovar Dublin, which can cause enteritis and systemic infections in humans, has been associated with antimicrobial resistance. Here, we report draft genome sequences of seven multidrug-resistant S. Dublin isolates from human samples. These sequences will contribute to an understanding of pathogenesis and resistance determinants in this serovar.

scholarly journals Piracy of Decay-Accelerating Factor (CD55) Signal Transduction by the Diffusely Adhering Strain Escherichia coli C1845 Promotes Cytoskeletal F-Actin Rearrangements in Cultured Human Intestinal INT407 Cells

1998 ◽  
Vol 66 (9) ◽  
pp. 4036-4042 ◽  
Author(s):  
Isabelle Peiffer ◽  
Alain L. Servin ◽  
Marie-Françoise Bernet-Camard
Keyword(s):  
Escherichia Coli ◽  
Signal Transduction ◽  
Protein Tyrosine Kinase ◽  
Cell Entry ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Decay Accelerating Factor ◽  
E Coli ◽  
Intestinal Cell Line ◽  
Fimbrial Adhesin

ABSTRACT Diffusely adhering Escherichia coli (DAEC) C1845 (clinical isolate) harboring the fimbrial adhesin F1845 can infect cultured human differentiated intestinal epithelial cells; this process is followed by the disassembly of the actin network in the apical domain. The aim of this study was to examine the mechanism by which DAEC C1845 promotes F-actin rearrangements. For this purpose, we used a human embryonic intestinal cell line (INT407) expressing the membrane-associated glycosylphosphatidylinositol (GPI) protein-anchored decay-accelerating factor (DAF), the receptor of the F1845 adhesin. We show here that infection of INT407 cells by DAEC C1845 can provoke dramatic F-actin rearrangements without cell entry. Clustering of phosphotyrosines was observed, revealing that the DAEC C1845-DAF interaction involves the recruitment of signal transduction molecules. A pharmacological approach with a subset of inhibitors of signal transduction molecules was used to identify the cascade of signal transduction molecules that are coupled to the DAF, that are activated upon infection, and that promote the F-actin rearrangements. DAEC C1845-induced F-actin rearrangements can be blocked dose dependently by protein tyrosine kinase, phospholipase Cγ, phosphatidylinositol 3-kinase, protein kinase C, and Ca2+inhibitors. F-actin rearrangements and blocking by inhibitors were observed after infection of the cells with two E. colirecombinants carrying the plasmids containing the fimbrial adhesin F1845 or the fimbrial hemagglutinin Dr, belonging to the same family of adhesins. These findings show that the DAEC Dr family of pathogens promotes alterations in the intestinal cell cytoskeleton by piracy of the DAF-GPI signal cascade without bacterial cell entry.

scholarly journals The Salmonella enterica Serovar Typhi Type IVB Self-Association Pili Are Detached from the Bacterial Cell by the PilV Minor Pilus Proteins

2006 ◽  
Vol 74 (9) ◽  
pp. 5414-5418 ◽  
Author(s):  
Connie K. P. Tam ◽  
Christina Morris ◽  
Jim Hackett
Keyword(s):  
Typhoid Fever ◽  
Bacterial Cell ◽  
Salmonella Enterica ◽  
Enteric Fever ◽  
Dna Supercoiling ◽  
Bacterial Membrane ◽  
Salmonella Enterica Serovar Typhi ◽  
Protein Molecules ◽  
Dna Fragment ◽  
Self Association

ABSTRACT Salmonella enterica serovar Typhi and some strains (Vi+) of serovar Dublin use type IVB pili to facilitate bacterial self-association, but only when the PilV proteins (potential minor pilus proteins) are not synthesized. Pilus-mediated self-association may be important in the pathogenesis of enteric fever. We have shown previously that the extent of DNA supercoiling controls the rate of Rci-catalyzed inversion of a DNA fragment which includes the C-terminal portions of the PilV proteins. This inversion therefore controls PilV synthesis as a high inversion rate prohibits transcription of pilV-encoding DNA. Here, we describe the manner in which PilV protein expression inhibits bacterial self-association and present data which suggest that incorporation of one or a few PilV protein molecules into a growing pilus, comprised of PilS subunits, causes the pilus to detach at the bacterial membrane. The bacteria are then unable to self-associate. We suggest that this phenomenon may be relevant to the pathogenesis of typhoid fever.

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