scholarly journals Gre factors-mediated control of hilD transcription is essential for the invasion of epithelial cells by Salmonella enterica serovar Typhimurium

2017 ◽  
Vol 13 (4) ◽  
pp. e1006312 ◽  
Author(s):  
Tania Gaviria-Cantin ◽  
Youssef El Mouali ◽  
Soazig Le Guyon ◽  
Ute Römling ◽  
Carlos Balsalobre
Keyword(s):  
Epithelial Cells ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Serovar Typhimurium

scholarly journals Salmonella enterica Serovar Typhimurium Invasion Is Repressed in the Presence of Bile

2000 ◽  
Vol 68 (12) ◽  
pp. 6763-6769 ◽  
Author(s):  
A. M. Prouty ◽  
J. S. Gunn
Keyword(s):  
Epithelial Cells ◽  
Cell Invasion ◽  
Type Iii Secretion ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Eukaryotic Cell ◽  
Intestinal Epithelial ◽  
Two Component System ◽  
Serovar Typhimurium ◽  
Invasive Capacity

ABSTRACT As enteric pathogens, the salmonellae have developed systems by which they can sense and adapt appropriately to deleterious intestinal components that include bile. Previously, growth in the presence of bile was shown to repress the transcription of prgH, a locus encoding components of the Salmonella pathogenicity island I (SPI-1) type III secretion system (TTSS) necessary for eukaryotic cell invasion. This result suggested an existing interaction between salmonellae, bile, and eukaryotic cell invasion. Transcription assays demonstrated that invasion gene regulators (e.g.,sirC and invF) are repressed by bile. However, bile does not interact with any of the invasion regulators directly but exerts its effect at or upstream of the two-component system at the apex of the invasion cascade, SirA-BarA. As suggested by the repression of invasion gene transcription in the presence of bile, Western blot analysis demonstrated that proteins secreted by the SPI-1 TTSS were markedly reduced in the presence of bile. Furthermore, Salmonella enterica serovar Typhimurium grown in the presence of bile was able to invade epithelial cells at only 4% of the level of serovar Typhimurium grown without bile. From these data, we propose a model whereby serovar Typhimurium uses bile as an environmental signal to repress its invasive capacity in the lumen of the intestine, but upon mucous layer penetration and association with intestinal epithelial cells, where the apparent bile concentration would be reduced, the system would become derepressed and invasion would be initiated.

scholarly journals Biofilm Formation by Salmonella enterica Serovar Typhimurium and Escherichia coli on Epithelial Cells following Mixed Inoculations

2005 ◽  
Vol 73 (8) ◽  
pp. 5198-5203 ◽  
Author(s):  
Cristina L. C. Esteves ◽  
Bradley D. Jones ◽  
Steven Clegg
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Salmonella Enterica ◽  
Biofilm Formation ◽  
Salmonella Enterica Serovar Typhimurium ◽  
E Coli ◽  
Serovar Typhimurium

ABSTRACT Biofilms were formed by inoculations of Salmonella enterica serovar Typhimurium and Escherichia coli on HEp-2 cells. Inoculations of S. enterica serovar Typhimurium and E. coli resulted in the formation of an extensive biofilm of S. enterica serovar Typhimurium. In experiments where an E. coli biofilm was first formed followed by challenge with S. enterica serovar Typhimurium, there was significant biofilm formation by S. enterica serovar Typhimurium. The results of this study indicate that S. enterica serovar Typhimurium can outgrow E. coli in heterologous infections and displace E. coli when it forms a biofilm on HEp-2 cells.

scholarly journals Disruption of Epithelial Barrier Integrity by Salmonella enterica Serovar Typhimurium Requires Geranylgeranylated Proteins

2003 ◽  
Vol 71 (2) ◽  
pp. 872-881 ◽  
Author(s):  
Farideh Tafazoli ◽  
Karl-Eric Magnusson ◽  
Limin Zheng
Keyword(s):  
Epithelial Cells ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Epithelial Barrier ◽  
Phosphatidylinositol 3 Kinase ◽  
Barrier Integrity ◽  
Actin Organization ◽  
Rho Family Gtpases ◽  
Serovar Typhimurium ◽  
Associated Proteins

ABSTRACT Epithelial cells that line the human intestinal mucosa constitute the initial sites of host invasion by bacterial pathogens. A number of bacteria, such as Salmonella and Yersinia spp., have been shown to disrupt the integrity of the epithelial barrier, although little is known about the mechanisms underlying that effect. We found that polarized MDCK-1 epithelial cells infected with invasive Salmonella enterica serovar Typhimurium SL1344 exhibited marked changes in F-actin organization, an increase in the paracellular flux of dextran, and a rapid decrease in transepithelial electrical resistance (TER). In contrast, infection with an isogenic noninvasive mutant (hilA) increased the TER in these cells. Pretreating MDCK-1 cells with the inhibitors for tyrosine kinase (genistein) or phosphatidylinositol 3-kinase (wortmannin) did not affect invasion and subsequent perturbation of the epithelial barrier by serovar Typhimurium. Instead, the geranylgeranyltransferase 1 inhibitor GGTI-298, but not the farnesyltransferase inhibitor FTI-277, clearly reversed the capacity of serovar Typhimurium to disrupt the epithelial barrier. The substrates for GGTI-298 include Rho family GTPases, as indicated by inhibiting prenylation of Rac1 and Cdc42. Infection with wild-type serovar Typhimurium increased the level of activated Rac1 and Cdc42 and caused these proteins to accumulate apically in MDCK-1 cells. This Salmonella-induced accumulation of Rac1 and Cdc42 and alteration of the junction-associated proteins ZO-1, occludin, and E-cadherin in MDCK-1 cells were markedly inhibited by GGTI-298. These results suggest that activation of geranylgeranylated proteins, including Rac1 and Cdc42, is critical for disruption of barrier integrity by serovar Typhimurium in polarized MDCK-1 cells.

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 Disruption of the Salmonella-Containing Vacuole Leads to Increased Replication of Salmonella enterica Serovar Typhimurium in the Cytosol of Epithelial Cells

2002 ◽  
Vol 70 (6) ◽  
pp. 3264-3270 ◽  
Author(s):  
John H. Brumell ◽  
Patrick Tang ◽  
Michelle L. Zaharik ◽  
B. Brett Finlay
Keyword(s):  
Epithelial Cells ◽  
Host Cell ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Host Cells ◽  
Intracellular Pathogen ◽  
Wild Type ◽  
Vacuolar Compartment ◽  
Serovar Typhimurium ◽  
Endosomal System

ABSTRACT Salmonella enterica serovar Typhimurium is a facultative intracellular pathogen that inhabits a vacuolar compartment, called the Salmonella-containing vacuole (SCV), in infected host cells. Maintenance of the SCV is accomplished by SifA, and mutants of this Salmonella pathogenicity island 2 type III effector replicate more efficiently in epithelial cells. Here we demonstrate that enhanced replication of sifA mutants occurs in the cytosol of these cells. Increased replication of wild-type bacteria was also observed in cells treated with wortmannin or expressing Rab5 Q79L or Rab7 N125I, all of which caused a loss of SCV integrity. Our findings demonstrate the requirement of the host cell endosomal system for maintenance of the SCV and that loss of this compartment allows increased replication of serovar Typhimurium in the cytosol of epithelial cells.

scholarly journals The CorA Mg2+ Channel Is Required for the Virulence of Salmonella enterica Serovar Typhimurium

2008 ◽  
Vol 190 (19) ◽  
pp. 6517-6523 ◽  
Author(s):  
Krisztina M. Papp-Wallace ◽  
Margaret Nartea ◽  
David G. Kehres ◽  
Steffen Porwollik ◽  
Michael McClelland ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mutant Strain ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Serovar Typhimurium ◽  
Microarray Studies ◽  
Virulence Effectors

ABSTRACT CorA is the primary Mg2+ channel in Salmonella enterica serovar Typhimurium. A corA mutant is attenuated in mice and defective for invasion of and replication within epithelial cells. Microarray studies show that several virulence effectors are repressed in a corA mutant strain, which ultimately manifests itself as a decrease in virulence.

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