Inside Front Cover: Inside Front Cover: Quantitative proteomic analysis of host epithelial cells infected by Salmonella enterica serovar Typhimurium

PROTEOMICS ◽  
2017 ◽  
Vol 17 (13-14) ◽  
pp. 1770112
Author(s):  
Linlu Qi ◽  
Mo Hu ◽  
Jiaqi Fu ◽  
Yanhua Liu ◽  
Mei Wu ◽  
...  
2017 ◽  
Vol 13 (4) ◽  
pp. e1006312 ◽  
Author(s):  
Tania Gaviria-Cantin ◽  
Youssef El Mouali ◽  
Soazig Le Guyon ◽  
Ute Römling ◽  
Carlos Balsalobre

2000 ◽  
Vol 68 (12) ◽  
pp. 6763-6769 ◽  
Author(s):  
A. M. Prouty ◽  
J. S. Gunn

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.


2005 ◽  
Vol 73 (8) ◽  
pp. 5198-5203 ◽  
Author(s):  
Cristina L. C. Esteves ◽  
Bradley D. Jones ◽  
Steven Clegg

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.


2003 ◽  
Vol 71 (2) ◽  
pp. 872-881 ◽  
Author(s):  
Farideh Tafazoli ◽  
Karl-Eric Magnusson ◽  
Limin Zheng

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.


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