Outer membrane protein OmpV mediates
            
              Salmonella enterica
            
            serovar typhimurium adhesion to intestinal epithelial cells via fibronectin and α1β1 integrin

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.

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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

Infection and Immunity ◽

10.1128/iai.68.6.3368-3376.2000 ◽

2000 ◽

Vol 68 (6) ◽

pp. 3368-3376 ◽

Cited By ~ 58

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.

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