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Salmonella Pathogenicity Island 1 undergoes decay in serovars adapted to swine and poultry

ABSTRACT: Salmonella Pathogenicity Island 1 undergoes decay in serovars adapted to swine and poultry

PROVIDER: PRJEB75724 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR13731783_1.fastq.gz	Fastqsanger.gz
	ERR13731783_2.fastq.gz	Fastqsanger.gz
	ERR13731784_1.fastq.gz	Fastqsanger.gz
	ERR13731784_2.fastq.gz	Fastqsanger.gz
	ERR13731785_1.fastq.gz	Fastqsanger.gz

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Proteomic comparison between two Salmonella serovars with differential pathogenicity in humans.

Project description:Salmonella infections are among the most common foodborne diseases worldwide. The Enteritidis and Dublin serovars of Salmonella enterica are closely related yet they differ significantly in pathogenicity and epidemiology. Enteritidis is a broad-host-range serovar that commonly causes gastroenteritis and infrequently causes invasive disease in humans. Dublin mainly colonizes cattle but upon infecting humans often results in invasive disease. The aim of this work was to elucidate the molecular factors responsible for the differential pathogenic behavior between both serovars. We performed a quantitative proteomic comparative analysis between one clinical isolate of each serovar grown in vitro under gut mimicking conditions (GMC). Compared to S. Enteritidis, the S. Dublin proteome was enriched in proteins linked to response to several stress conditions, such as those encountered during host infection, as well as to virulence. The S. Enteritidis proteome contained proteins related to central anaerobic metabolism pathways that were undetected in S. Dublin. Similar differences were also found at the transcriptional level, as mRNA levels correlated with proteomic results for 17 of the 20 genes tested in 4 natural isolates of each serovar grown in GMC. This work reveals proteomic differences between two Salmonella serovars with markedly different invasive and host-range characteristics, grown in an infection relevant condition, which were not evident in previous comparative genomic analyses.

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Poultry body temperature contributes to invasion control through reduced expression of Salmonella pathogenicity island 1 genes in Salmonella enterica serovars Typhimurium and Enteritidis.

Project description:Salmonella enterica serovars Typhimurium (S. Typhimurium) and Enteritidis (S. Enteritidis) are foodborne pathogens, and outbreaks are often associated with poultry products. Chickens are typically asymptomatic when colonized by these serovars; however, the factors contributing to this observation are uncharacterized. Whereas symptomatic mammals have a body temperature between 37°C and 39°C, chickens have a body temperature of 41°C to 42°C. Here, in vivo experiments using chicks demonstrated that numbers of viable S. Typhimurium or S. Enteritidis bacteria within the liver and spleen organ sites were ?4 orders of magnitude lower than those within the ceca. When similar doses of S. Typhimurium or S. Enteritidis were given to C3H/HeN mice, the ratio of the intestinal concentration to the liver/spleen concentration was 1:1. In the avian host, this suggested poor survival within these tissues or a reduced capacity to traverse the host epithelial layer and reach liver/spleen sites or both. Salmonella pathogenicity island 1 (SPI-1) promotes localization to liver/spleen tissues through invasion of the epithelial cell layer. Following in vitro growth at 42°C, SPI-1 genes sipC, invF, and hilA and the SPI-1 rtsA activator were downregulated compared to expression at 37°C. Overexpression of the hilA activators fur, fliZ, and hilD was capable of inducing hilA-lacZ at 37°C but not at 42°C despite the presence of similar levels of protein at the two temperatures. In contrast, overexpression of either hilC or rtsA was capable of inducing hilA and sipC at 42°C. These data indicate that physiological parameters of the poultry host, such as body temperature, have a role in modulating expression of virulence.

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