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Infect. Immun. doi:10.1128/IAI.00366-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Net replication of Salmonella enterica serovars Typhimurium and Choleraesuis in porcine intestinal mucosa and nodes is associated with their differential virulence

Enteric Bacterial Pathogens Laboratory, Division of Microbiology, Institute for Animal Health, Compton, Berkshire, RG20 7NN, United Kingdom

^* To whom correspondence should be addressed. Email: mark-p.stevens{at}bbsrc.ac.uk.

	Abstract

Salmonella enterica is a facultative intracellular pathogen of worldwide importance and causes a spectrum of diseases depending on serovar- and host-specific factors. Oral infection of pigs with S. enterica serovar Typhimurium strain 4/74 produces acute enteritis but is rarely fatal whereas serovar Choleraesuis strain A50 causes systemic disease with a high mortality rate. Using a porcine ligated ileal loop model we observed that systemic virulence of S. Choleraesuis A50 is not associated with enhanced intestinal invasion, secretory responses or neutrophil recruitment compared to S. Typhimurium 4/74. The net growth in vivo of S. Choleraesuis A50 and S. Typhimurium 4/74 was monitored following oral inoculation of pigs using strains harbouring pHSG422, which exhibits temperature-sensitive replication. Analysis of plasmid partitioning revealed that the enteric virulence of S. Typhimurium 4/74 relative to S. Choleraesuis A50 is associated with rapid replication in the intestinal wall, whereas systemic virulence of S. Choleraesuis A50 associated with enhanced persistence in intestinal mesenteric lymph nodes. Faster replication of S. Typhimurium compared to S. Choleraesuis in the intestinal mucosa was associated with greater induction of the pro-inflammatory cytokines TNF, IL-8 and IL-18 as detected by reverse transcriptase-PCR analysis of transcripts from infected mucosa. During replication in batch culture and porcine alveolar macrophages, transcription of genes encoding components of Type III secretion systems-1 (sipC) and -2 (sseC) was observed to be significantly higher in S. Typhimurium 4/74 than S. Choleraesuis A50 and this may contribute to the differences in epithelial invasion and intracellular proliferation. The rapid induction of pro-inflammatory responses by strain 4/74 may explain why pigs confine S. Typhimurium infection to the intestines, whereas slow replication of S. Choleraesuis may enable it to evade host innate immunity and thus disseminate by stealth.

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