The Capsule Encoding the viaB Locus Reduces Interleukin-17 Expression and Mucosal Innate Responses in the Bovine Intestinal Mucosa during Infection with Salmonella enterica Serotype Typhi

Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Ave., Davis, CA 95616-8645, USA.
Infection and Immunity (Impact Factor: 3.73). 10/2007; 75(9):4342-50. DOI: 10.1128/IAI.01571-06
Source: PubMed


The viaB locus contains genes for the biosynthesis and export of the Vi capsular antigen of Salmonella enterica serotype Typhi. Wild-type serotype Typhi induces less CXC chemokine production in tissue culture models than does an isogenic
viaB mutant. Here we investigated the in vivo relevance of these observations by determining whether the presence of the viaB region prevents inflammation in two animal models of gastroenteritis. Unlike S. enterica serotype Typhimurium, serotype Typhi or a serotype Typhi viaB mutant did not elicit marked inflammatory changes in the streptomycin-pretreated mouse model. In contrast, infection of bovine
ligated ileal loops with a serotype Typhi viaB mutant resulted in more fluid accumulation and higher expression of the chemokine growth-related oncogene alpha (GROα) and
interleukin-17 (IL-17) than did infection with the serotype Typhi wild type. There was a marked upregulation of IL-17 expression
in both the bovine ligated ileal loop model and the streptomycin-pretreated mouse model, suggesting that this cytokine is
an important component of the inflammatory response to infection with Salmonella serotypes. Introduction of the cloned viaB region into serotype Typhimurium resulted in a significant reduction of GROα and IL-17 expression and in reduced fluid secretion.
Our data support the idea that the viaB region plays a role in reducing intestinal inflammation in vivo.

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Available from: Manuela Raffatellu
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    • "Chemokines are signaling molecules responsible for recruitment of leukocytes. Previous work demonstrated increased expression of C-X-C chemokines during Salmonella infection in the bovine intestine [9], [32], [52], [53]. For additional confirmation of microarray results, gene expression patterns from previously published work were compared to the expression patterns in the data presented here and were found to be consistent. "
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    • "Another major inflammatory pathway in the mucosa is controlled by the release of IL-23. The levels of IL-17 and IL-22 increase dramatically within 2–5 h post-infection in bovine or avian ligated loops.22,23 Such an early amplification of host inflammatory responses could involve the stimulation of antigen-experienced T cells by IL-23, inducing the release of IL-17 and IL-22. "
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    • "In addition, it has been reported that a switch from pro-inflammatory to an anti-inflammatory mode occurred and inhibited production of cytokines in the acute phase of typhoid fever patients [39]. It can also be explained by the 'stealth' tactics of S. Typhi, evading recognition of TLR4 and TLR5, impairing identification of its invasion to prevent a typical antibacterial host response, which results in suppression of neutrophil recruitment [40] and weak induction of acute phase responses [41]. "
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