title: 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.
abstract: 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 (GROalpha) 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 GROalpha 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.
authors.affiliation: Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Ave., Davis, CA 95616-8645, USA.
authors.forename: Manuela
authors.initials: M
authors.lastname: Raffatellu
authors.forename: Renato L
authors.initials: RL
authors.lastname: Santos
authors.forename: Daniela
authors.initials: D
authors.lastname: Chessa
authors.forename: R Paul
authors.initials: RP
authors.lastname: Wilson
authors.forename: Sebastian E
authors.initials: SE
authors.lastname: Winter
authors.forename: Carlos A
authors.initials: CA
authors.lastname: Rossetti
authors.forename: Sara D
authors.initials: SD
authors.lastname: Lawhon
authors.forename: Hiutung
authors.initials: H
authors.lastname: Chu
authors.forename: Tsang
authors.initials: T
authors.lastname: Lau
authors.forename: Charles L
authors.initials: CL
authors.lastname: Bevins
authors.forename: L Garry
authors.initials: LG
authors.lastname: Adams
authors.forename: Andreas J
authors.initials: AJ
authors.lastname: Bäumler
mesh_terms: D000818:Animals; D000942:Antigens, Bacterial / Q000235:genetics / Q000502:physiology*; D016667:Bacterial Capsules / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology*; D002417:Cattle; D002465:Cell Movement / Q000235:genetics / Q000276:immunology; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000235:genetics / Q000276:immunology; D005819:Genetic Markers; D018928:Immunity, Mucosal / Q000235:genetics; D018836:Inflammation Mediators / Q000378:metabolism / Q000502:physiology; D020381:Interleukin-17 / Q000037:antagonists & inhibitors* / Q000096:biosynthesis / Q000235:genetics; D007413:Intestinal Mucosa / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009504:Neutrophils / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D009876:Operon / Q000235:genetics; D011135:Polysaccharides, Bacterial / Q000235:genetics / Q000502:physiology*; D012481:Salmonella Infections, Animal / Q000276:immunology* / Q000473:pathology / Q000517:prevention & control; D012485:Salmonella typhi / Q000235:genetics* / Q000276:immunology
chemical_list: D000942:Antigens, Bacterial; D005819:Genetic Markers; D018836:Inflammation Mediators; D020381:Interleukin-17; D011135:Polysaccharides, Bacterial