Cellular changes and cytokine expression in the ilea of gnotobiotic piglets resulting from peroral Salmonella typhimurium challenge
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
9393822
PubMed Central
PMC175755
DOI
10.1128/iai.65.12.5244-5249.1997
Knihovny.cz E-resources
- MeSH
- Cytokines immunology MeSH
- Germ-Free Life * MeSH
- Ileum immunology microbiology pathology MeSH
- Swine, Miniature MeSH
- Swine MeSH
- Salmonella typhimurium * MeSH
- Salmonella Infections, Animal immunology pathology MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Cytokines MeSH
Two stable rough mutants of Salmonella spp. were studied as live peroral vaccines. The SF1591 mutant of S. typhimurium (Ra chemotype) protected germ-free piglets against subsequent infection with virulent smooth S. typhimurium LT2, whereas a deep-rough mutant of S. minnesota mR595 (Re chemotype) did not. We investigated cytokine and leukocyte profiles in the ilea of gnotobiotic piglets colonized for 1 week either with rough mutants alone or with rough mutants followed by S. typhimurium LT2. The ileal mucosae of piglets associated with strain SF1591 alone were not inflamed. Villi contained activated macrophages, and enterocytes expressed transforming growth factor beta (TGF-beta). Subsequent infection of piglets with S. typhimurium LT2 resulted in immigration of alphabeta T cells and immunoglobulin A (IgA) response. In contrast, the ileal mucosae of piglets associated with strain mR595 alone expressed heat shock proteins and inflammatory cytokines but not TGF-beta. Acellular villi contained numerous gammadelta T cells but no alphabeta T cells. After subsequent challenge with the LT2 strain, most piglets died of sepsis. Intestinal mucosae contained IgG but no IgA. These findings suggest the importance of cytokine signals in the regulation of intestinal responses against Salmonella infection.
See more in PubMed
Infect Immun. 1991 Dec;59(12):4491-6 PubMed
Folia Microbiol (Praha). 1989;34(2):157-64 PubMed
Microb Pathog. 1991 Nov;11(5):347-56 PubMed
Nature. 1992 Jun 18;357(6379):588-9 PubMed
Clin Immunol Immunopathol. 1992 Oct;65(1):1-9 PubMed
Folia Biol (Praha). 1992;38(3-4):202-15 PubMed
Immunology. 1992 Oct;77(2):219-27 PubMed
Cell Immunol. 1993 Oct 15;151(2):336-44 PubMed
Infect Immun. 1993 Nov;61(11):4569-74 PubMed
Infect Agents Dis. 1993 Apr;2(2):55-73 PubMed
Vet Immunol Immunopathol. 1994 May;41(1-2):31-40 PubMed
Infect Immun. 1995 Mar;63(3):1134-7 PubMed
J Exp Med. 1996 Jul 1;184(1):271-6 PubMed
Immunol Today. 1996 Aug;17(8):352-4 PubMed
Immunol Today. 1996 Feb;17(2):57-9 PubMed
Infect Immun. 1997 Dec;65(12):5238-43 PubMed
J Interferon Res. 1985 Winter;5(1):45-53 PubMed
Immunology. 1988 Jul;64(3):539-44 PubMed
J Clin Immunol. 1992 Mar;12(2):61-74 PubMed
Defined Pig Microbiota Mixture as Promising Strategy against Salmonellosis in Gnotobiotic Piglets
Cytokines in Salmonella infection
Effect of controlled antigenic stimulation on lymphocyte subsets in pigs and pig fetuses
Salmonellosis: lessons drawn from a germ-free pig model
Pathogenicity and protective effect of rough mutants of Salmonella species in germ-free piglets