title: Impact of Salmonella Typhimurium DT104 virulence factors invC and sseD on the onset, clinical course, colonization patterns and immune response of porcine salmonellosis.
abstract: The present study was conducted to study the impact of the virulence factors invC and sseD of the two type III secretion systems of Salmonella enterica serovar Typhimurium (S. Typhimurium) on the pathogenesis of the porcine S. Typhimurium DT104 infection. For this purpose, two S. Typhimurium mutant strains with a disrupted invC gene of the Salmonella pathogenicity island 1 or with a disrupted sseD gene of the Salmonella pathogenicity island 2 have been studied in experimental infection of pigs. Twenty-two 7-week-old male hybrid pigs were either infected with one of the mutants or the wild-type S. Typhimurium DT104 strain. Each group was examined for clinical signs, Salmonella shedding rate and the specific antibody response. Survival and replication were evaluated by qualitative and quantitative determination of the colonization rate. The humoral and cellular immune responses were examined using isotype-specific ELISA and quantitative real-time PCR of IL-2, IL-4, IL-10, IL-12 and IFN-gamma. The results proved that both mutants had a lower virulence (with marked differences between both mutants) than the wild-type and that both virulence factors have importance in porcine salmonellosis. Only pigs infected with the wild-type S. Typhimurium DT104 exhibited typical clinical symptoms of salmonellosis like anorexia, vomiting, disturbed demeanour, fever and diarrhoea. Deletion of the invC gene resulted in a significantly reduced colonization rate. Interestingly, the mRNA expression of both type-1 and type-2 cytokines were significantly decreased in pigs infected with either the invC-mutant and the sseD-mutant strain.
authors.affiliation: Institute of Animal Hygiene and Veterinary Public Health, University Leipzig, An den Tierkliniken 1, 04103 Leipzig, Germany.
authors.forename: Steffi
authors.initials: S
authors.lastname: Brumme
authors.forename: Thorsten
authors.initials: T
authors.lastname: Arnold
authors.forename: Haukur
authors.initials: H
authors.lastname: Sigmarsson
authors.forename: Jörg
authors.initials: J
authors.lastname: Lehmann
authors.forename: Holger C
authors.initials: HC
authors.lastname: Scholz
authors.forename: Wolf-Dietrich
authors.initials: WD
authors.lastname: Hardt
authors.forename: Andreas
authors.initials: A
authors.lastname: Hensel
authors.forename: Uwe
authors.initials: U
authors.lastname: Truyen
authors.forename: Uwe
authors.initials: U
authors.lastname: Roesler
mesh_terms: D000818:Animals; D000917:Antibody Formation; D001426:Bacterial Proteins / Q000235:genetics / Q000502:physiology*; D016207:Cytokines / Q000032:analysis / Q000096:biosynthesis / Q000235:genetics; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods / Q000662:veterinary; D005243:Feces / Q000382:microbiology; D015964:Gene Expression Regulation, Bacterial; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000235:genetics; D007111:Immunity, Cellular; D008297:Male; D008565:Membrane Proteins / Q000235:genetics; D009154:Mutation; D016133:Polymerase Chain Reaction / Q000379:methods / Q000662:veterinary; D006180:Proton-Translocating ATPases / Q000235:genetics / Q000502:physiology*; D011897:Random Allocation; D012481:Salmonella Infections, Animal / Q000276:immunology / Q000382:microbiology*; D012486:Salmonella typhimurium / Q000235:genetics / Q000276:immunology / Q000472:pathogenicity*; D013552:Swine; D013553:Swine Diseases / Q000276:immunology / Q000382:microbiology*; D037521:Virulence Factors / Q000235:genetics / Q000502:physiology*
chemical_list: D001426:Bacterial Proteins; D016207:Cytokines; D008565:Membrane Proteins; C440638:SPI-2 protein, Salmonella; C419942:Spi1 protein, Salmonella; C502376:SseD protein, Salmonella typhimurium; D037521:Virulence Factors; C088598:invC protein, Salmonella typhimurium; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; D006180:Proton-Translocating ATPases