title: Immune dynamics following infection of avian macrophages and epithelial cells with typhoidal and non-typhoidal Salmonella enterica serovars; bacterial invasion and persistence, nitric oxide and oxygen production, differential host gene expression, NF-κB signalling and cell cytotoxicity.
abstract: Poultry-derived food is a common source of infection of human with the non-host-adapted salmonellae while fowl typhoid and pullorum disease are serious diseases in poultry. Development of novel immune-based control strategies against Salmonella infection necessitates a better understanding of the host-pathogen interactions at the cellular level. Intestinal epithelial cells are the first line of defence against enteric infections and the role of macrophages is crucial in Salmonella infection and pathogenesis. While gene expression following Salmonella infection has been investigated, a comparison between different serovars has not been, as yet, extensively studied in poultry. In this study, chicken macrophage-like cells (HD11) and chick kidney epithelial cells (CKC) were used to study and compare the immune responses and mechanisms that develop after infection with different Salmonella serotypes. Salmonella serovars Typhimurium, Enteritidis, Hadar and Infantis showed a greater level of invasion and/or uptake characters when compared with S. Pullorum or S. Gallinarum. Nitrate and reactive oxygen species were greater in Salmonella-infected HD11 cells with the expression of iNOS and nuclear factor-κB by chicken macrophages infected with both systemic and broad host range serovars. HD11 cells revealed higher mRNA gene expression for CXCLi2, IL-6 and iNOS genes in response to S. Enteritidis infection when compared to S. Pullorum-infected cells. S. Typhimurium- and S. Hadar-infected HD11 showed higher gene expression for CXCLi2 versus S. Pullorum-infected cells. Higher mRNA gene expression levels of pro-inflammatory cytokine IL-6, chemokines CXCLi1 and CXCLi2 and iNOS genes were detected in S. Typhimurium- and S. Enteritidis-infected CKC followed by S. Hadar and S. Infantis while no significant changes were observed in S. Pullorum or S. Gallinarum-infected CKC.
authors.affiliation: Animal Infection and Immunity Research Group, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, Leicestershire, LE12 5RD, UK.
authors.forename: Ahmed
authors.initials: A
authors.lastname: Setta
authors.forename: Paul A
authors.initials: PA
authors.lastname: Barrow
authors.forename: Pete
authors.initials: P
authors.lastname: Kaiser
authors.forename: Michael A
authors.initials: MA
authors.lastname: Jones
mesh_terms: D000818:Animals; D015153:Blotting, Western / Q000662:veterinary; D002460:Cell Line; D002470:Cell Survival / Q000276:immunology; D002645:Chickens; D016207:Cytokines / Q000235:genetics / Q000276:immunology; D004847:Epithelial Cells / Q000276:immunology / Q000382:microbiology; D054884:Host-Pathogen Interactions / Q000276:immunology; D008264:Macrophages / Q000276:immunology / Q000382:microbiology*; D016328:NF-kappa B / Q000276:immunology*; D009569:Nitric Oxide / Q000276:immunology*; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000276:immunology; D011201:Poultry Diseases / Q000276:immunology / Q000382:microbiology*; D012313:RNA / Q000737:chemistry / Q000235:genetics; D026361:Reactive Nitrogen Species / Q000032:analysis / Q000276:immunology; D017382:Reactive Oxygen Species / Q000276:immunology*; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000662:veterinary; D012475:Salmonella / Q000235:genetics / Q000276:immunology*; D012481:Salmonella Infections, Animal / Q000276:immunology* / Q000382:microbiology
chemical_list: D016207:Cytokines; D016328:NF-kappa B; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D012313:RNA; D052247:Nitric Oxide Synthase Type II