title: Immune reaction and survivability of salmonella typhimurium and salmonella infantis after infection of primary avian macrophages.
abstract: Salmonella serovars are differentially able to infect chickens. The underlying causes are not yet fully understood. Aim of the present study was to elucidate the importance of Salmonella Pathogenicity Island 1 and 2 (SPI-1 and -2) for the virulence of two non-host-specific, but in-vivo differently invasive, Salmonella serovars in conjunction with the immune reaction of the host. Primary avian splenic macrophages were inoculated with Salmonella enterica sub-species enterica serovar (S.) Typhimurium and S. Infantis. The number and viability of intracellular bacteria and transcription of SPI-1 and -2 genes by the pathogens, as well as transcription of immune-related proteins, surface antigen expression and nitric oxide production by the macrophages, were compared at different times post inoculation. After infection, both of the Salmonella serovars were found inside the primary macrophages. Invasion-associated SPI-1 genes were significantly higher transcribed in S. Infantis- than S. Typhimurium-infected macrophages. The macrophages counteracted the S. Infantis and S. Typhimurium infection with elevated mRNA expression of inducible nitric oxide synthase (iNOS), interleukin (IL)-12, IL-18 and lipopolysaccharide-induced tumor necrosis factor alpha factor (LITAF) as well as with an increased synthesis of nitric oxide. Despite these host cell attacks, S. Typhimurium was better able than S. Infantis to survive within the macrophages and transcribed higher rates of the SPI-2 genes spiC, ssaV, sifA, and sseA. The results showed similar immune reactions of primary macrophages after infection with both of the Salmonella strains. The more rapid and stronger transcription of SPI-2-related genes by intracellular S. Typhimurium compared to S. Infantis might be responsible for its better survival in avian primary macrophages.
authors: Institute of Molecular Pathogenesis, 'Friedrich-Loeffler-Institut' (Federal Research Institute for Animal Health), Jena, Germany.
authors: Maria
authors: M
authors: Braukmann
authors: Institute of Bacterial Infections and Zoonoses, 'Friedrich-Loeffler-Institut' (Federal Research Institute for Animal Health), Jena, Germany.
authors: Ulrich
authors: U
authors: Methner
authors: Institute of Molecular Pathogenesis, 'Friedrich-Loeffler-Institut' (Federal Research Institute for Animal Health), Jena, Germany.
authors: Angela
authors: A
authors: Berndt
mesh_terms: D000818:Animals; D000942:Antigens, Bacterial / Q000276:immunology; D017209:Apoptosis / Q000235:genetics; D002478:Cells, Cultured; D002645:Chickens / Q000235:genetics / Q000276:immunology* / Q000382:microbiology*; D015169:Colony Count, Microbial; D005434:Flow Cytometry; D005798:Genes, Bacterial; D054884:Host-Pathogen Interactions / Q000235:genetics / Q000276:immunology; D007109:Immunity / Q000235:genetics; D008264:Macrophages / Q000276:immunology / Q000382:microbiology*; D050296:Microbial Viability; D008858:Microscopy, Phase-Contrast; D009569:Nitric Oxide / Q000096:biosynthesis; D010641:Phenotype; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D012475:Salmonella / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity; D012481:Salmonella Infections, Animal / Q000235:genetics / Q000276:immunology* / Q000382:microbiology; D012486:Salmonella typhimurium / Q000235:genetics / Q000276:immunology / Q000472:pathogenicity; D013154:Spleen / Q000473:pathology; D014158:Transcription, Genetic; D014774:Virulence / Q000235:genetics
chemical_list: D000942:Antigens, Bacterial; D012333:RNA, Messenger; D009569:Nitric Oxide