title: Survival of Salmonella serovar Typhimurium inside porcine monocytes is associated with complement binding and suppression of the production of reactive oxygen species.
abstract: The development of the carrier state in swine after infection with Salmonella serovar Typhimurium (S. Typhimurium) has not been elucidated yet. Possibly, phagocytes like macrophages play a crucial role. It was the aim of the present study to characterize the interaction of a S. Typhimurium strain and its hilA and ssrA mutants with porcine peripheral blood monocytes (PBM). Exposure of porcine PBM to S. Typhimurium induced the production of reactive oxygen species (ROS), requiring bacterial protein synthesis. The numbers of intracellular bacteria sharply decreased over a period of 3h. Monocytes obtained from different pigs differed markedly in their ROS production and in their ability to kill the bacteria. Interestingly, high ROS production did not coincide with increased intracellular killing. Using diphenylene iodonium inhibition of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, it was shown that bacterial killing was ROS-dependent only within 1h post inoculation, but was ROS-independent from 1h post inoculation onwards. This might be explained by the finding that metabolically active Salmonella bacteria were capable of suppressing the respiratory burst activity in a SPI-1- and SPI-2-independent manner without causing measurable cell damage. Opsonization with complement did not alter the ROS production. Nevertheless, it increased intracellular survival of the bacteria. In conclusion, survival of S. Typhimurium inside porcine PBM is promoted by suppression of respiratory burst activity and complement binding.
authors.affiliation: Department of Pathology, Bacteriology and Avian Diseases, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820 Merelbeke, Belgium. eef.donne@ugent.be
authors.forename: E
authors.initials: E
authors.lastname: Donné
authors.forename: F
authors.initials: F
authors.lastname: Pasmans
authors.forename: F
authors.initials: F
authors.lastname: Boyen
authors.forename: F
authors.initials: F
authors.lastname: Van Immerseel
authors.forename: C
authors.initials: C
authors.lastname: Adriaensen
authors.forename: J-P
authors.initials: JP
authors.lastname: Hernalsteens
authors.forename: R
authors.initials: R
authors.lastname: Ducatelle
authors.forename: F
authors.initials: F
authors.lastname: Haesebrouck
mesh_terms: D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000276:immunology; D002353:Carrier State / Q000382:microbiology / Q000662:veterinary*; D003165:Complement System Proteins / Q000276:immunology / Q000378:metabolism*; D003601:Cytotoxicity Tests, Immunologic / Q000662:veterinary; D008163:Luminescent Measurements / Q000662:veterinary; D009000:Monocytes / Q000276:immunology / Q000382:microbiology*; D016254:Mutagenesis, Insertional; D012329:RNA, Bacterial / Q000235:genetics / Q000276:immunology; D026361:Reactive Nitrogen Species / Q000276:immunology; D017382:Reactive Oxygen Species / Q000276:immunology / Q000378:metabolism*; D012481:Salmonella Infections, Animal / Q000276:immunology / Q000382:microbiology*; D012486:Salmonella typhimurium / Q000276:immunology / Q000502:physiology*; D013552:Swine; D013553:Swine Diseases / Q000276:immunology / Q000382:microbiology*; D015534:Trans-Activators / Q000235:genetics / Q000276:immunology
chemical_list: D001426:Bacterial Proteins; C102236:HilA protein, Salmonella; D012329:RNA, Bacterial; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D015534:Trans-Activators; C096222:tmRNA; D003165:Complement System Proteins