title: Stress induced Salmonella Typhimurium recrudescence in pigs coincides with cortisol induced increased intracellular proliferation in macrophages.
abstract: Salmonella Typhimurium infections in pigs often result in the development of carriers that intermittently excrete Salmonella in very low numbers. During periods of stress, for example transport to the slaughterhouse, recrudescence of Salmonella may occur, but the mechanism of this stress related recrudescence is poorly understood. Therefore, the aim of the present study was to determine the role of the stress hormone cortisol in Salmonella recrudescence by pigs. We showed that a 24 h feed withdrawal increases the intestinal Salmonella Typhimurium load in pigs, which is correlated with increased serum cortisol levels. A second in vivo trial demonstrated that stress related recrudescence of Salmonella Typhimurium in pigs can be induced by intramuscular injection of dexamethasone. Furthermore, we found that cortisol, but not epinephrine, norepinephrine and dopamine, promotes intracellular proliferation of Salmonella Typhimurium in primary porcine alveolar macrophages, but not in intestinal epithelial cells and a transformed cell line of porcine alveolar macrophages. A microarray based transcriptomic analysis revealed that cortisol did not directly affect the growth or the gene expression or Salmonella Typhimurium in a rich medium, which implies that the enhanced intracellular proliferation of the bacterium is probably caused by an indirect effect through the cell. These results highlight the role of cortisol in the recrudescence of Salmonella Typhimurium by pigs and they provide new evidence for the role of microbial endocrinology in host-pathogen interactions.
authors.affiliation: Department of Pathology, Bacteriology and Avian Diseases, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820 Merelbeke, Belgium. Elin.verbrugghe@ugent.be.
authors.forename: Elin
authors.initials: E
authors.lastname: Verbrugghe
authors.forename: Filip
authors.initials: F
authors.lastname: Boyen
authors.forename: Alexander
authors.initials: A
authors.lastname: Van Parys
authors.forename: Kim
authors.initials: K
authors.lastname: Van Deun
authors.forename: Siska
authors.initials: S
authors.lastname: Croubels
authors.forename: Arthur
authors.initials: A
authors.lastname: Thompson
authors.forename: Neil
authors.initials: N
authors.lastname: Shearer
authors.forename: Bregje
authors.initials: B
authors.lastname: Leyman
authors.forename: Freddy
authors.initials: F
authors.lastname: Haesebrouck
authors.forename: Frank
authors.initials: F
authors.lastname: Pasmans
mesh_terms: D000818:Animals; D058491:Bacterial Load / Q000662:veterinary; D002460:Cell Line; D049109:Cell Proliferation; D015169:Colony Count, Microbial / Q000662:veterinary; D004797:Enzyme-Linked Immunosorbent Assay / Q000662:veterinary; D004847:Epithelial Cells / Q000378:metabolism* / Q000382:microbiology; D015964:Gene Expression Regulation, Bacterial; D006854:Hydrocortisone / Q000097:blood / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000382:microbiology; D016676:Macrophages, Alveolar / Q000378:metabolism* / Q000382:microbiology; D012481:Salmonella Infections, Animal / Q000382:microbiology*; D012486:Salmonella typhimurium / Q000235:genetics* / Q000378:metabolism; D013312:Stress, Physiological; D013552:Swine; D013553:Swine Diseases / Q000382:microbiology*
chemical_list: D006854:Hydrocortisone