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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.

Stress induced Salmonella Typhimurium recrudescence in pigs coincides with cortisol induced increased intracellular proliferation in macrophages