Immunomodulatory effect of stress hormones on porcine neutrophil functions during Actinobacillus pleuropneumoniae infection.

Stress contributes to disease outcomes and can influence the signaling and interactions of immune cells. This study aimed to evaluate the influence of three selected stress hormones cortisol, epinephrine and norepinephrine, at in vivo-relevant concentrations, on the antimicrobial activity of porcine neutrophils during infection with Actinobacillus pleuropneumoniae (A.pp). We analyzed whether stress hormones affect the antimicrobial activity of neutrophils. Reactive oxygen species (ROS) production, cell size, and granularity were measured using flow cytometry. Neutrophil extracellular trap (NET) formation was quantified using confocal immunofluorescence microscopy, and transmission electron microscopy was employed to analyze the formation of vesicular NETs. ROS production and NET formation experiments were also conducted under infection with A.pp. The survival of A.pp in the presence of stress hormone-treated neutrophils was assessed. The antimicrobial activity of neutrophils was altered in a concentration-dependent manner by all tested stress hormones: neutrophils produced higher amounts of ROS and released significantly more NETs under A.pp infection, in particular vesicular NET formation. However, A.pp growth in the presence or absence of neutrophils was not affected by stress hormones. Future studies are needed to characterize the role of vesicular NETs as stress response reactions. In conclusion, this study contributes to a better understanding of the innate immune cells, particularly porcine neutrophils, in infections within stressed hosts.