Abstract
Simple SummaryIn modern livestock husbandry, animals may face stressful events like weaning, regrouping, or transportation, all of which can impair animal welfare and health. Research in model organisms has revealed that stress hormones, such as glucocorticoids and catecholamines, strongly modulate the immune system and thus the animals’ ability to fight infections. In the pig, knowledge about this relationship is rare, and results from rodents cannot readily be transferred due to some physiological differences. Therefore, the effects of glucocorticoids and catecholamines on porcine immune cell proliferation and the production of the pro-inflammatory cytokine TNFα were investigated in an in vitro study. Blood was obtained from catheterized pigs to exclude pre-exposure to stress hormones. Glucocorticoids exerted inhibitory effects on both investigated immune functions. Catecholamines, on the other hand, showed diverse effects on lymphocyte proliferation and TNFα production of particular immune cell types. This suggests that studies from model species are not entirely transferrable to pigs. Future research should extend the preliminary findings on cytokine production and focus on the molecular mechanisms and health impacts of stress hormones in pigs.Stress hormones exert important modulating influences on the functionality of immune cells. Despite its major role as a livestock animal and its increasing use as an animal model, knowledge about this relationship in the domestic pig is rare. This study therefore aimed to characterize the effect of glucocorticoids and catecholamines on the proliferation and cytokine production of porcine peripheral blood mononuclear cells (PBMC). Blood was obtained from donor pigs equipped with indwelling catheters to exclude stress hormone exposition before in vitro testing. PBMC were stimulated in the presence of cortisol, adrenaline or noradrenaline at concentrations resembling low to high stress conditions. Proliferation was determined via 3H-thymidine incorporation, and TNFα producers were quantified by intracellular cytokine staining. Cortisol led to a decrease in mitogen-induced lymphocyte proliferation and the number of TNFα producing cells. In contrast, catecholamines increased proliferation while exerting repressive or no effects on the number of cytokine producers. Remarkably, in concentrations presumably found in lymphatic tissue in stress situations, noradrenaline suppressed lymphocyte proliferation completely. The shown repressive effects might especially have implications on health and welfare in pigs. The obtained results provide a preliminary database for extended studies on the molecular mechanisms of glucocorticoid and catecholamine actions on porcine immune cells.
Highlights
The physiological stress response enables the body to cope with threats via predominantly adaptive alterations in cardiac function, energy metabolism and the immune system [1,2,3]
peripheral blood mononuclear cells (PBMC) were stimulated with ConA, this inhibitory effect occurred at a concentration of 10−8 M and higher, whereas the proliferation of pokeweed mitogen (PWM)-stimulated PBMC was first inhibited upon addition of 10−7 M
Catecholamines generally had an enhancing impact on lymphocyte proliferation, but the magnitude of the effect of adrenaline or noradrenaline action was dependent on CA dose and mitogen (Figure 1c–f)
Summary
The physiological stress response enables the body to cope with threats via predominantly adaptive alterations in cardiac function, energy metabolism and the immune system [1,2,3]. Efforts to reduce the use of antibiotics in animal husbandry require a well-functioning immune system and the prevention of stress-induced immunosuppression. For these reasons, it is of utmost importance to understand the actions of the particular stress hormones on different immune functions. ADR and NA can exert effects similar to cortisol with lower proliferation [10] and cytokine production [11,12] They may lead to immune activation [13,14], depending on experimental conditions, such as dose or the timing of treatment [15]
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