The degree to which homeostasis becomes unbalanced and leads to distress is largely influenced by the impact of stress hormones on target cells. Glucocorticoids (primarily cortisol in farm animals) are the main effector endpoints of the neuroendocrine response to stressors, and result from activation of the hypothalamus-pituitary-adrenal (HPA) axis (Fig. 1). Systemic cortisol concentrations increase several minutes after a perceived threat and can last for a number of hours and recur in waves if the threat (stressor) is not removed. The well-known antiinflammatory and immunosuppressive effects of cortisol may serve as physiological downregulators of initiated immune responses following infection or tissue damage. However, contemporary management stressors that significantly and repeatedly activate the HPA axis in otherwise healthy animals cause pronounced changes in immune cell physiology, leading to disease susceptibility and clinical pathology.
Another pathway that mediates stress responses in animals is the sympatho-adrenal axis (Fig. 1). Activation of this neurotransmitter axis results in release of ad-renergic hormones (mainly the catecholamines, adrenaline, and noradrenaline) from the medullae of the adrenal glands and from nerves that innervate lymphoid tissues and blood vessels. Catecholamine secretion occurs seconds following perceived threats, enabling rapid increases in heart and respiration rate and constriction of small blood vessels in peripheral tissues to increase blood flow to the brain, liver, and muscles, and enhancing awareness and athletic prowess to facilitate the fight-or-flight response. However, like HPA axis activation, catechol-amine responses may be inappropriate and harmful to immunity and health in the context of exposure to recurring or chronic stressors.
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