Enhancing versus suppressive effects of stress hormones on skin immune function

Delayed-type hypersensitivity (DTH) reactions are antigen-specific cell-med iated immune responses that, depending on the antigen, mediate beneficial ( e.g., resistance to viruses, bacteria, and fungi) or harmful (e.g., allergi c dermatitis and autoimmunity) aspects of immune function. Contrary to the idea that stress suppresses immunity, we have reported that short-duration stressors significantly enhance skin DTH and that a stress-induced traffick ing of leukocytes to the skin may mediate this immunoenhancement, Here, we identify the hormonal mediators of a stress-induced enhancement of skin imm unity. Adrenalectomy, which eliminates the glucocorticoid and epinephrine s tress response, eliminated the stress-induced enhancement of skin DTH. Low- dose corticosterone or epinephrine administration significantly enhanced sk in DTH and produced a significant increase in the number of T cells in lymp h nodes draining the site of the DTH reaction. In contrast, high-dose corti costerone, chronic corticosterone, or low-dose dexamethasone administration significantly suppressed skin DTH, These results suggest a role for adrena l stress hormones as endogenous immunoenhancing agents. These results also show that hormones released during an acute stress response may help prepar e the immune system for potential challenges (e.g., wounding or infection) for which stress perception by the brain may serve as an early warning sign al.