MET-ENKEPHALIN MODULATES STRESS-INDUCED ALTERATIONS OF THE IMMUNE-RESPONSE IN MICE

Overnight restraint stress of mice decreased ConA-driven lymphocyte pr oliferation, plaque-forming cell response to sheep red blood cells (SR BC), and NK activity in the spleen, but the phagocytic activity was en hanced. Injection of methionine-enkephalin (MENK), 10 mg/kg, IP, 30 mi n before restraint, abolished these changes (except for the NK activit y) and attenuated the stress-induced elevation of glucocorticoids. How ever, MENK itself affected the immune responses like stress: It decrea sed NK activity and the PFC response and enhanced phagocytic activity. Contrary to results with stress, MENK had no effect on cell prolifera tion. The opioid-receptor antagonist naloxone given before restraint r eversed the stress-induced enhancement of phagocytosis and the decreas e of T-cell proliferation. Alterations of the immune responses induced by restraint stress seem to be mediated by at least two mechanisms: a ctivation of the hypothalamus-pituitary-adrenal (HPA) axis and the sec retion of opioid peptides. MENK injected before stress may interfere w ith either or both mechanisms. T or B lymphocytes seem to be affected by the activation of the HPA axis, and phagocytes by a direct opioid a ction, whereas NK cells seem to be under the influence of another cont rol mechanism.