Marotti T, Gabrilovac J, Rabatic S, Smejkal-Jagar L, Rocic B, Haberstock H
Department of Experimental Biology and Medicine, Rudjer Boskovic Institute, Zagreb, Croatia.
Pharmacol Biochem Behav. 1996 May;54(1):277-84. doi: 10.1016/0091-3057(95)02112-4.
Overnight restraint stress of mice decreased ConA-driven lymphocyte proliferation, plaque-forming cell response to sheep red blood cells (SRBC), and NK activity in the spleen, but the phagocytic activity was enhanced. Injection of methionine-enkephalin (MENK), 10 mg/kg, i.p., 30 min before restraint, abolished these changes (except for the NK activity) and attenuated the stress-induced elevation of glucocorticoids. However, MENK itself affected the immune responses like stress: It decreased NK activity and the PFC response and enhanced phagocytic activity. Contrary to results with stress, MENK had no effect on cell proliferation. The opioid-receptor antagonist naloxone given before restraint reversed the stress-induced enhancement of phagocytosis and the decrease of T-cell proliferation. Alterations of the immune responses induced by restraint stress seem to be mediated by at least two mechanisms: activation of the hypothalamus-pituitary-adrenal (HPA) axis and the secretion of opioid peptides. MENK injected before stress may interfere with 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 action, whereas NK cells seem to be under the influence of another control mechanism.
小鼠过夜束缚应激降低了刀豆蛋白A驱动的淋巴细胞增殖、对绵羊红细胞（SRBC）的空斑形成细胞反应以及脾脏中的自然杀伤（NK）活性，但吞噬活性增强。在束缚前30分钟腹腔注射10 mg/kg甲硫氨酸脑啡肽（MENK）可消除这些变化（NK活性除外），并减弱应激诱导的糖皮质激素升高。然而，MENK本身对免疫反应的影响与应激类似：它降低了NK活性和空斑形成细胞反应，并增强了吞噬活性。与应激结果相反，MENK对细胞增殖没有影响。束缚前给予阿片受体拮抗剂纳洛酮可逆转应激诱导的吞噬作用增强和T细胞增殖减少。束缚应激诱导的免疫反应改变似乎至少由两种机制介导：下丘脑-垂体-肾上腺（HPA）轴的激活和阿片肽的分泌。应激前注射MENK可能会干扰其中一种或两种机制。T或B淋巴细胞似乎受HPA轴激活的影响，吞噬细胞受阿片类物质的直接作用影响，而NK细胞似乎受另一种控制机制的影响。
