Brown R, Price R J, King M G, Husband A J
Department of Psychology, University of Newcastle, Shortland, Australia.
Brain Behav Immun. 1989 Dec;3(4):320-30. doi: 10.1016/0889-1591(89)90031-7.
A single, brief (8 h) period of sleep deprivation (DEP) was found to suppress secondary antibody response to sheep red blood cells in rats. This decrease could be totally prevented if either interleukin-1 beta (IL-1) or muramyl dipeptide (MDP) was administered at the beginning of the DEP vigil. Twenty-five units of IL-1 or 250 micrograms/kg MDP was found to be immunosuppressive in sleeping rats but, paradoxically, the combination of such doses with DEP alleviated this effect. Increased colonic temperatures associated with antigen and/or adjuvant administration were not related to the differences in antibody levels between sleeping and DEP animals. Activation of hypothalamic dopamine in IL-1-treated rats following DEP suggests that this monoamine transmitter system may participate in the observed protective activity of IL-1. The present findings extend the immune adjuvant effects of both IL-1 and MDP to protection of the host against behaviorally induced immunosuppression.
研究发现，单次短暂（8小时）的睡眠剥夺（DEP）会抑制大鼠对绵羊红细胞的二次抗体反应。如果在睡眠剥夺期开始时给予白细胞介素-1β（IL-1）或胞壁酰二肽（MDP），这种降低完全可以预防。发现25单位的IL-1或250微克/千克的MDP对睡眠中的大鼠具有免疫抑制作用，但矛盾的是，这些剂量与睡眠剥夺相结合可减轻这种作用。与抗原和/或佐剂给药相关的结肠温度升高与睡眠和睡眠剥夺动物之间抗体水平的差异无关。睡眠剥夺后，IL-1处理的大鼠下丘脑多巴胺的激活表明，这种单胺递质系统可能参与了观察到的IL-1的保护活性。目前的研究结果将IL-1和MDP的免疫佐剂作用扩展到保护宿主免受行为诱导的免疫抑制。
