Harden Lois M, du Plessis Irné, Poole Stephen, Laburn Helen P
Brain Function Research Group, School of Physiology, Medical School, University of the Witwatersrand, 7 York Road, Parktown, Gauteng, Johannesburg, South Africa.
Brain Behav Immun. 2008 Aug;22(6):838-49. doi: 10.1016/j.bbi.2007.12.006. Epub 2008 Feb 5.
Pro-inflammatory cytokines interleukin (IL)-6 and IL-1 beta can act in the brain (centrally) to cause fever. Sickness behaviors which accompany fever also appear to involve the central action of IL-1 beta. We injected species-homologous rat IL-6 and IL-1 beta directly into the brains of conscious rats to examine the effect of these cytokines on fever, and two behaviors affected by sickness, voluntary wheel-running and food intake. Male Sprague-Dawley rats selected for their predisposition to spontaneously run on running wheels were used in the experiment. Each rat was anaesthetized and had a temperature-sensitive radiotransmitter implanted intra-abdominally, and a 23-gauge stainless steel guide cannula inserted stereotaxically over the lateral cerebral ventricle. Rats were randomly assigned to receive intracerebroventricular injections of three doses of either IL-1 beta or IL-6 (100 ng, 1 ng or 0.1 ng IL-1 beta and 200 ng, 20 ng or 2 ng IL-6), or one of three different combinations of IL-1 beta and IL-6. Rats receiving either IL-1 beta or IL-6 showed a dose-dependent increase in body temperature and decrease in wheel-running (ANOVA, p<0.0001). Only rats receiving the highest dose of IL-1 beta significantly decreased food intake and body mass compared to rats receiving vehicle (ANOVA, p<0.001). Doses of IL-1 beta and IL-6 which, when injected on their own were non-pyrogenic and did not affect food intake and body mass, induced fever and anorexia when they were co-injected centrally. These results show that species-homologous rat IL-6 and IL-1 beta can act directly within the brain to decrease voluntary activity and suggest they also can act synergistically to induce anorexia and fever.
促炎细胞因子白细胞介素(IL)-6和IL-1β可作用于大脑(中枢)引起发热。伴随发热出现的疾病行为似乎也涉及IL-1β的中枢作用。我们将同种大鼠IL-6和IL-1β直接注射到清醒大鼠的大脑中,以研究这些细胞因子对发热以及受疾病影响的两种行为——自主轮转运动和食物摄入的作用。实验选用了因倾向于在转轮上自发奔跑而被挑选出的雄性斯普拉格-道利大鼠。每只大鼠均接受麻醉,并在腹腔内植入一个对温度敏感的无线电发射器,同时通过立体定位在侧脑室上方插入一根23号不锈钢引导套管。大鼠被随机分配接受脑室内注射三种剂量的IL-1β或IL-6(100 ng、1 ng或0.1 ng IL-1β以及200 ng、20 ng或2 ng IL-6),或者IL-1β和IL-6的三种不同组合之一。接受IL-1β或IL-6注射的大鼠体温呈剂量依赖性升高,轮转运动减少(方差分析,p<0.0001)。与接受赋形剂注射的大鼠相比,只有接受最高剂量IL-1β注射的大鼠食物摄入量和体重显著下降(方差分析,p<0.001)。单独注射时无致热作用且不影响食物摄入量和体重的IL-1β和IL-6剂量,在脑室内联合注射时会引起发热和厌食。这些结果表明,同种大鼠IL-6和IL-1β可直接在脑内发挥作用,降低自主活动,并提示它们也可协同作用诱导厌食和发热。