Brain interleukin-1 as a mediator of stress responses

外周免疫功能受各种应激源的影响，但应激诱导免疫调节的机制尚不清楚。脑白介素1参与应激诱导的肾上腺皮质激活已有报道，本研究以大鼠和小鼠为实验动物，探讨脑白介素1在应激诱导的免疫调节中的可能作用。当小鼠和/或大鼠受到束缚应激时，血清IL-6水平在1小时内升高，随后IL-6mRNA在肝和脾中的表达增加。肝组织免疫组织化学检测显示，应激诱导的IL-6主要表达于肝实质细胞。向脑室注射抗IL-1抗体时，血清对应激的IL-6反应大大减弱，但脑室内注射微量IL-1则可模拟这种反应。应激后即刻脑组织IL-1mRNA水平升高。根据这些结果，我得出结论，外周IL-6对束缚应激的反应是由脑IL-1介导的。

Peripheral immune functions are modified by various stressors, but the mechanisms of the stress-induced immunomodulation are poorly understood. There have been reports that brain interleukin (IL)-1 is involved in the stress-induced adrenocortical activation, In this study, I have investigated about possible roles of brain IL-1 in the stress-induced immunomodulation using rats and mice as experimental animals. When mice and/or rats were subjected to immobilization stress, the serum IL-6 level rose in 1 hr, following increased expression of IL-6 mRNA in both the liver and the spleen. Immunohistochemical examinations of liver tissue revealed that the stress induced IL-6 mainly in hepatic parenchymal cells. The serum IL-6 response to the stress was much attenuated when an antibody against IL-1 was injected into the cerebral ventricle, but mimicked by an intracerebroventricular injection of minute amounts of IL-1. It was also found that the brain IL-1 mRNA level rose immediately after the stress. From these results, I conclude that the peripheral IL-6 response to immobilization stress is mediated by brain IL-1.