Brain mechanisms of stress-induced immunomodulation

应激诱导免疫调节的脑机制

基本信息

批准号：
09670072
负责人：
TAKE Sachiko
金额：
$ 1.98万
依托单位：
KYUSHU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09670072/
关键词：
Stress Hypothalamus Cytokines Cytotoxicity of natural killer cells c-Fos Prostaglandin E_2 RNase Protection Assay Th1 Th2 balance Thl NK括牲定量化RT-PCR

项目摘要

It is well known that various kinds of stressors modulate immune functions, suggesting the brain control of the immune system. In the present study we attempted to reveal the brain mechanisms of stress-induced modulation of cellular immune functions and have found those findings below :(1)Immobilization stress activated neurons of the hypothalamic nuclei, especially those of the paraventricular nucleus of the hypothalamus (PVN), which regulates both the sympathetic nervous system and the hypothalamic pituitary adrenocortical axis. Prostaglandin E2 induced by immobilization stress in the PVN may play a role in suppressing NK activity with the mediation of the sympathetic nervous system.(2)The PVN and teh ventromedial hypothalamus (VMH) tonically activated and the preoptic hypothalamus (POA) and the lateral hypothalamus (LH) tonically inhibited the activity of the splenic sympathetic nervous system.(3)Non-inflamatory stress such as immobilization stress enhanced the expression of mRNA fo … More r immune cytokines such as IFN-alpha, IL-1beta, TNFalpha, TNFbeta, IL-3, IL-6, and IL-10. Especially IFNalpha and lL-1 beta induce by immobilization stress in the hypothalamus were strongly suggested to be involved immobilization stress-induced modulation of the cellular immunity mediated by the splenic sympathetic nervous system.(4)It is suggested that immobilization stress-induced shift of Thl/Th2 balance from Th1 (cellular immunity) toward Th2 (humoral immunity) may be involved in the immobilization stress-induced modulation of the immunity.(5)Activation of the LH and suppression of the hippocampus are suggested to be involved in stress-induced enhancement of the cellular immunity.Taken all things together, it is suggested that stress-induced cytokines in the hypothalamus modulate the activity of the sympathetic nervous system, which modulates the cellular immunity directly or with the mediation of splenic cytokines induced in the spleen. In addition, the hippocampus and the LH may be involved stress-induced enhancement of the cellular immunity. Less

众所周知，各种压力源都会调节免疫功能，这表明大脑对免疫系统的控制。在本研究中，我们试图揭示压力诱导的细胞免疫功能调节的大脑机制，并发现了以下发现:( 1）固定应激激活下丘脑核的神经元，特别是下丘脑室旁核（PVN）的神经元，它调节交感神经系统和下丘脑垂体肾上腺皮质轴。 PVN固定应激诱导的前列腺素E2可能在交感神经系统的介导下发挥抑制NK活性的作用。(2)PVN和下丘脑腹内侧区(VMH)强直性激活、视前下丘脑(POA)和外侧丘脑下丘脑（LH）强直性抑制脾交感神经系统的活动。（3）非炎症应激，例如固定应激增强了 IFN-α、IL-1β、TNFα、TNFβ、IL-3、IL-6 和 IL-10 等免疫细胞因子的 mRNA 表达，尤其是固定应激诱导的 IFNα 和 IL-1β。强烈建议下丘脑中的细胞免疫调节参与由脾交感神经系统介导的固定应激诱导的细胞免疫调节。（4）这表明固定应激诱导的Thl/Th2平衡从Th1（细胞免疫）向Th2（体液免疫）的转变可能参与了固定应激诱导的免疫调节。（5）LH的激活和海马的抑制被认为是参与应激诱导的细胞免疫增强。综合考虑，下丘脑中应激诱导的细胞因子调节交感神经系统的活性，交感神经系统直接或介导调节细胞免疫此外，脾脏中诱导的海马和LH可能参与应激诱导的细胞免疫的增强。