Brain mechanisms of stress-induced immunomodulation
Grant-in-Aid for Scientific Research (C)
Environmental physiology (including Physical medicine and Nutritional physiology)
|Research Institution||KYUSHU UNIVERSITY|
TAKE Sachiko School of Medicine, Kyushu University, Assistant, 医学部, 助手 (80253425)
|Project Fiscal Year
1997 – 1998
Completed(Fiscal Year 1998)
|Budget Amount *help
¥3,100,000 (Direct Cost : ¥3,100,000)
Fiscal Year 1998 : ¥900,000 (Direct Cost : ¥900,000)
Fiscal Year 1997 : ¥2,200,000 (Direct Cost : ¥2,200,000)
|Keywords||Stress / Hypothalamus / Cytokines / Cytotoxicity of natural killer cells / c-Fos / Prostaglandin E_2 / RNase Protection Assay / Th1 / Th2 balance / ストレス / 視床下部 / サイトカイン / NK活性 / Prostaglandin E2 / Th2バランス / Thl / NK括牲 / 定量化RT-PCR|
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
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
Research Output (13results)