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Cytokines and Hypothalamo-Autonomic Control of Immune System

细胞因子和下丘脑-免疫系统的自主控制

基本信息

批准号：
06044180
负责人：
HOTI Tstsuro
金额：
$ 2.62万
依托单位：
KYUSHU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for international Scientific Research
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1995
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-06044180/
关键词：
Splenic sympathetic nerve Interleukin-1 beta Interferon alpha Interleukin-6 Prostaglandin E2 Anterventral region of the III vetricle Endotoxin Kupffer cell 第3脳室壁前腹側領域インターロイキン-1β 視索前野細胞性免疫脾臓交感神経 PACAP

项目摘要

What we found in this project is as follows ;1) : Suppression of splenic natural killer (NK) cell activity by noradrenaline released from splenic sympathetic nerve (SSN) terminals is one of the mechanisms of immobilization (IM) -induced immunosppression. 2) : Brain IL-1 beta induces reduction of the SSN.3) : Immunosuppression induced by both IFN alpha and IL-1 beta in the brain is due to an sctivation of CRF system which leads to an enhancement of SSN.4) : EPI receptors for PGE2 are partly involved in the activation of the brain CRF system. 5) : The medial preoptic area (MPO), which is the most potent acting site of INF alpha, is involved in the central regulation of immunity by its suppressive influence on the SSN.6) : Splenic NK activity decreases during dynamic phase of the ventromedial hypothalamus (VMH) lesioning-induced hyperphagia, while it increases during static phase. 7) : Neurons in the anteroventromedial region of the III ventricle projecting to the MPO and the paraventricular nucleus play an important role in the blood-borne cytokine-brain signal transduction. 8) : Inhibition of the dorsal vagal motoneurons by IL-1 beta through the prostanoids is considered to be one of the mechanisms of the IL-1 beta-induced suppression of gastric acid secretion. 9) : IM stress elevates plasma IL-6 concentration. 10) : Plasma IL-6 response to IM stress was attenuated by partial hepatectomy or by partial sympathectomy in the liver. 11) : Some Kupffer (K) cells and endothelial cells in the liver obtained from rats immobilized showed significant IL-6 like immunoreactivity against anti-murine IL-6 antiserum. 12) : Norepinephrine stimulated the IL-6 production in the K cells obtained by in vitro culture preparation. 13) : The basal endotoxin (LPS) level in the portal plasma was higher than that in the systemic venous plasma. 14) : The portal LPS content increased during IM stress, whereas that in the systemic venous plasma did not change remarkably.

结果表明：1）脾交感神经（SSN）末梢释放的去甲肾上腺素抑制脾NK细胞活性是制动（IM）诱导免疫抑制的机制之一。2):脑IL-1 β诱导SSN的减少。3）：脑中IFN α和IL-1 β诱导的免疫抑制是由于CRF系统的激活导致SSN的增强。4）：PGE 2的EPI受体部分参与脑CRF系统的激活。5):视前内侧区（MPO）是INF α最有效的作用部位，通过其对SSN的抑制作用参与免疫的中枢调节。6）：脾NK活性在下丘脑腹内侧（VMH）损伤诱导的摄食过多的动态阶段降低，而在静态阶段增加。7):第三脑室前腹内侧区投射到髓过氧化物酶和室旁核的神经元在血传脑-脑信号转导中起重要作用。8):IL-1 β通过前列腺素类抑制背迷走神经运动神经元被认为是IL-1 β诱导的胃酸分泌抑制的机制之一。9)IM应激可升高血浆IL-6浓度。10)部分肝切除术或部分肝交感神经切除术可减弱血浆IL-6对IM应激的反应。11):肝枯否细胞和内皮细胞对鼠IL-6抗血清呈明显的IL-6样免疫反应。12)去甲肾上腺素刺激体外培养的K细胞产生IL-6。13)门静脉血浆中基础内毒素（LPS）水平高于体静脉血浆。14)：IM应激期间门脉LPS含量增加，而体静脉血浆中的LPS含量变化不明显。