| Project/Area Number |
06044180
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
HOTI Tstsuro Kyushu University, Professor, 医学部, 教授 (00022814)
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| Co-Investigator(Kenkyū-buntansha) |
ARIMURA Akira Tulane University, Professor, チューレン大学・米日生物医学研究所, 教授
ECKHART Simo ドイツ国, マックスプランク生理学臨床研究所, 教授
TAKE Sachiko Kyushu University, Associate Professor, 医学部, 助手 (80253425)
TAKAKI Atsushi Kyushu University, Associate Professor, 医学部, 助手 (30243934)
KATAFUCHI Toshihiko Kyushu University, Associate Professor, 医学部, 講師 (80177401)
AOU Shyuji Kyushu University, Associate Professor, 医学部, 助教授 (40150908)
SIMON Eckhart Max-Planck Institute, Professor
RIEDEL Walte ドイツ国, マックスプランク生理学臨床研究所, 教授
SIMON Eckhar ドイツ国, マックスプランク生理学臨床研究所, 教授
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 1995: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1994: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | 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 |
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| Research Abstract |
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.
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