Cytokines and Hypothalamo-Autonomic Control of Immune System

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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.