Schauenstein K, Rinner I, Felsner P, Mangge H
Department of General and Experimental Pathology, University of Graz, School of Medicine, Austria.
Padiatr Padol. 1992;27(4):81-5.
The purpose of this article is to review recent experimental data from our laboratory on immune-neuroendocrine communications, whereby the following findings will be discussed: (i) Experiments using an experimental stress model in rats revealed different doses of a defined stressor to exert opposite effects on the in vitro reactivity of peripheral blood lymphocytes (PBL). Stress effects are also dependent on the tissue origin of lymphocytes, and they seem to be exclusively mediated by adrenal hormones. (ii) The balance between the sympathetic and parasympathetic nervous system may be critical in extrinsic immunoregulation: Experimentally induced hypercatecholaminemia in rats seem to protect lymphocytes from immunosuppressing effects of other, endogenous stress hormones, but causes suppression of PBL activation, if beta-receptors are blocked at the same time. Chronic cholinergic stimuli exert enhancing effects on the cells of the thymus. (iii) A defect in the immune-neuroendocrine crosstalk may contribute to the occurrence of forbidden immune reactions, as has been shown in spontaneous and experimentally induced autoimmune diseases in animals models. Recent data indicate that the parasympathetic nervous system is involved in the transmission of immune messages to the central nervous system.
本文旨在综述我们实验室最近关于免疫-神经内分泌通讯的实验数据,据此将讨论以下发现:(i)使用大鼠实验性应激模型的实验表明,不同剂量的特定应激源对外周血淋巴细胞(PBL)的体外反应性产生相反作用。应激效应还取决于淋巴细胞的组织来源,且似乎完全由肾上腺激素介导。(ii)交感神经系统和副交感神经系统之间的平衡在外源性免疫调节中可能至关重要:实验诱导的大鼠高儿茶酚胺血症似乎能保护淋巴细胞免受其他内源性应激激素的免疫抑制作用,但如果同时阻断β受体,则会导致PBL活化受到抑制。慢性胆碱能刺激对胸腺细胞有增强作用。(iii)免疫-神经内分泌串扰缺陷可能导致禁忌免疫反应的发生,动物模型中的自发性和实验性自身免疫性疾病已证明了这一点。最近的数据表明,副交感神经系统参与了免疫信息向中枢神经系统的传递。