细胞因子和抑郁症

Cytokines and Depression

在心理神经免疫学领域，越来越多的证据表明神经和免疫之间存在双向交流通路，免疫系统可能在一些心理精神障碍中具有重要作用。“抑郁症的细胞因子假说”认为细胞因子作为神经调质，可能在抑郁症的病因和病理过程中具有重要作用。这个假说得到了很多证据的支持。而在动物身上应用前炎性细胞因子也能够引起与人类抑郁症行为症状非常类似的“病态行为”。研究认为外周细胞因子通过信号传导进入脑内与中枢产生的细胞因子共同作用于下丘脑--垂体--肾上腺轴和5-羟色胺系统，从而导致抑郁症。细胞因子的中枢效应可以解释很多抑郁症状，“抑郁症的细胞因子假说”为探讨抑郁症状的机制和治疗抑郁症提供了一个新的视角。

In the research field of psycholoneuroimmunology， accumulating evidence has indicated the existence of reciprocal communication pathway between nervous and immune system. “The cytokine hypothesis of depression” implies that proinflammatory cytokines， acting as neuromudulators， represent the key factor in the central mediation of the behavioral， neuroendocrine and neurochemical features of depression. This view is supported by various findings. Administration of proinflammatory cytokine in animal induces “sickness behavior”， which is very similar to the behavioral symptoms of depression in humans. Cytokines produced by peripheral immune activity， which could signal to the brain via a fast neural pathway and a slower humoral pathway， together with the cytokines produced within central nervous system exert central effects. Cytokines may cause hypothalamic-pituitary adrenal axis hyperactivity by disturbing the negative feedback inhibition of circulating corticosteroids on the hypothalamic-pituitary adrenal axis. Otherwise， cytokines may reduce 5-hydroxytryptamin level by lowering the availability of its precursor tryptophan through activation of the trypyophan-metabolising enzyme indoleamine-2， 3-dioxygenase.The central effects of cytokines appear to be able to account for most of the symptoms occurring in depression， and “cytokine hypothesis of depression” has created new perspectives in the mechanism study and the therapy of depressive symptoms.