Leonard B E, Song C
Department of Pharmacology, University College, Galway, Ireland.
Pharmacol Biochem Behav. 1996 May;54(1):299-303. doi: 10.1016/0091-3057(95)02158-2.
There is clinical and experimental evidence that various aspects of the immune and endocrine systems are severely compromised in chronic stress and depression. For example, it has been shown that a reduced lymphocyte response occurs to mitogens in depressed patients, effects that are not reversed by chronic antidepressant treatment. By contrast, monocyte phagocytosis is increased, while neutrophil phagocytosis is decreased in depressed patients. Such changes are normalized by effective antidepressant treatment. The results of such studies and others that demonstrate alterations in noncellular immune processed in depression indicate that the changes in immune function correlate with the severity and duration of the external and/or internal stressful stimuli. There is evidence that some of the immune changes are a reflection of increased plasma glucocorticoids that characterize both stress and depression. However, it is also apparent that the cytokines, prostaglandins, and corticotrophic releasing factor (CRF) also play an important role in initiating the behavioral and pathophysiological changes that are characteristic of both depression and chronic stress. This review attempts to critically assess the interplay between CRF, the immune and neurotransmitter systems, and behavior in chronic stress and depression.
有临床和实验证据表明，在慢性应激和抑郁症中，免疫和内分泌系统的各个方面都受到严重损害。例如，研究表明，抑郁症患者对有丝分裂原的淋巴细胞反应降低，而慢性抗抑郁治疗并不能逆转这种效应。相比之下，抑郁症患者的单核细胞吞噬作用增强，而中性粒细胞吞噬作用减弱。有效的抗抑郁治疗可使这些变化恢复正常。这些研究以及其他表明抑郁症中非细胞免疫过程发生改变的研究结果表明，免疫功能的变化与外部和/或内部应激刺激的严重程度和持续时间相关。有证据表明，某些免疫变化反映了血浆糖皮质激素的增加，这是应激和抑郁症的共同特征。然而，同样明显的是，细胞因子、前列腺素和促肾上腺皮质激素释放因子（CRF）在引发抑郁症和慢性应激所特有的行为和病理生理变化中也起着重要作用。本综述试图批判性地评估CRF、免疫和神经递质系统以及慢性应激和抑郁症中的行为之间的相互作用。
