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Stress and the immune system in the etiology of anxiety and depression.

机译:压力和免疫系统在焦虑和抑郁的病因中。

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摘要

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.
机译:有临床和实验证据表明,慢性应激和抑郁严重损害了免疫和内分泌系统的各个方面。例如,已经显示在抑郁的患者中对有丝分裂原的淋巴细胞应答降低,这种作用不能通过慢性抗抑郁药治疗来逆转。相比之下,抑郁症患者的单核细胞吞噬作用增加,而中性粒细胞吞噬作用减少。通过有效的抗抑郁药治疗可以使此类变化正常化。此类研究的结果以及其他证明抑郁症中非细胞免疫过程发生改变的结果表明,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增加,反映了压力和抑郁。但是,也很明显,细胞因子,前列腺素和皮质营养释放因子(CRF)在引发行为和病理生理变化方面也起着重要作用,这些行为和病理生理变化是抑郁症和慢性应激的特征。这篇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行为之间的相互作用。

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