Psychological and biological mechanisms of cytokine induced depression

N. Hepgul, V. Mondelli, C. Pariante
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引用次数: 17

Abstract

Abstract Depression is frequently seen in patients with medical illnesses yet the link between medical illnesses and depression remains unclear. There is increasing data to suggest that the array of depressive symptoms experienced by the medically-ill may involve inflammation. The activation of the immune system and the subsequent release of innate immune products such as cytokines can have important effects on behaviour. The treatment of choice for chronic viral hepatitis C, interferon-alpha IFN-α, acutely induces the production and release of other innate immune cytokines, and has been indicated to cause clinically significant depression in 30% of patients receiving treatment. This in turn can impair quality of life and affect treatment compliance. We and others use IFN-α induced depression as a model to identify alterations in psychological and biological pathways that predispose to depression in the medically-ill, and thus provide an explanatory link between inflammation and the subsequent behavioural changes. In this editorial, we aim to describe the main biological pathways involved in IFN-induced depression and to discuss psychological, clinical and biological factors that have been found to predict those who will develop more severe psychiatric symptoms during treatment with IFN-α. Among these, particular attention would be given to psychological traits, genetic polymorphisms regulating inflammation and serotonergic function, and changes in plasma levels of pro-inflammatory cytokines.
细胞因子诱导抑郁的心理和生物学机制
抑郁症常见于内科疾病患者,但内科疾病与抑郁症之间的联系尚不清楚。越来越多的数据表明,病人所经历的一系列抑郁症状可能与炎症有关。免疫系统的激活和随后的先天免疫产物(如细胞因子)的释放对行为有重要影响。慢性病毒性丙型肝炎的首选治疗干扰素-α IFN-α可急性诱导其他先天免疫细胞因子的产生和释放,并已被证明可导致30%接受治疗的患者出现临床显著的抑郁。这反过来又会损害生活质量并影响治疗依从性。我们和其他人使用IFN-α诱导的抑郁症作为模型,以确定心理和生物学途径的变化,这些变化易导致疾病中的抑郁症,从而提供炎症和随后的行为变化之间的解释联系。在这篇社论中,我们的目的是描述IFN诱导抑郁症的主要生物学途径,并讨论已发现的心理、临床和生物学因素,这些因素可以预测那些在IFN-α治疗期间会出现更严重的精神症状的人。其中,应特别注意心理特征、调节炎症和血清素能功能的遗传多态性以及血浆促炎细胞因子水平的变化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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