Kenis Gunter, Maes Michael
Department of Psychiatry and Neuropsychology, University of Maastricht, Maastricht, The Netherlands.
Int J Neuropsychopharmacol. 2002 Dec;5(4):401-12. doi: 10.1017/S1461145702003164.
There is now evidence that major depression is associated with an up-regulation of the inflammatory response system (IRS). One of the major factors in this IRS activation is the hyperproduction of pro-inflammatory cytokines. Recently, a number of studies examined whether there is a causative role of these inflammatory mediators in the aetiology of major depression. Studies with animal models and cytokine immune therapy in humans suggest that pro-inflammatory cytokines induce depressive symptomatology. Moreover, these depressive symptoms can be effectively reversed by antidepressant treatment. Thus, it may be suggested that antidepressants suppress pro-inflammatory cytokine production and/or action, resulting in improvement of depressive symptoms. The influence of antidepressants on cytokine production has been examined in culture systems in vitro, and in animal models of depression - in which cytokine production is induced by endotoxin administration. Results suggest that antidepressants of several classes decrease the production of pro-inflammatory cytokines such as interferon-gamma and tumour necrosis factor-alpha, and increase that of interleukin-10, an anti-inflammatory cytokine. Further, the effect of antidepressive treatment on cytokine secretion and on plasma levels of cytokines in depressed patients has been studied. Unfortunately, different approaches to examine cytokine production and different techniques to measure cytokines in plasma are used in these studies. Despite this, current data indicate a normalization of cytokine plasma levels and cytokine production after antidepressant treatment. It is clear, however, that more research is warranted and we strongly argue the need for higher standardization in the methodology used to examine the cytokine network in depressed patients.
目前有证据表明，重度抑郁症与炎症反应系统（IRS）的上调有关。该IRS激活的主要因素之一是促炎细胞因子的过度产生。最近，一些研究探讨了这些炎症介质在重度抑郁症病因中是否具有因果作用。对动物模型和人类细胞因子免疫疗法的研究表明，促炎细胞因子会诱发抑郁症状。此外，这些抑郁症状可通过抗抑郁治疗有效逆转。因此，可能有人认为抗抑郁药可抑制促炎细胞因子的产生和/或作用，从而改善抑郁症状。抗抑郁药对细胞因子产生的影响已在体外培养系统以及抑郁症动物模型中进行了研究，在这些模型中，通过给予内毒素诱导细胞因子的产生。结果表明，几类抗抑郁药可降低促炎细胞因子如干扰素-γ和肿瘤坏死因子-α的产生，并增加抗炎细胞因子白细胞介素-10的产生。此外，还研究了抗抑郁治疗对抑郁症患者细胞因子分泌和血浆细胞因子水平的影响。不幸的是，这些研究中使用了不同的方法来检测细胞因子的产生，以及不同的技术来测量血浆中的细胞因子。尽管如此，目前的数据表明抗抑郁治疗后细胞因子血浆水平和细胞因子产生恢复正常。然而，很明显，仍需要更多的研究，我们强烈主张在用于检测抑郁症患者细胞因子网络的方法上需要更高的标准化。
