Effects of antidepressants on the production of cytokines
Effects of antidepressants on the production of cytokines
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DOI：
10.1017/s1461145702003164
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发表时间：
2002-12-01
影响因子：
4.8
通讯作者：
Maes, M
中科院分区：
文献类型：
--
作者：
Kenis, G;Maes, M
现在有证据表明，重度抑郁症与炎症反应系统(IRS)的上调有关。这种IRS激活的主要因素之一是促炎细胞因子的过度产生。最近，一些研究考察了这些炎症介质在抑郁症的病因中是否起到了致病作用。对动物模型和人类细胞因子免疫疗法的研究表明，促炎细胞因子会导致抑郁症状。此外，这些抑郁症状可以通过抗抑郁药物治疗有效地逆转。因此，可能提示抗抑郁药抑制促炎细胞因子的产生和/或作用，从而导致抑郁症状的改善。在体外培养系统和抑郁症动物模型中，已经研究了抗抑郁药物对细胞因子产生的影响--在这些动物模型中，细胞因子的产生是由内毒素诱导的。结果表明，几种类型的抗抑郁药减少了促炎症细胞因子的产生，如干扰素-γ和肿瘤坏死因子-a，而增加了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，在这些研究中使用了不同的方法来检测细胞因子的产生和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，在抗抑郁治疗后，细胞因子血浆水平和细胞因子产生已正常化。然而，很明显，更多的研究是有必要的，我们强烈认为，在用于检查抑郁症患者细胞因子网络的方法中需要更高的标准化。
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-a, 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.