Department of Psychiatry, Kuopio University Hospital and University of Eastern Finland, Kuopio, Finland.
BMC Psychiatry. 2012 Jan 9;12:2. doi: 10.1186/1471-244X-12-2.
Inflammatory mediators in both the peripheral circulation and central nervous system (CNS) are dysregulated in major depressive disorder (MDD). Nevertheless, relatively little is known about the role of the T-helper (Th)-2 effector cytokines interleukin (IL)-5 and IL-13 in MDD.
We examined the serum levels of these cytokines and a Th-1 comparison cytokine, interferon (IFN)-γ, in 116 individuals (MDD, n = 58; controls, n = 58).
In our basic multivariate model controlling for the effects of potential confounders on the associations between MDD and the examined cytokines, each 1-unit increase in the serum IL-5 level increased the likelihood of belonging to the MDD group by 76% (OR 1.76, 95% CI 1.03-2.99, p = 0.04; model covariates: age, gender, marital status, daily smoking and alcohol use). The likelihood further increased in models additionally controlling for the effects of the use of antidepressants and NSAIDS, and a diagnosis of asthma. No such associations were detected with regard to IL-13 (OR 1.08, 95% CI 0.96-1.22, p = 0.22) or IFN-γ (OR 1.02, 95% CI 0.99-1.05, p = 0.23).
Elevated levels of IL-5, which uses the neural plasticity-related RAS GTPase-extracellular signal-regulated kinase (Ras-ERK) pathway to mediate its actions in the central nervous system (CNS), could be one of the factors underlying the depression-related changes in CNS plasticity.
在外周循环和中枢神经系统(CNS)中,炎症介质在重度抑郁症(MDD)中失调。然而,关于辅助性 T 细胞(Th)-2 效应细胞因子白细胞介素(IL)-5 和 IL-13 在 MDD 中的作用,人们知之甚少。
我们检测了 116 个人(MDD 组,n = 58;对照组,n = 58)的血清细胞因子水平,包括这些细胞因子和 Th-1 对照细胞因子干扰素(IFN)-γ。
在我们的基本多元模型中,控制潜在混杂因素对 MDD 和所检查细胞因子之间关联的影响,血清 IL-5 水平每增加 1 个单位,MDD 组的可能性增加 76%(OR 1.76,95%CI 1.03-2.99,p = 0.04;模型协变量:年龄、性别、婚姻状况、每日吸烟和饮酒)。在另外控制抗抑郁药和 NSAIDs 的使用以及哮喘诊断影响的模型中,这种可能性进一步增加。而对于 IL-13(OR 1.08,95%CI 0.96-1.22,p = 0.22)或 IFN-γ(OR 1.02,95%CI 0.99-1.05,p = 0.23)则没有发现这种关联。
IL-5 水平升高,它使用与神经可塑性相关的 Ras GTPase-细胞外信号调节激酶(Ras-ERK)途径在中枢神经系统(CNS)中发挥作用,可能是导致 CNS 可塑性与抑郁相关变化的因素之一。