Jiang Mingdi, Qin Ping, Yang Xu
Section of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan 430079, China.
National Centre for Suicide Research and Prevention, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
J Affect Disord. 2014 Sep;166:22-9. doi: 10.1016/j.jad.2014.04.027. Epub 2014 May 10.
Depression is often present in patients with asthma and vice versa. In this review, we aimed to summarize reports on the comorbidity of depression and asthma, and to seek evidence that the biological mechanisms of allergy may have an important role linking asthma and depression.
To explore the relationship and pathway underpinning this comorbidity, we reviewed medical articles and undertook a meta-analysis of epidemiological studies on (i) incidence of asthma in patients with depression; (ii) morbidity of depression in patients with asthma; (iii) concentration of cytokines in depressed subjects.
High level of comorbidity of asthma and depression was consistently demonstrated in 10 studies of patients with asthma and four studies of patients with depression. In search of biological connection of the two illnesses, thirty-eight studies were included for Meta-analyses examining differences in allergy related cytokines between patients with depression and non-depressive subjects. In people with depression, concentration of monocytes related cytokines such as IL-1 (1.56ng/mL, 95% CI: 0.00-3.12, p=0.05) was significantly higher than that in non-depressive control subjects. At the same time, some other inflammatory factors including IL-4 (5.77pg/mL, 95% CI: 2.34-9.21, p=0.00010), IL-6 (1.44ng/mL, 95% CI: 1.05-1.82, p<0.00001) and TNF-α(3.01ng/mL, 95% CI: 1.76-4.26, p<0.00001) were extremely significantly higher in depressed people compared with the controls. There was no significant differences of the T cell related cytokine levels, IFN-γ (-0.16ng/mL, 95% CI: -0.85-7.73, p=0.97), accompanied with IL-10 (0.67ng/mL, 95% CI: -0.84-2.18, p=0.38) between depressive and non-depressive groups.
The varying levels of certain cytokines play an important role in arousing and remitting asthma and depression. That suggests inflammatory response could be a common pathway adjusting both depression and asthma.
抑郁症常存在于哮喘患者中，反之亦然。在本综述中，我们旨在总结关于抑郁症与哮喘共病的报告，并寻找证据证明过敏的生物学机制可能在连接哮喘和抑郁症方面发挥重要作用。
为探究这种共病的关系及潜在途径，我们查阅了医学文章，并对以下方面的流行病学研究进行了荟萃分析：（i）抑郁症患者中哮喘的发病率；（ii）哮喘患者中抑郁症的发病率；（iii）抑郁症患者体内细胞因子的浓度。
在10项针对哮喘患者的研究和4项针对抑郁症患者的研究中，均一致表明哮喘与抑郁症的共病率很高。为寻找这两种疾病的生物学联系，纳入了38项研究进行荟萃分析，以检验抑郁症患者与非抑郁症患者在过敏相关细胞因子方面的差异。在抑郁症患者中，单核细胞相关细胞因子如IL-1的浓度（1.56ng/mL，95%置信区间：0.00 - 3.12，p = 0.05）显著高于非抑郁症对照受试者。同时，包括IL-4（5.77pg/mL，95%置信区间：2.34 - 9.21，p = 0.00010）、IL-6（1.44ng/mL，95%置信区间：1.05 - 1.82，p < 0.00001）和TNF-α（3.01ng/mL，95%置信区间：1.76 - 4.26，p < 0.00001）在内的一些其他炎症因子在抑郁症患者中比对照组极显著更高。抑郁症组与非抑郁症组之间T细胞相关细胞因子水平，即IFN-γ（-0.16ng/mL，95%置信区间：-0.85 - 7.73，p = 0.97）以及IL-10（0.67ng/mL，95%置信区间：-0.84 - 2.18，p = 0.38）没有显著差异。
某些细胞因子水平的变化在引发和缓解哮喘及抑郁症方面发挥着重要作用。这表明炎症反应可能是调节抑郁症和哮喘的共同途径。
