Cassano Paolo, Bui Eric, Rogers Andrew H, Walton Zandra E, Ross Rachel, Zeng Mary, Nadal-Vicens Mireya, Mischoulon David, Baker Amanda W, Keshaviah Aparna, Worthington John, Hoge Elizabeth A, Alpert Jonathan, Fava Maurizio, Wong Kwok K, Simon Naomi M
1 Center for Anxiety and Traumatic Stress Disorders, Department of Psychiatry, Massachusetts General Hospital, Boston, MA, USA.
2 Dana-Farber Cancer Institute, Boston, MA, USA.
Aust N Z J Psychiatry. 2017 Jan;51(1):23-31. doi: 10.1177/0004867416652736. Epub 2016 Sep 29.
There is mixed evidence in the literature on the role of inflammation in major depressive disorder. Contradictory findings are attributed to lack of rigorous characterization of study subjects, to the presence of concomitant medical illnesses, to the small sample sizes, and to the limited number of cytokines tested.
Subjects aged 18-70 years, diagnosed with major depressive disorder and presenting with chronic course of illness, as well as matched controls ( n = 236), were evaluated by trained raters and provided blood for cytokine measurements. Cytokine levels in EDTA plasma were measured with the MILLIPLEX Multi-Analyte Profiling Human Cytokine/Chemokine Assay employing Luminex technology. The Wilcoxon rank-sum test was used to compare cytokine levels between major depressive disorder subjects and healthy volunteers, before (interleukin [IL]-1β, IL-6, and tumor necrosis factor-α) and after Bonferroni correction for multiple comparisons (IL-1α, IL-2, IL-3, IL-4, IL-5, IL-7, IL-8, IL-10, IL-12(p40), IL-12(p70), IL-13, IL-15, IFN-γ-inducible protein 10, Eotaxin, interferon-γ, monotype chemoattractant protein-1, macrophage inflammatory protein-1α, granulocyte-macrophage colony-stimulating factor and vascular endothelial growth factor).
There were no significant differences in cytokine levels between major depressive disorder subjects and controls, both prior to and after correction for multiple analyses (significance set at p ⩽ 0.05 and p ⩽ 0.002, respectively).
Our well-characterized examination of cytokine plasma levels did not support the association of major depressive disorder with systemic inflammation. The heterogeneity of major depressive disorder, as well as a potential sampling bias selecting for non-inflammatory depression, might have determined our findings discordant with the literature.
关于炎症在重度抑郁症中的作用,文献中的证据并不一致。相互矛盾的研究结果归因于研究对象缺乏严格的特征描述、存在合并的内科疾病、样本量小以及所检测的细胞因子数量有限。
年龄在18 - 70岁、被诊断为重度抑郁症且病程为慢性的受试者,以及匹配的对照组(n = 236),由经过培训的评估人员进行评估,并提供血液用于细胞因子检测。采用Luminex技术的MILLIPLEX多分析物人类细胞因子/趋化因子检测法测量乙二胺四乙酸(EDTA)血浆中的细胞因子水平。采用Wilcoxon秩和检验比较重度抑郁症受试者与健康志愿者之间的细胞因子水平,在多重比较的Bonferroni校正之前(白细胞介素[IL]-1β、IL-6和肿瘤坏死因子-α)以及之后(IL-1α、IL-2、IL-3、IL-4、IL-5、IL-7、IL-8、IL-10、IL-12(p40)、IL-12(p70)、IL-13、IL-15、γ-干扰素诱导蛋白10、嗜酸性粒细胞趋化因子、γ-干扰素、单核细胞趋化蛋白-1、巨噬细胞炎性蛋白-1α、粒细胞-巨噬细胞集落刺激因子和血管内皮生长因子)。
在多重分析校正之前和之后,重度抑郁症受试者与对照组之间的细胞因子水平均无显著差异(显著性分别设定为p⩽0.05和p⩽0.002)。
我们对细胞因子血浆水平进行的特征明确的检测不支持重度抑郁症与全身炎症之间的关联。重度抑郁症的异质性,以及可能存在的选择非炎症性抑郁症的抽样偏差,可能导致了我们的研究结果与文献不一致。