CAS Key Laboratory of Mental Health, Institute of Psychology, Beijing, China; Department of Psychology, University of Chinese Academy of Sciences, Beijing, 100049, China.
CAS Key Laboratory of Mental Health, Institute of Psychology, Beijing, China; Department of Psychology, University of Chinese Academy of Sciences, Beijing, 100049, China.
J Affect Disord. 2019 Apr 1;248:52-58. doi: 10.1016/j.jad.2019.01.029. Epub 2019 Jan 28.
Many studies have shown that the disturbance of pro-inflammatory and/or anti-inflammatory cytokines is involved in the modulation of traumatic stress and related psychiatric disorders, typically posttraumatic stress disorder (PTSD). However, the specific immune alterations associated with PTSD symptoms are still unclear. The present study compared levels of pro- and anti-inflammatory cytokines between PTSD and non-PTSD controls, and investigated the relationships of immune changes with PTSD symptomatology.
In this study, 51 earthquake-exposed PTSD patients and 136 earthquake-exposed healthy controls were recruited. We assessed trauma exposure, PTSD and depression severity, and quantified a panel of pro- inflammatory cytokines, including interleukin (IL)-1β, IL-2, IL-6, IL-8, tumor necrosis factor alpha (TNF-α), interferon ϒ (IFN), and anti-inflammatory cytokines, including IL-4, IL-10 and IL-13 with enzyme-linked immunosorbent assays. Additionally, total pro-inflammatory cytokines score and total anti-inflammatory cytokines score were calculated to reflect the status of two balance system.
Behavioral data showed that the PTSD group had greater severity of depression, as well as total symptoms and every symptom cluster in the seven-factor model of PTSD compared to the non-PTSD control group. Immune data showed that PTSD subjects had higher levels of IL-1β and TNFα, as well as total pro-inflammatory cytokine scores compared to controls, suggesting an increase of inflammatory activity in PTSD. In all subjects, the IL-1β levels were correlated with PCL scores, after controlling for covariates, including age, education, marital status and gender, trauma exposure severity and depression.
The current study did not include a non-traumatized healthy control group, and PTSD was assessed using a self-reported measure.
Thus, by including a control group comprised entirely of earthquake-exposed individuals as means to discriminate specific alterations of cytokine levels in PTSD, these findings suggest that the increased inflammatory cytokines, especially IL-1β, may play a role in the pathophysiology of PTSD.
许多研究表明，促炎和/或抗炎细胞因子的紊乱参与了创伤后应激和相关精神障碍的调节，通常是创伤后应激障碍（PTSD）。然而，与 PTSD 症状相关的特定免疫改变仍不清楚。本研究比较了 PTSD 和非 PTSD 对照组之间促炎和抗炎细胞因子的水平，并研究了免疫变化与 PTSD 症状的关系。
在这项研究中，招募了 51 名地震暴露后 PTSD 患者和 136 名地震暴露后健康对照者。我们评估了创伤暴露、PTSD 和抑郁严重程度，并使用酶联免疫吸附试验定量了一组促炎细胞因子，包括白细胞介素（IL）-1β、IL-2、IL-6、IL-8、肿瘤坏死因子-α（TNF-α）、干扰素-γ（IFN）和抗炎细胞因子，包括 IL-4、IL-10 和 IL-13。此外，还计算了总促炎细胞因子评分和总抗炎细胞因子评分，以反映两个平衡系统的状态。
行为数据显示，与非 PTSD 对照组相比，PTSD 组的抑郁严重程度更高，以及 PTSD 的七种症状模型中的总症状和每个症状群。免疫数据显示，与对照组相比，PTSD 患者的 IL-1β 和 TNFα 水平以及总促炎细胞因子评分更高，提示 PTSD 中炎症活动增加。在所有受试者中，IL-1β 水平与 PCL 评分相关，在控制协变量（包括年龄、教育、婚姻状况和性别、创伤暴露严重程度和抑郁）后。
本研究没有包括非创伤性健康对照组，并且 PTSD 是使用自我报告的测量来评估的。
因此，通过包括一个完全由地震暴露者组成的对照组来区分 PTSD 中细胞因子水平的特定改变，这些发现表明，增加的炎症细胞因子，特别是 IL-1β，可能在 PTSD 的发病机制中起作用。
