BackgroundMany 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. MethodsIn 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 (IFNϒ), 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. ResultsBehavioral 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. LimitationsThe current study did not include a non-traumatized healthy control group, and PTSD was assessed using a self-reported measure. ConclusionsThus, 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.