Department of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy.
Department of Biotechnology, Chemistry and Pharmacy, University of Siena, 53100 Siena, Italy.
Int J Environ Res Public Health. 2023 Feb 8;20(4):2937. doi: 10.3390/ijerph20042937.
Several heterogeneous pathophysiology pathways have been hypothesized for being involved in the onset and course of Post-Traumatic Stress Disorder (PTSD). This systematic review aims to summarize the current evidence on the role of inflammation and immunological dysregulations in PTSD, investigating possible peripheral biomarkers linked to the neuroimmune response to stress. A total of 44 studies on the dysregulated inflammatory and metabolic response in subjects with PTSD with respect to controls were included. Eligibility criteria included full-text publications in the English language, human adult samples, studies involving both subjects with a clinical diagnosis of PTSD and a healthy control group. The research was focused on specific blood neuroimmune biomarkers, namely IL-1β, TNF-α, IL-6 and INF-γ, as well as on the potential harmful role of reduced antioxidant activity (involving catalase, superoxide dismutase and glutathione peroxidase). The possible role of the inflammatory-altered tryptophan metabolism was also explored. The results showed conflicting data on the role of pro-inflammatory cytokines in individuals with PTSD, and a lack of study regarding the other mediators investigated. The present research suggests the need for further studies in human samples to clarify the role of inflammation in the pathogenesis of PTSD, to define potential peripheral biomarkers.
已经假设了几种不同的病理生理学途径与创伤后应激障碍（PTSD）的发生和病程有关。本系统评价旨在总结炎症和免疫失调在 PTSD 中的作用的现有证据，研究与应激的神经免疫反应相关的可能外周生物标志物。共纳入了 44 项关于 PTSD 患者与对照组之间炎症和代谢失调反应的研究。纳入标准包括全文发表于英文期刊、以人类成年样本为研究对象、包含 PTSD 临床诊断患者和健康对照组的研究。研究集中在特定的血液神经免疫生物标志物上，即白细胞介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和干扰素-γ（INF-γ），以及抗氧化活性降低（涉及过氧化氢酶、超氧化物歧化酶和谷胱甘肽过氧化物酶）的潜在有害作用。还探讨了炎症改变的色氨酸代谢的可能作用。结果显示，在 PTSD 个体中，促炎细胞因子的作用存在矛盾的数据，而且对于其他研究的介质缺乏研究。目前的研究表明，需要在人类样本中进一步研究炎症在 PTSD 发病机制中的作用，以确定潜在的外周生物标志物。
