C-Reactive Protein: Marker of risk for post-traumatic stress disorder and its potential for a mechanistic role in trauma response and recovery.
C-Reactive Protein: Marker of risk for post-traumatic stress disorder and its potential for a mechanistic role in trauma response and recovery.
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DOI：
10.1111/ejn.15031
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发表时间：
2022-05
期刊：
影响因子：
--
通讯作者：
Risbrough VB
中科院分区：
文献类型：
--
作者：
Friend SF;Nachnani R;Powell SB;Risbrough VB
越来越多的证据表明炎症在PTSD和应激障碍的病理生理学中起作用。PTSD与较高的循环炎症蛋白水平相关。啮齿类动物模型表明，炎症促进严重应激后的持久回避和唤醒行为（例如，捕食者暴露和社会失败），表明炎症可能在创伤性疾病中起机械作用。C反应蛋白（CRP）是一种先天性急性期反应物，由肝脏在急性感染和慢性疾病后产生。越来越多的研究报告PTSD诊断与外周CRP升高、CRP基因突变和免疫信号通路中CRP基因表达变化相关。CRP被合理地确定为PTSD和创伤暴露的潜在标志物，但它是否以及如何发挥机制作用尚不清楚。在这篇综述中，我们讨论了目前对PTSD免疫机制的理解，特别关注先天免疫信号因子CRP。我们发现，尽管有一致的证据表明CRP与PTSD症状和风险相关，但关于CRP如何导致PTSD中的CNS炎症，从而导致PTSD症状的数据很少。我们讨论了CRP调节外周和中枢神经系统应激反应的潜在机制，沿着未来的研究领域探讨CRP和其他先天免疫信号因子在调节创伤反应中的作用。总的来说，我们发现CRP可能有助于中枢炎症，但它如何做到这一点是一个需要进一步研究的领域。这篇综述描述了我们目前对C反应蛋白（CRP）如何可能在机制上导致PTSD病理的理解。我们讨论了CRP调节外周和中枢神经系统应激反应的机制，沿着未来的研究领域探讨CRP和其他免疫信号因子在调节创伤反应中的作用。总的来说，证据表明CRP可以促进中枢炎症，但它如何做到这一点是一个需要进一步研究的领域。
Increasing evidence indicates that inflammation plays a role in PTSD and stress disorder pathophysiology. PTSD is consistently associated with higher circulating inflammatory protein levels. Rodent models demonstrate that inflammation promotes enduring avoidance and arousal behaviors after severe stressors (e.g., predator exposure and social defeat), suggesting that inflammation may play a mechanistic role in trauma disorders. C‐reactive protein (CRP) is an innate acute phase reactant produced by the liver after acute infection and chronic disease. A growing number of investigations report associations with PTSD diagnosis and elevated peripheral CRP, CRP gene mutations, and CRP gene expression changes in immune signaling pathways. CRP is reasonably established as a potential marker of PTSD and trauma exposure, but if and how it may play a mechanistic role is unclear. In this review, we discuss the current understanding of immune mechanisms in PTSD with a particular focus on the innate immune signaling factor, CRP. We found that although there is consistent evidence of an association of CRP with PTSD symptoms and risk, there is a paucity of data on how CRP might contribute to CNS inflammation in PTSD, and consequently, PTSD symptoms. We discuss potential mechanisms through which CRP could modulate enduring peripheral and CNS stress responses, along with future areas of investigation probing the role of CRP and other innate immune signaling factors in modulating trauma responses. Overall, we found that CRP likely contributes to central inflammation, but how it does so is an area for further study. This review describes our current understanding of how C‐reactive protein (CRP), potentially contributes mechanistically to PTSD pathology. We discuss the mechanisms through which CRP could modulate enduring peripheral and CNS stress responses, along with future areas of investigation probing the role of CRP and other immune signaling factors in modulating trauma responses. Overall, the evidence suggests that CRP can contribute to central inflammation, but how it does so is an area for further study.
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