Monitoring the Neuroinflammatory Response Following Acute Brain Injury.
Monitoring the Neuroinflammatory Response Following Acute Brain Injury.
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DOI：
10.3389/fneur.2017.00351
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发表时间：
2017
影响因子：
3.4
通讯作者：
Helmy A
中科院分区：
文献类型：
--
作者：
Thelin EP;Tajsic T;Zeiler FA;Menon DK;Hutchinson PJA;Carpenter KLH;Morganti-Kossmann MC;Helmy A
创伤性脑损伤（TBI）和蛛网膜下腔出血（SAH）是导致发病率和死亡率的主要原因。在最初的损伤之后，患者可能会因继发性脑损伤而恶化。潜在的分子和细胞级联反应包含先天免疫系统的组成部分。有不同的方法来评估和监测脑炎在神经重症监护病房。这篇叙述性综述的目的是描述在急性背景下监测TBI和SAH患者炎症活动的技术。分析中枢神经系统（CNS）室室（包括脑脊液和细胞外液）中的促炎性和抗炎性细胞因子是监测脑炎症活动替代标志物的最常用方法。这些隔室中的每一个都有不同的生物学特性，反映了局部过程以及全身和中枢神经系统炎症之间的串扰。细胞因子与预后以及持续的继发性损伤进展相关。除了体液介质的动态、局部分析外，通过正电子发射断层扫描成像可以提供炎症细胞活性的整体体内测量，从而揭示初始损伤后的长期过程。与脑损伤后急性激活的先天免疫系统相比，适应性免疫系统可能在慢性期发挥更大的作用，t细胞介导的对脑特异性蛋白的自身反应性证明了这一点。评估神经炎症最困难的方面是确定所监测的过程对大脑是有害还是有益，因为积累的数据表明这些炎症级联反应在损伤后具有双重作用。总之，脑损伤后复杂损伤级联的炎症成分可以使用不同的方式进行监测。使用多模式监测方法可能有助于开发针对炎症级联不同方面的治疗方法，并改善TBI和SAH后的预后。
Traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) are major contributors to morbidity and mortality. Following the initial insult, patients may deteriorate due to secondary brain damage. The underlying molecular and cellular cascades incorporate components of the innate immune system. There are different approaches to assess and monitor cerebral inflammation in the neuro intensive care unit. The aim of this narrative review is to describe techniques to monitor inflammatory activity in patients with TBI and SAH in the acute setting. The analysis of pro- and anti-inflammatory cytokines in compartments of the central nervous system (CNS), including the cerebrospinal fluid and the extracellular fluid, represent the most common approaches to monitor surrogate markers of cerebral inflammatory activity. Each of these compartments has a distinct biology that reflects local processes and the cross-talk between systemic and CNS inflammation. Cytokines have been correlated to outcomes as well as ongoing, secondary injury progression. Alongside the dynamic, focal assay of humoral mediators, imaging, through positron emission tomography, can provide a global in vivo measurement of inflammatory cell activity, which reveals long-lasting processes following the initial injury. Compared to the innate immune system activated acutely after brain injury, the adaptive immune system is likely to play a greater role in the chronic phase as evidenced by T-cell-mediated autoreactivity toward brain-specific proteins. The most difficult aspect of assessing neuroinflammation is to determine whether the processes monitored are harmful or beneficial to the brain as accumulating data indicate a dual role for these inflammatory cascades following injury. In summary, the inflammatory component of the complex injury cascade following brain injury may be monitored using different modalities. Using a multimodal monitoring approach can potentially aid in the development of therapeutics targeting different aspects of the inflammatory cascade and improve the outcome following TBI and SAH.
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