The role of markers of inflammation in traumatic brain injury.
The role of markers of inflammation in traumatic brain injury.
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DOI：
10.3389/fneur.2013.00018
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发表时间：
2013
影响因子：
3.4
通讯作者：
Morganti-Kossmann MC
中科院分区：
文献类型：
--
作者：
Woodcock T;Morganti-Kossmann MC
在创伤性冲击的几分钟内，在受伤的大脑中引发了强烈的炎症反应。这种创伤后尖叫的复杂性涉及细胞成分，包括常驻胶质细胞、小胶质细胞和星形胶质细胞的激活以及血液白细胞的浸润。第二部分涉及分泌免疫介质，其可分为以下亚组：原型促炎细胞因子（白细胞介素-1，肿瘤坏死因子，白细胞介素-6），抗炎细胞因子这些细胞因子包括细胞因子（IL-4、白细胞介素-10和TGF-β）和趋化性细胞因子或趋化因子，其特异性地驱动实质和外周免疫细胞在受损脑区域中的积累。这种机制已经在动物模型中得到证实，主要是在啮齿动物以及人脑中。虽然体液免疫应答在创伤性脑损伤（TBI）后的急性期特别明显，但胶质细胞的激活似乎是持续数月的相当长的效应。细胞因子和细胞类型的复杂相互作用设置了一个事件网络，其随后与相邻的病理级联交叉，包括氧化应激、兴奋性毒性或修复性事件，包括血管生成、瘢痕形成和神经发生。公认的是，神经炎症负责有益和有害的影响，有助于继发性脑损伤，但也促进神经修复。虽然这些介质是免疫激活的明确标志物，但细胞因子在多大程度上可以被定义为反映脑损伤的诊断因素或作为长期结果的预测因子还需要进一步证实。在临床研究中，一些研究组报告了脑脊液或脑实质内组织中成比例的细胞因子产生，并伴有初始脑损伤、死亡率或不良结局评分。然而，细胞因子作为生物标志物的有效性并没有被广泛接受。这篇综述文章将讨论来自临床和实验室研究的证据，探索免疫标志物作为TBI分类和预后相关性的有效性。
Within minutes of a traumatic impact, a robust inflammatory response is elicited in the injured brain. The complexity of this post-traumatic squeal involves a cellular component, comprising the activation of resident glial cells, microglia, and astrocytes, and the infiltration of blood leukocytes. The second component regards the secretion immune mediators, which can be divided into the following sub-groups: the archetypal pro-inflammatory cytokines (Interleukin-1, Tumor Necrosis Factor, Interleukin-6), the anti-inflammatory cytokines (IL-4, Interleukin-10, and TGF-beta), and the chemotactic cytokines or chemokines, which specifically drive the accumulation of parenchymal and peripheral immune cells in the injured brain region. Such mechanisms have been demonstrated in animal models, mostly in rodents, as well as in human brain. Whilst the humoral immune response is particularly pronounced in the acute phase following Traumatic brain injury (TBI), the activation of glial cells seems to be a rather prolonged effect lasting for several months. The complex interaction of cytokines and cell types installs a network of events, which subsequently intersect with adjacent pathological cascades including oxidative stress, excitotoxicity, or reparative events including angiogenesis, scarring, and neurogenesis. It is well accepted that neuroinflammation is responsible of beneficial and detrimental effects, contributing to secondary brain damage but also facilitating neurorepair. Although such mediators are clear markers of immune activation, to what extent cytokines can be defined as diagnostic factors reflecting brain injury or as predictors of long term outcome needs to be further substantiated. In clinical studies some groups reported a proportional cytokine production in either the cerebrospinal fluid or intraparenchymal tissue with initial brain damage, mortality, or poor outcome scores. However, the validity of cytokines as biomarkers is not broadly accepted. This review article will discuss the evidence from both clinical and laboratory studies exploring the validity of immune markers as a correlate to classification and outcome following TBI.
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