Closed head injury - an inflammatory disease?
Closed head injury - an inflammatory disease?
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DOI：
10.1016/j.brainresrev.2004.12.028
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发表时间：
2005-04-01
影响因子：
--
通讯作者：
Stahel, PF
中科院分区：
文献类型：
--
作者：
Schmidt, OI;Heyde, CE;Stahel, PF
闭合性头部损伤（CHI）仍然是工业化国家年轻人死亡和持续神经功能障碍的主要原因。过去几年的研究工作已经提供了证据表明，损伤脑中的颅内炎症反应有助于神经病理学后遗症，这在很大程度上是头部损伤后不良后果的原因。脑损伤患者复苏早期出现的缺氧和低血压进一步加剧了缺血/再灌注介导的脑损伤引起的炎症反应。CHI后的深刻的内源性神经炎性反应，其在遗传学上旨在保护鞘内室免受入侵病原体和修复受损的脑组织，有助于脑水肿的发展，血脑屏障的破坏，并最终导致迟发性神经元细胞死亡。然而，除了这些有害的影响，神经炎症最近已被证明介导脑损伤后的神经修复机制。神经炎症的这种“双重效应”是过去几年广泛的实验和临床研究的焦点，并导致了对CHI后调节颅内炎症反应的细胞和分子机制的扩展的基础知识。因此，头部损伤最近已经演变为一种炎症和免疫性疾病，而不仅仅是一种纯粹的创伤学、神经学或神经外科实体。本综述将总结迄今已知的创伤后神经炎症后CHI的机制，从临床和实验研究的数据的基础上，特别关注促炎细胞因子，趋化因子和补体系统的作用。(c)2004 Elsevier B. V.保留所有权利。
Closed head injury (CHI) remains the leading cause of death and persisting neurological impairment in young individuals in industrialized nations. Research efforts in the past years have brought evidence that the intracranial inflammatory response in the injured brain contributes to the neuropathological sequelae which are, in large part, responsible for the adverse outcome after head injury. The presence of hypoxia and hypotension in the early resuscitative period of brain-injured patients further aggravates the inflammatory response in the brain due to ischemia/reperfusion-mediated injuries. The profound endogenous neuroinflammatory response after CHI, which is phylogenetically aimed at defending the intrathecal compartment from invading pathogens and repairing lesioned brain tissue, contributes to the development of cerebral edema, breakdown of the blood-brain barrier, and ultimately to delayed neuronal cell death. However, aside from these deleterious effects, neuroinflammation has been recently shown to mediate neuroreparative mechanisms after brain injury as well. This "dual effect" of neuroinflammation was the focus of extensive experimental and clinical research in the past years and has lead to an expanded basic knowledge on the cellular and molecular mechanisms which regulate the intracranial inflammatory response after CHI. Thus, head injury has recently evolved as an inflammatory and immunological disease much more than a pure traumatological, neurological, or neurosurgical entity. The present review will summarize the so far known mechanisms of posttraumatic neuroinflammation after CHI, based on data from clinical and experimental studies, with a special focus on the role of pro-inflammatory cytokines, chemokines, and the complement system. (c) 2004 Elsevier B.V. All rights reserved.