Inflammatory response in acute traumatic brain injury: a double-edged sword
Inflammatory response in acute traumatic brain injury: a double-edged sword
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DOI：
10.1097/00075198-200204000-00002
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发表时间：
2002-04
影响因子：
3.3
通讯作者：
M. Morganti‐Kossmann;M. Rancan;P. Stahel;T. Kossmann
中科院分区：
文献类型：
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作者：
M. Morganti‐Kossmann;M. Rancan;P. Stahel;T. Kossmann
炎症是创伤性脑损伤病理生理学的重要组成部分。虽然中枢神经系统与其他器官不同，因为它几乎完全与血脑屏障介导的血流隔离，但脑内免疫激活的主要步骤与其他器官相似。这些过程中的关键参与者是在原发性损伤后几分钟内释放的大量免疫介质。它们引导一系列事件，包括粘附分子的表达、细胞浸润以及炎性分子和生长因子的额外分泌，从而导致再生或细胞死亡。问题是：炎症对受伤的脑组织有多大程度的好处，它又是如何导致继发性脑损伤和进行性神经元丧失的？这篇综述简要报告了最近的证据支持双重的，有益的，或有害的作用，创伤性脑损伤后的神经炎症。
Inflammation is an important part of the pathophysiology of traumatic brain injury. Although the central nervous system differs from the other organs because of the almost complete isolation from the blood stream mediated by the blood–brain barrier, the main steps characterizing the immune activation within the brain follow a scenario similar to that in other organs. The key players in these processes are the numerous immune mediators released within minutes of the primary injury. They guide a sequence of events including expression of adhesion molecules, cellular infiltration, and additional secretion of inflammatory molecules and growth factors, resulting in either regeneration or cell death. The question is this: to what extent is inflammation beneficial for the injured brain tissue, and how does it contribute to secondary brain damage and progressive neuronal loss? This review briefly reports recent evidence supporting the dual, the beneficial, or the deleterious role of neuroinflammation after traumatic brain injury.