Division of Neurosurgery, Department of Clinical Neurosciences, University of Cambridge, Box 167, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 0QQ, UK.
Prog Neurobiol. 2011 Nov;95(3):352-72. doi: 10.1016/j.pneurobio.2011.09.003. Epub 2011 Sep 16.
There is an increasing recognition that following traumatic brain injury, a cascade of inflammatory mediators is produced, and contributes to the pathological consequences of central nervous system injury. This review summarises the key literature from pre-clinical models that underlies our understanding of innate inflammation following traumatic brain injury before focussing on the growing evidence from human studies. In addition, the underlying molecular mediators responsible for blood brain barrier dysfunction have been discussed. In particular, we have highlighted the different sampling methodologies available and the difficulties in interpreting human data of this sort. Ultimately, understanding the innate inflammatory response to traumatic brain injury may provide a therapeutic avenue in the treatment of central nervous system disease.
人们越来越认识到，在创伤性脑损伤后，会产生一连串的炎症介质，从而导致中枢神经系统损伤的病理后果。这篇综述总结了基础临床模型中的关键文献，这些文献为我们理解创伤性脑损伤后的固有炎症提供了依据，然后着重讨论了来自人类研究的日益增多的证据。此外，还讨论了导致血脑屏障功能障碍的潜在分子介质。特别是，我们强调了不同的采样方法以及解释此类人类数据的困难。最终，了解创伤性脑损伤的固有炎症反应可能为治疗中枢神经系统疾病提供一种治疗途径。
