Cytokines and innate inflammation in the pathogenesis of human traumatic brain injury

被引:214
作者
Helmy, Adel [1 ]
De Simoni, Maria-Grazia [2 ]
Guilfoyle, Mathew R. [1 ]
Carpenter, Keri L. H. [1 ,3 ]
Hutchinson, Peter J. [1 ,3 ]
机构
[1] Univ Cambridge, Addenbrookes Hosp, Div Neurosurg, Dept Clin Neurosci, Cambridge CB2 0QQ, England
[2] Mario Negri Inst Pharmacol Res, Lab Inflammat & Nervous Syst Dis, I-20156 Milan, Italy
[3] Univ Cambridge, Addenbrookes Hosp, Wolfson Brain Imaging Ctr, Dept Clin Neurosci, Cambridge CB2 0QQ, England
基金
英国医学研究理事会;
关键词
Traumatic brain injury; Cytokines; Inflammation; Blood brain barrier; Cerebrospinal fluid; Microdialysis; TUMOR-NECROSIS-FACTOR; ENDOTHELIAL GROWTH-FACTOR; CLOSED-HEAD INJURY; CENTRAL-NERVOUS-SYSTEM; VASCULAR-PERMEABILITY-FACTOR; REDUCES CONTUSION VOLUME; FOCAL CEREBRAL-ISCHEMIA; CORTICAL IMPACT INJURY; FLUID PRODUCTION-RATE; NEURONAL CELL-DEATH;
D O I
10.1016/j.pneurobio.2011.09.003
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
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. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码:352 / 372
页数:21
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