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

Prog Neurobiol. 2011 Nov;95(3):352-72. doi: 10.1016/j.pneurobio.2011.09.003. Epub 2011 Sep 16.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiopoietins / physiology
  • Animals
  • Biomarkers
  • Blood-Brain Barrier / physiology
  • Brain Injuries / drug therapy
  • Brain Injuries / pathology
  • Brain Injuries / physiopathology*
  • Brain Injuries / therapy
  • Complement System Proteins / physiology
  • Cytokines / blood
  • Cytokines / metabolism
  • Cytokines / physiology*
  • Humans
  • Inflammation / pathology
  • Inflammation / physiopathology*
  • Interleukins / physiology
  • Tumor Necrosis Factor-alpha / physiology
  • Vascular Endothelial Growth Factor A / physiology

Substances

  • Angiopoietins
  • Biomarkers
  • Cytokines
  • Interleukins
  • Tumor Necrosis Factor-alpha
  • Vascular Endothelial Growth Factor A
  • Complement System Proteins