Inflammatory response in acute traumatic brain injury: a double-edged sword

Curr Opin Crit Care. 2002 Apr;8(2):101-5. doi: 10.1097/00075198-200204000-00002.


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.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain Injuries / physiopathology*
  • Cytokines / physiology*
  • Encephalitis / complications
  • Encephalitis / physiopathology*
  • Humans
  • Intercellular Adhesion Molecule-1 / physiology
  • Interleukin-10 / physiology
  • Interleukin-6 / physiology
  • Leukocytes / physiology
  • Mice
  • Transforming Growth Factor beta / physiology
  • Tumor Necrosis Factor-alpha / physiology


  • Cytokines
  • Interleukin-6
  • Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1
  • Interleukin-10