AI Article Synopsis
- Inflammation plays a critical role in the effects of traumatic brain injury (TBI), initiating immune responses within the brain despite its isolation by the blood-brain barrier.
- Immune mediators are quickly released after injury, leading to a sequence of events that can either promote regeneration or cause cell death in brain tissue.
- Recent studies highlight the complex nature of neuroinflammation, revealing both beneficial and harmful effects on brain recovery and potential secondary damage.
Article Abstract
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.
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| http://dx.doi.org/10.1097/00075198-200204000-00002 | DOI Listing |
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