Role of cerebral inflammation after traumatic brain injury: A revisited concept

Neuroinflammation occuring after traumatic brain injury (TBI) is a complex phenomenon comprising distinct cellular and molecular events involving the injured as well as the healthy cerebral tissue. Although immunoactivation o nly represents a one of the many cascades initiated in the pathophysiology of TBI, the exact function of each mediator, activated cell types or pathop hysiological mechanism, needs to be further elucidated. It is widely accept ed that inflammatory events display dual and opposing roles promoting, on t he one hand, the repair of the injured tissue and, on the other hand, causi ng additional brain damage mediated by the numerous neurotoxic substances r eleased. Most of the data supporting these hypotheses derive from experimen tal work based on both animal models and cultured neuronal cells. More rece ntly, evidence has been provided that a complete elimination of selected in flammatory mediators is rather detrimental as shown by the attenuation of n eurological recovery. However, there are conflicting results reported on th is issue which strongly depend on the experimental setting used. The histor y of immunoactivation in neurotrauma is the subject of this review article, giving particular emphasis to the comparison of clinical versus experiment al studies performed over the last 10 years. These results also are evaluat ed with respect to other neuropathologies, which are years ahead as compare d to the research in TBI. The possible reciprocal influence of peripheral a nd intrathecal activation of the immune system will also be discussed. To c onclude, the future directions of research in the field of neurotrauma is c onsidered.