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.
*Department of Trauma Surgery, The Alfred Hospital, Prahran, Australia; †Department of Surgery, Division of Trauma Surgery, University Hospital, Zurich, Switzerland; and ‡Department of Trauma and Reconstructive Surgery, University Hospital Benjamin Franklin, The Free University of Berlin, Berlin, Germany.
Correspondence to Maria Cristina Morganti-Kossmann, PhD, Department of Trauma Surgery, Alfred Hospital and Monash University, Commercial Rd., Prahran, Victoria, 3181, Australia; e-mail: email@example.com
The work presented by M.C.M.-K. and T.K. has been supported by the Swiss National Science Foundation grants 31-36375. 92, 31-42490.94, and 31-52482.97, and by the Foundations Hartmann-Müller and Olga-Meyenfisch.