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Mediators of Inflammation
Volume 2006 (2006), Article ID 90123, 6 pages
Research Communication

Spatiotemporal Pattern of Neuroinflammation After Impact-Acceleration Closed Head Injury in the Rat

1Department of Neurosurgery, University Hospital Antwerp, Edegem 2650, Belgium
2Department of Neurology, Heinrich-Heine University, Düsseldorf 40225, Germany
3Department of Life Sciences, Janssen Research Foundation, Beerse 2340, Belgium
4Julius-Maximilians University, Heinrich-Heine University, Würzburg 97080, Belgium
5Department of Intensive Care Medicine, University Hospital Antwerp, Edegem 2650, Belgium

Received 21 September 2005; Accepted 20 October 2005

Copyright © 2006 Servan Rooker et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Inflammatory processes have been implicated in the pathogenesis of traumatic brain damage. We analyzed the spatiotemporal expression pattern of the proinflammatory key molecules: interleukin-1β, interleukin-6, tumor necrosis factor-α, and inducible nitric oxide synthase in a rat closed head injury (CHI) paradigm. 51 rats were used for RT-PCR analysis after CHI, and 18 for immunocytochemistry. We found an early upregulation of IL-1β, IL-6, and TNF-α mRNA between 1 h and 7 h after injury; the expression of iNOS mRNA only revealed a significant increase at 4 h. After 24 h, the expression decreased towards baseline levels, and remained low until 7 d after injury. Immunocytochemically, IL-1β induction was localized to ramified microglia in areas surrounding the primary impact place as well as deeper brain structures. Our study shows rapid induction of inflammatory gene expression that exceeds by far the primary impact site and might therefore contribute to tissue damage at remote sites.