©2004 by MEDIMOND S.r.l. 115 E912C0022 Inhibition of Neurogenic Inflammation Attenuates the Inflammatory Response Following Traumatic Brain Injury in Rats K. Reardon 1 , D. Heath 1 , A. Nimmo 2 , R. Vink 3 and K. Whitfield 1 1 School of Pharmacy & Molecular Sciences and 2 School of Biomedical Sciences, James Cook University, Townsville, Queensland; 3 Department of Pathology, University of Adelaide, Adelaide, South Australia, Australia. Summary A profound inflammatory response is initiated following traumatic brain injury (TBI). It has been proposed that serum IL-6 levels may serve as a marker for the severity of the injury. Using the rat impact-accelera- tion model of TBI, the study examined whether drugs which are able to inhibit neurogenic inflammation (capsaicin, NK1 antagonist), might in- fluence the post-traumatic inflammatory response. In non-treated animals, TBI resulted in a significant increase in serum IL-6 levels. However, in animals pre-treated with capsaicin prior to injury, or treated with an NK1 antagonist following injury, this rise in IL-6 levels was not observed. We conclude that the inhibition of neurogenic inflammation may attenuate the inflammatory reaction associated with TBI, and help improve out- come. Introduction Traumatic brain injury (TBI) results in a profound inflammatory re- sponse within the central nervous system, which is characterised by the increased production of a number of pro-inflammatory mediators, includ- ing tumour necrosis factor alpha, interleukin-1beta and interleukin-6 (IL- 6) (1). These mediators are considered to have both detrimental and beneficial effects in terms of neural outcome following TBI. On one hand they contribute to neuronal cell death and dysfunction, whilst on the other they establish the foundation for reparative processes. Whilst the tissue