• Keira Kamm, Wayne Vanderkolk, Chuck Lawrence, Mark Jonker, and Alan T Davis.
• Grand Rapids/Michigan State University General Surgery Residency, Department of Trauma, Spectrum Butterworth Hospital, 221 Michigan Street NE, Grand Rapids, MI 49503, USA. kkamm@siumed.edu
• J Trauma. 2006 Jan 1;60(1):152-7.

BackgroundUsing a model of traumatic brain injury (TBI) in the rat, this study was undertaken to characterize the short-term biochemical changes of IL-1beta, IL-10, and tumor necrosis factor TNF-alpha to determine whether injury in the brain elicits a systemic cytokine response.MethodsSprague-Dawley rats were subjected to a TBI using a weight-drop model and then killed at various time points after injury. Samples of blood, brain, and liver were recovered and analyzed for concentrations of IL-1beta, IL-10, and TNF-alpha as well as IL-1beta and IL-10 mRNA expression in liver and brain.ResultsIn brain, IL-1beta increased in the first hour after injury, peaked at 8 hours, and declined during the final 16 hours. IL-10 quickly increased during the first 4 hours and then gradually rose over the last 20 hours. Analysis of liver showed no upregulation of these markers and plasma IL-1beta and IL-10 were unchanged compared with controls. Although not upregulated in brain, TNF-alpha showed a statistically significant (p < 0.05) rise in plasma from 14 +/- 16 pg/mL at 20 minutes to 91 +/- 28 pg/mL at 24 hours.ConclusionUsing a model of TBI, we have demonstrated that there is a rise in both IL-1beta and IL-10 in the injured rat brain within the first 24 hours after injury without a corresponding rise in either plasma or liver. Therefore, it appears as if two strong indicators of brain injury severity are expressed and possibly carry out their actions solely in the brain.

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