Recent studies in animal models and in humans have demonstrated an acute inflammatory response to traumatic brain injury (TBI), including upregulation of endothelial adhesion molecules and accumulation of neutrophils in brain. Interleukin-8 (IL-8) is a proinflammatory cytokine with neutrophil chemotactic and activating properties. We hypothesized that IL-8 would be increased in CSF in children with severe TBI. CSF was obtained between 0 and 48 h after severe TBI (GCS < 8) from 17 children, ages 2 mo to 16 y. Children were managed with standard neurointensive care including continuous CSF drainage from intraventricular catheters. Control CSF was obtained from 11 children who were evaluated and ruled out for meningitis (no CSF pleocytosis and negative bacterial cultures). CSF was also obtained from 5 children with culture-proven bacterial meningitis to compare TBI with CNS infection. IL-8 was measured by ELISA (R&D Systems, Minneapolis, MN).

Results Values in the Table are median(range). * p < 0.05 vs. Control (ANOVA on ranks and Dunn's test). IL-8 remained increased at 13-24 h (1064 [0-4309]) and 25-48 h (511 [6-1996]) after TBI (p = 0.16 vs. 0-12 h by repeated measures ANOVA). IL-8 was increased in children ≤ 4 y vs. children > 4y of age (p < 0.05).

Table 1 No caption available.
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Conclusions: This is the first report of CSF IL-8 in children after TBI. A sustained increase (to 48 h) in CSF IL-8 was observed, in some cases with concentrations similar to those seen in children with bacterial meningitis. The data are consistent with an acute inflammatory component to TBI in children, and suggest an association between CSF IL-8 and age ≤ 4 y(a group known to be at high risk for poor outcome after TBI1. These data suggest that IL-8 is involved in the acute inflammatory response to TBI and may be a potential target for anti-inflammatory therapy.

Support:NS30318, and the Charles Schertz Fellowship from the Dept. of Anesthesiology and CCM, University of Pittsburgh, Pittsburgh, PA.