Cortical interleukin-1 beta elevation after traumatic brain injury in the rat: no effect of two selective antagonists on motor recovery.

Interleukin-1 is an inflammatory cytokine implicated in secondary responses to traumatic brain injury. We utilized a specific IL-beta enzyme-linked immunoadsorbant assay to examine the expression of IL-beta after lateral fluid percussion brain injury in the rat. IL-beta was significantly elevated in the ipsilateral injured cortex at 4 h after injury. Increased levels of IL-beta were also observed at 12, 24 and 72 h after injury, although such changes did not reach statistical significance. To determine whether injury-induced IL-beta expression may contribute to subsequent neurological impairment, we treated rats with either of two structurally different, selective IL-1 antagonists and monitored neurological recovery 1, 7 and 14 days later. Intracerebroventricular treatment with either the endogenous interleukin-1 receptor antagonist (10 microg) at 15 min, 2, 4, 6, and 8 h after injury or soluble IL-1 receptors (10 microg) at 15 min, 4 and 8 h after injury did not significantly alter outcome in a series of motor tasks. These data suggest that cortical elevations of IL-beta follow traumatic brain injury, but they may not contribute to subsequent neurological impairment.