• Ido Yatsiv, Maria C Morganti-Kossmann, Daniel Perez, Charles A Dinarello, Daniela Novick, Menachem Rubinstein, Viviane I Otto, Mario Rancan, Thomas Kossmann, Claudio A Redaelli, Otmar Trentz, Esther Shohami, and Philip F Stahel.
• Pediatric Intensive Care Unit and Department of Pharmacology, Hebrew University Hadassah Medical Center, Jerusalem, Israel.
• J. Cereb. Blood Flow Metab. 2002 Aug 1;22(8):971-8.

AbstractProinflammatory cytokines are important mediators of neuroinflammation after traumatic brain injury. The role of interleukin (IL)-18, a new member of the IL-1 family, in brain trauma has not been reported to date. The authors investigated the posttraumatic release of IL-18 in murine brains following experimental closed head injury (CHI) and in CSF of CHI patients. In the mouse model, intracerebral IL-18 was induced within 24 hours by ether anesthesia and sham operation. Significantly elevated levels of IL-18 were detected at 7 days after CHI and in human CSF up to 10 days after trauma. Published data imply that IL-18 may play a pathophysiological role in inflammatory CNS diseases; therefore its inhibition may ameliorate outcome after CHI. To evaluate the functional aspects of IL-18 in the injured brain, mice were injected systemically with IL-18-binding protein (IL-18BP), a specific inhibitor of IL-18, 1 hour after trauma. IL-18BP-treated mice showed a significantly improved neurological recovery by 7 days, accompanied by attenuated intracerebral IL-18 levels. This demonstrates that inhibition of IL-18 is associated with improved recovery. However, brain edema at 24 hours was not influenced by IL-18BP, suggesting that inflammatory mediators other than IL-18 induce the early detrimental effects of intracerebral inflammation.

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