期刊
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
卷 22, 期 8, 页码 971-978出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00004647-200208000-00008
关键词
inflammatory response; traumatic brain injury; CSF
资金
- NIAID NIH HHS [AI-15614] Funding Source: Medline
Proinflammatory 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, I hour after trauma, IL-18BP-treated mice showed a significantly improved neurological recovery by 7 clays, 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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