1. ^*School of Biological Sciences, University of Manchester, Manchester, United Kingdom
2. ^†Inserm M0103, CEA SHFJ, Orsay, France
3. ^‡UMR CNRS 6551, Center Cycéron, Caen, France
4. ^§Douglas Hospital Research Center, McGill University, Montreal, Quebec, Canada
5. Hyogo College of Medicine, Osaka University, Osaka, Japan

Correspondence: Nancy J Rothwell, 1.124 Stopford Building, School of Biological Sciences, University of Manchester, Oxford Road, Manchester M13 9PT, U.K. E-mail: nancy.rothwell@man.ac.uk

¹Dr. Wheeler is currently affiliated with the Montreal Neurological Institute, Montreal, QC, Canada.

Received 11 October 2002; Revised 13 January 2003; Accepted 15 January 2003.

Abstract

There is now extensive evidence to show that the cytokine interleukin-1 (IL-1) contributes directly to reversible and permanent ischemic brain damage in rodents. Because interleukin-18 (IL-18) shares many structural and functional similarities with IL-1, the authors tested the hypothesis that IL-18 contributes directly to ischemic brain damage in mice exposed to focal, reversible (15-minute or 30-minute) middle cerebral artery occlusion. IL-18 expression was not induced acutely by middle cerebral artery occlusion, and deletion of the IL-18 gene (IL-18 knockout mice) did not affect infarct volume. The present results suggest that IL-18 does not contribute to acute ischemic brain damage.