Background: Administration of anti-CD11B, a monoclonal antibody directed against the leukocyte adhesion molecule CD11B, results in decreased neutrophil infiltration into injured tissue after experimental ischemia. We determined the effect of anti-CD11B administration on neutrophil migration and neurologic functioning after experimental cortical trauma. Methods: Injuries were produced by a pneumatic impactor. Treatment animals received anti-CD11B after injury. Neurologic functioning was quantitated at 1, 12, and 24 hours after injury. Neutrophil migration was assessed with the myeloperoxidase assay. Results: Neutrophil influx was increased in injured cortex after trauma. Anti-CD11B significantly reduced neutrophil influx. There was no significant improvement in neurologic functioning after MAb administration. Conclusions: These results show there is marked neutrophil response to injury as produced with the pneumatic contusion model. This migration may be significantly attenuated by administration of a anti-CD11B.
|Original language||English (US)|
|Number of pages||10|
|Journal||Journal of Trauma - Injury, Infection and Critical Care|
|State||Published - Jun 2000|