Abstract
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) |
|---|---|
| Pages (from-to) | 1081-1090 |
| Number of pages | 10 |
| Journal | Journal of Trauma - Injury, Infection and Critical Care |
| Volume | 48 |
| Issue number | 6 |
| DOIs | |
| State | Published - Jun 2000 |
| Externally published | Yes |
Keywords
- Animal models
- Brain injury
- Cellular adhesion molecules
- Inflammation
ASJC Scopus subject areas
- Surgery
- Critical Care and Intensive Care Medicine