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.
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.
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.
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.
From the University of North Carolina-Chapel Hill Division of Neurosurgery (K.D.W.), Chapel Hill, North Carolina; Nathan Kline Institute for Psychiatric Research (C.A.B.), Orangeburg, New York; Department of Biomedical Engineering (L.H.), University of Michigan, Ann Arbor, Michigan; Department of Pathology (C.H.M.), University of California-Davis, Davis, California; and (K.B.Q.) Lewiston, Maine.
Address for reprints: Kyle D. Weaver, MD, Division of Neurosurgery, University of North Carolina-Chapel Hill, 148 Burnett-Womack/CB#7060, Chapel Hill, NC 27599-7060.
Submitted for publication October 4, 1999.
Accepted for publication March 1, 2000.
This work was supported by the Distinguished Medical Scholars Program of the University of North Carolina-Chapel Hill School of Medicine.