Administration of either anti-intercellular adhesion molecule-1 or a nonspecific control antibody improves recovery after traumatic brain injury in the rat.

Intercellular adhesion molecule-1 (ICAM-1) is an endothelial protein that facilitates invasion of leukocytes into the CNS in response to injury or inflammation. ICAM-1 expression correlates with the severity of clinical head injuries, but its importance in secondary injury events is not fully understood. Therefore, we evaluated ICAM-1 expression and the effect of anti-ICAM-1 treatment on motor recovery and neutrophil invasion after traumatic brain injury induced via the lateral fluid-percussion method in the rat. ICAM-1 was expressed in large and small blood vessels within the injured cortex at 10 and 24 h after injury. Repeated administration of anti-ICAM-1 antibody (clone 1A29) at 1, 10, and again at 24 h after injury significantly improved performance in two of three motor tests, compared to saline controls. Equal doses of nonspecific control antibody (IgG) also significantly improved motor test scores, compared to saline controls. Cortical myeloperoxidase activity, an indicator of neutrophil invasion, was significantly reduced 26 h after injury in animals treated with anti-ICAM-1. Animals treated with IgG showed a trend toward reduction that did not reach significance. These data suggest that ICAM-1 may be involved in neutrophil invasion and neurological dysfunction after TBI, but also implicate a role for a nonspecific antibody effect in improved functional outcome.