Involvement of an intercellular adhesion molecule 1-dependent pathway in the pathogenesis of secondary changes after spinal cord injury in rats.

The intercellular adhesion molecule 1 (ICAM-1) plays an important role in immune responses by promoting infiltration of neutrophils into tissues; however, its implication in the secondary destructive pathomechanism after the initial mechanical injury to the spinal cord has not been clarified yet. This study was conducted to examine the role of ICAM-1 in this process after spinal cord injury (SCI) in rats. The expression of ICAM-1 mRNA was investigated by the reverse transcription-PCR method and the effect of monoclonal antibody (mAb) to ICAM-1 on SCI was evaluated by measuring various parameters. ICAM-1 mRNA expression correlated with the severity of injury and reached its maximum level 6 h after SCI. Intravenous injection of ICAM-1 mAb (1 mg/kg) 30 min after SCI reduced motor disturbance and enhanced recovery. Moreover, it significantly suppressed myeloperoxidase activity by 43.0% and spinal cord edema by 1.1% in the injured spinal cord tissue. The posttraumatic drop in spinal cord blood flow was also improved. These results suggest that ICAM-1 is deeply involved in the secondary self-destructive process after mechanical injury of the spinal cord and should be an effective target for developing a pharmacological treatment for SCI.