Influence of percussion trauma on expression of intercellular adhesion molecule-1 (ICAM-1) by human cerebral microvascular endothelium.

Abstract

Brain injury is associated with the production of oxygen free radicals (OFR) and the accumulation of polymorphonuclear leukocytes (PMN) at the site of injury, both of which may be involved in the evolution of secondary cerebral injury. Intercellular adhesion molecule-1 (ICAM-1) is responsible for adherence of PMNs. We sought to determine whether percussion trauma altered the expression of ICAM-1 and to determine the effect of OFR scavengers on ICAM-1 expression after percussion trauma. Prospective controlled laboratory research using passage 2 human cerebral microvascular endothelium (HCME). Cell lysates were collected over 24 hours and analyzed for ICAM-1 by enzyme-linked immunosorbent assay (ELISA) after trauma or incubation with tumor necrosis factor (TNF)-alpha. OFR scavengers were added immediately after trauma with or without previous incubation with TNF-alpha. Sublethal percussion trauma did not alter ICAM-1 expression by HCME. TNF-alpha upregulated ICAM-1 in percussed and nonpercussed cells with maximal ICAM-1 expression at 24 hours (p < 0.01, ANOVA). However, percussion trauma significantly blunted the response of HCME to TNF-alpha. The addition of OFR scavengers after percussion trauma alone had no effect on ICAM-1 expression at 24 hours, but restored the response of percussed HCME to TNF-alpha. Percussion trauma alters the response of HCME to cytokine-induced ICAM-1 upregulation, and the normal response is restored by OFR scavengers. This suggests that HCME become dysfunctional after percussion trauma and this dysfunction may be mediated by OFR.