INTERCELLULAR-ADHESION MOLECULE-1 (ICAM-1) IS EXPRESSED ON HUMAN NEUTROPHILS AND IS ESSENTIAL FOR NEUTROPHIL ADHERENCE AND AGGREGATION

This study investigated the expression and regulation of intercellular adhesion molecule-1 (ICAM-1) on human polymorphonuclear neutrophils ( PMNs), and its potential role in PMN-PMN adherence and aggregation as observed during systemic inflammatory response syndrome. Normal human PMNs were found to express ICAM-1 with 90% positive population, and th is expression was augmented by endotoxin (lipopolysaccharide, LPS) and tumor necrosis factor-alpha (TNF-alpha) stimulation. The presence of ICAM-1 mRNA in human PMNs was further detected by reverse transcriptio n-polymerase chain reaction before and after LPS and TNF-alpha treatme nt. Furthermore, incubation of PMNs with LPS and TNF-alpha resulted in significant increases in PMN-PMN adherence and aggregation, while add ition of either anti ICAM-1 mAb or anti CD11b/CD18 mAb significantly i nhibited LPS and TNF-alpha-mediated PMN-PMN adherence and aggregation. These novel findings demonstrate that ICAM-1 is expressed on human PM Ns and responsible for PMN aggregation, and suggest that the interacti on between ICAM-1 and CD11b/CD18 may be the molecular basis for PMN ag gregation and clumping in the microcirculation during systemic inflamm atory response syndrome.