Peer-Reviewed Journal Details
Mandatory Fields
Wang, J. H.,Sexton, D. M.,Redmond, H. P.,Watson, R. W. G.,Croke, D. T.,BouchierHayes, D.;
1997
Shock
Intercellular adhesion molecule-1 (ICAM-1) is expressed on human neutrophils and is essential for neutrophil adherence and aggregation
Validated
()
Optional Fields
8
55
357
361357
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 this 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 transcription-polymerase chain reaction before and after LPS and TNF-alpha treatment. Furthermore, incubation of PMNs with LPS and TNF-alpha resulted in significant increases in PMN-PMN adherence and aggregation, while addition of either anti ICAM-1 mAb or anti CD11b/CD18 mAb significantly inhibited LPS and TNF-alpha-mediated PMN-PMN adherence and aggregation. These novel findings demonstrate that ICAM-1 is expressed on human PMNs and responsible for PMN aggregation, and suggest that the interaction between ICAM-1 and CD11b/CD18 may be the molecular basis for PMN aggregation and clumping in the microcirculation during systemic inflammatory response syndrome.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 this 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 transcription-polymerase chain reaction before and after LPS and TNF-alpha treatment. Furthermore, incubation of PMNs with LPS and TNF-alpha resulted in significant increases in PMN-PMN adherence and aggregation, while addition of either anti ICAM-1 mAb or anti CD11b/CD18 mAb significantly inhibited LPS and TNF-alpha-mediated PMN-PMN adherence and aggregation. These novel findings demonstrate that ICAM-1 is expressed on human PMNs and responsible for PMN aggregation, and suggest that the interaction between ICAM-1 and CD11b/CD18 may be the molecular basis for PMN aggregation and clumping in the microcirculation during systemic inflammatory response syndrome.
1073-23221073-2322
://WOS:A1997YD37600007://WOS:A1997YD37600007
Grant Details