Intercellular adhesion molecule-1 (ICAM-1) is expressed on human neutrophils and is essential for neutrophil adherence and aggregation

• Published in: Shock (Augusta, Ga.) Ga.), 1997-11, Vol.8 (5), p.357-361
• Main Authors: Wang, J H, Sexton, D M, Redmond, H P, Watson, R W, Croke, D T, Bouchier-Hayes, D
• Format: Article
• Language: English
• Subjects: Adult; Antibodies, Monoclonal - pharmacology; Base Sequence; CD18 Antigens - immunology; Cell Adhesion - drug effects; Cell Adhesion - physiology; Cell Aggregation - drug effects; Cell Aggregation - physiology; DNA Primers - genetics; Gene Expression - drug effects; Humans; In Vitro Techniques; Intercellular Adhesion Molecule-1 - genetics; Intercellular Adhesion Molecule-1 - immunology; Intercellular Adhesion Molecule-1 - physiology; Lipopolysaccharides - pharmacology; Macrophage-1 Antigen - immunology; Neutrophils - drug effects; Neutrophils - physiology; Polymerase Chain Reaction; RNA, Messenger - genetics; RNA, Messenger - metabolism; Tumor Necrosis Factor-alpha - pharmacology
• ISSN: 1073-2322
• DOI: 10.1097/00024382-199711000-00007

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.