Intercellular adhesion molecule-1 (ICAM-1) is a cytokine-inducible adhesion molecule, expressed on cells of multiple lineages at the site of inflammation. Cytofluorometric analysis revealed that CD16-positive peripheral blood polymorphonuclear leukocytes (PMNs, neutrophils) expressed ICAM-1 on their surface, and it was upregulated by in vitro stimulation with tumor necrosis factor (TNF), GM-CSF and Staphylococcus aureus. The S. aureus-induced stimulation of ICAM-1 expression was inhibited by pentoxifylline (PTX). As TNF is a potent inducer of ICAM-1 expression, it is concluded that in these experiments the inhibition of TNF production by PTX concomitantly resulted in the inhibition of the upregulation of ICAM-1. However, the inhibition of granulocyte apoptosis by PTX might be of importance in this process. The present study provides evidence that cytokine-stimulated neutrophils are able to express the adhesion molecule ICAM-1 and this may allow ICAM-1-positive neutrophils to physically interact with LFA-1-positive inflammatory cells. The preliminary results demonstrate that the basal expression of ICAM-1 on PMNs of septic patients is higher than that in the case of normal blood donors. Further studies will elucidate the in vivo relevance of cytokine-induced neutrophil ICAM-1 expression and the potential role of its inhibition by PTX in inflammatory response disorders.

Keywords:
Polymorphonuclear granulocytes, Intracellular adhesion molecule-1, Tumor necrosis factor, Staphylococcus, Pentoxifylline, Sepsis
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© 1997 S. Karger AG, Basel
1997
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