Granulocyte colony‐stimulating factor down‐regulates the surface expression of the human leucocyte adhesion molecule‐1 on human neutrophils in vitro and in vivo

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Abstract
Summary. The leucocyte adhesion molecule‐1 (LAM‐1) is the human homologue of the murine peripheral lymph node homing receptor, MEL‐14, and might play a crucial role in neutrophil localization at inflammatory sites. We have reported previously that recombinant human granulocyte colony‐stimulating factor (rhG‐CSF) stimulates or enhances several neutrophil functions in vivo, as well as in vitro. To further explore the possible role of G‐CSF in inflammation we studied the effect of rhG‐CSF on the surface expression of LAM‐1 on human neutrophils, both in vitro and in vivo. The expression of LAM‐1 by human neutrophils was investigated by indirect immunofluorescence using flow cytometry and monoclonal antibodies anti‐Leu‐8 and TQ1. A whole blood analysis was performed to minimize in vitro manipulation. Most circulating human neutrophils expressed LAM‐1 on the cell surface. Brief exposure of neutrophils to rhG‐CSF in vitro decreased the surface expression of LAM‐1. rhG‐CSF down‐regulated neutrophil LAM‐1 expression in a time‐ and dose‐dependent manner. Neutrophils from healthy volunteers and from patients who were receiving rhG‐CSF exhibited a decreased expression of LAM‐1 after rhG‐CSF administration, and the expression thereafter returned or overshot the pretreatment level after stopping rhG‐CSF administration. These findings indicate that rhG‐CSF down‐regulates the surface expression of LAM‐1 on human neutrophils in vivo, as well as in vitro, and G‐CSF might participate in neutrophil‐endothelial cell interaction in inflamed tissue.