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

• Published in: British journal of haematology Vol. 84; no. 4; p. 574
• Main Authors: Ohsaka, A, Saionji, K, Sato, N, Mori, T, Ishimoto, K, Inamatsu, T
• Format: Journal Article
• Language: English
• Published: England 01.08.1993
• Subjects: Antigens, CD - drug effects; CD11 Antigens; Cell Adhesion - physiology; Cell Adhesion Molecules - drug effects; Cell Adhesion Molecules - metabolism; Cells, Cultured; Dose-Response Relationship, Drug; Granulocyte Colony-Stimulating Factor - pharmacology; Humans; In Vitro Techniques; L-Selectin; Membrane Glycoproteins - drug effects; Neutrophils - metabolism; Recombinant Proteins - pharmacology; Time Factors
• ISSN: 0007-1048
• DOI: 10.1111/j.1365-2141.1993.tb03130.x

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.