title: Granulocyte colony-stimulating factor down-regulates the surface expression of the human leucocyte adhesion molecule-1 on human neutrophils in vitro and in vivo.
abstract: 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.
authors.affiliation: Department of Internal Medicine, Hitachi General Hospital, Ibaraki, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Ohsaka
authors.forename: K
authors.initials: K
authors.lastname: Saionji
authors.forename: N
authors.initials: N
authors.lastname: Sato
authors.forename: T
authors.initials: T
authors.lastname: Mori
authors.forename: K
authors.initials: K
authors.lastname: Ishimoto
authors.forename: T
authors.initials: T
authors.lastname: Inamatsu
mesh_terms: D015703:Antigens, CD / Q000187:drug effects; D018845:CD11 Antigens; D002448:Cell Adhesion / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000187:drug effects* / Q000378:metabolism; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D019041:L-Selectin; D008562:Membrane Glycoproteins / Q000187:drug effects; D009504:Neutrophils / Q000378:metabolism*; D011994:Recombinant Proteins / Q000494:pharmacology; D013997:Time Factors
chemical_list: D015703:Antigens, CD; D018845:CD11 Antigens; D015815:Cell Adhesion Molecules; D008562:Membrane Glycoproteins; D011994:Recombinant Proteins; D019041:L-Selectin; D016179:Granulocyte Colony-Stimulating Factor