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Chemotactic Activity of Recombinant Human Granulocyte Colony-Stimulating Factor

Recombinant human granulocyte colony-stimulating factor (rhG-CSF) induced migration across polycarbonate filters of human polymorphonuclear leukocytes (PMN). rhG-CSF was active in inducing PMN migration at concentrations ≥10 to 100 U/mL (7 to 70 ng/mL). rhG-CSF did not contain appreciable levels of...

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Bibliographic Details
Published in:Blood 1988-11, Vol.72 (5), p.1456-1460
Main Authors: Wang, Ji Ming, Chen, Zhen Guo, Colella, Silvia, Bonilla, Mary Ann, Welte, Karl, Bordignon, Claudio, Mantovani, Alberto
Format: Article
Language:English
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Summary:Recombinant human granulocyte colony-stimulating factor (rhG-CSF) induced migration across polycarbonate filters of human polymorphonuclear leukocytes (PMN). rhG-CSF was active in inducing PMN migration at concentrations ≥10 to 100 U/mL (7 to 70 ng/mL). rhG-CSF did not contain appreciable levels of endotoxin contamination as assessed by Limulus amebocyte assay, and Polymixin B did not affect the chemotactic activity of rhG-CSF. A monoclonal anti-G-CSF antibody blocked the induction of migration by G-CSF, thus establishing that the cytokine was responsible for the activity of the recombinant preparation. Checkerboard analysis was performed by seeding different concentrations of G-CSF above and/or below the filter and revealed that the migratory response to this cytokine was best observed in the presence of a positive concentration gradient between the lower and upper compartments of the chamber, thus indicating an actual chemotactic effect. When different migrating cells were examined, rhG-CSF was inactive on large granular lymphocytes and endothelial cells under conditions in which appropriate reference attractants were active. In contrast, rhG-CSF elicited a chemotactic response in monocytes inhibited by specific antibody. Thus, G-CSF is a chemotactic signal for phagocytes. This cytokine, when produced at inflammatory sites, may contribute to the recruitment of phagocytes from the blood compartment to amplify resistance against certain noxious agents.
ISSN:0006-4971
1528-0020
DOI:10.1182/blood.V72.5.1456.1456