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- Arup Chakraborty
- Section of Infectious Diseases, Department of Medicine, and
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- Eric R. Hentzen
- Section of Leukocyte Biology, Department of Pediatrics, Baylor College of Medicine; and
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- Scott M. Seo
- Section of Leukocyte Biology, Department of Pediatrics, Baylor College of Medicine; and
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- C. Wayne Smith
- Section of Leukocyte Biology, Department of Pediatrics, Baylor College of Medicine; and
説明
<jats:p> Granulocyte colony stimulating factor (G-CSF) is well known for its ability to drive the maturation and mobilization of neutrophils. G-CSF also appears to have the potential to activate functions of mature neutrophils, influencing recruitment at sites of inflammation and tissue injury. We investigated the ability of G-CSF to stimulate adhesion of isolated blood neutrophils. G-CSF induced significant adherence to intercellular adhesion molecule (ICAM)-1 that was both macrophage antigen-1 (Mac-1) and leukocyte function-associated antigen-1 dependent. The kinetics of G-CSF-stimulated adhesion to ICAM-1 peaked at 11 min without detectable surface upregulation of Mac-1. This was in marked contrast to chemokines, in which peak activation of adhesion is seen within 1 min of stimulation. In contrast to chemokine-induced adhesion, G-CSF stimulation was not inhibited by pertussis toxin. G-CSF also augmented the attachment of neutrophils to activated human umbilical vein endothelial cells (HUVEC) through specific effects on neutrophils, because HUVEC appear to lack functional G-CSF receptors. </jats:p>
収録刊行物
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- American Journal of Physiology-Cell Physiology
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American Journal of Physiology-Cell Physiology 284 (1), C103-C110, 2003-01-01
American Physiological Society