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Articles in PresS, published online ahead of print September 18, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00165.2002
Submitted on April 11, 2002
Accepted on September 16, 2002
1 Medicine-ID, Baylor College of Medicine, Houston, TX, USA; Pediatrics-Leuk Biol, Baylor College of Medicine, Houston, TX, USA
2 Pediatrics-Leuk Biol, Baylor College of Medicine, Houston, TX, USA
* To whom correspondence should be addressed. E-mail: arupc{at}bcm.tmc.edu.
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 ICAM-1 that was both Mac-1 and LFA-1 dependent. The kinetics of G-CSF-stimulated adhesion to ICAM-1 peaked at 11 minutes without detectable surface upregulation of Mac-1. This was in marked contrast to chemokines where peak activation of adhesion is seen within 1 minute 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, since HUVEC appear to lack functional G-CSF receptors.
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