|Chakraborty, Arup - BAYLOR COLLEGE MED|
|Hentzen, Eric - BAYLOR COLLEGE MED|
|Seo, Scott - BAYLOR COLLEGE MED|
|Smith, C Wayne|
Submitted to: American Journal of Physiology - Cell Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 16, 2002
Publication Date: January 1, 2003
Citation: Chakraborty, A., Hentzen, E.R., Seo, S., Smith, W.C. 2003. Granulocyte colony-stimulating factor promotes adhesion of neutrophils. American Journal of Physiology - Cell Physiology.284(1):C103-C110. Interpretive Summary: This paper discusses new data on the ability of a hormone called granulocyte colony stimulating factor (G-CSF) to increase the function of white blood cells. While these functions are important in resistance to infection, they may contribute to tissue injury if inflammation is enhanced.
Technical Abstract: 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.