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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #147483
Title: GRANULOCYTE COLONY-STIMULATING FACTOR PROMOTES ADHESION OF NEUTROPHILS

Author
item CHAKRABORTY, ARUP - BAYLOR COLLEGE MED
item HENTZEN, ERIC - BAYLOR COLLEGE MED
item SEO, SCOTT - BAYLOR COLLEGE MED
item Smith, Wayne

Submitted to: American Journal of Physiology - Cell Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/16/2002
Publication Date: 1/1/2003
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.