Granulocyte colony-stimulating factor promotes adhesion of neutrophils

被引:37
作者
Chakraborty, A
Hentzen, ER
Seo, SM
Smith, CW
机构
[1] Baylor Coll Med, Dept Med, Infect Dis Sect, Houston, TX 77030 USA
[2] Baylor Coll Med, Dept Pediat, Sect Leukocyte Biol, Houston, TX 77030 USA
[3] Rice Univ, Dept Biomed Engn, Houston, TX 77030 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 2003年 / 284卷 / 01期
关键词
granulocyte colony-stimulating factor; intracellular adhesion molecule-1; leukocyte function-associated antigen-1; macrophage antigen-1; adhesion; polymorphonuclear neutrophils;
D O I
10.1152/ajpcell.00165.2002
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:C103 / C110
页数:8
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