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, and LTB4 on the
adhesive kinetics of LFA-1 and Mac-1 on human neutrophils
1 Institute of Biosciences and Bioengineering, Rice University, Houston 77005; 2 Speros P. Martel Section of Leukocyte Biology, Department of Pediatrics, and 3 Structural and Computational Biology and Molecular Biophysics Program, Baylor College of Medicine, Houston, Texas 77030
Firm adhesion of
rolling neutrophils on inflamed endothelium is dependent on
2 (CD18)-integrins and activating stimuli. LFA-1 (CD11a/CD18) appears to be more important than Mac-1 (CD11b/CD18) in
neutrophil emigration at inflammatory sites, but little is known of the
relative binding characteristics of these two integrins under
conditions thought to regulate firm adhesion. The present study
examined the effect of chemoattractants on the kinetics of LFA-1 and
Mac-1 adhesion in human neutrophils. We found that subnanomolar
concentrations of interleukin-8, Gro-
, and leukotriene B4 (LTB4) induced rapid and optimal rates of
LFA-1-dependent adhesion of neutrophils to intercellular adhesion
molecule (ICAM)-1-coated beads. These optimal rates of LFA-1 adhesion
were transient and decayed within 1 min after chemoattractant
stimulation. Mac-1 adhesion was equally rapid initially but continued
to rise for 
6 min after stimulation. A fourfold higher density of
ICAM-1 on beads markedly increased the rate of binding to LFA-1 but did not change the early and narrow time window for the optimal rate of
adhesion. Using well-characterized monoclonal antibodies, we showed
that activation of LFA-1 and Mac-1 by Gro- was completely blocked by
anti-CXC chemokine receptor R2, but activation of these integrins by
interleukin-8 was most effectively blocked by anti-CXC chemokine
receptor R1. The topographical distribution of beads also reflected
significant differences between LFA-1 and Mac-1. Beads bound to Mac-1
translocated to the cell uropod within 4 min, but beads bound to LFA-1
remained bound to the lamellipodial regions at the same time. These
kinetic and topographical differences may indicate distinct functional
contributions of LFA-1 and Mac-1 on neutrophils.
intercellular adhesion molecule-1; inflammation; chemokine; emigration; integrin; interleukin-8; leukotriene B4
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