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*
Department of Chemical Engineering, Bioengineering Laboratory, State University of New York, Buffalo, NY 14260;
Department of Pediatrics, Section of Leukocyte Biology, Baylor College of Medicine, Houston, TX 77005; and
Division of Biomedical Engineering, University of California, Davis, CA 95616
We examined the relative contributions of LFA-1, Mac-1, and ICAM-3
to homotypic neutrophil adhesion over the time course of formyl peptide
stimulation at shear rates ranging from 100 to 800 s-1.
Isolated human neutrophils were sheared in a cone-plate viscometer and
the kinetics of aggregate formation was measured by flow cytometry. The
efficiency of cell adhesion was computed by fitting the aggregate
formation rates with a model based on two-body collision theory.
Neutrophil homotypic adhesion kinetics varied with shear rate and was
most efficient at 800 s-1, where 
40% of the collisions
resulted in adhesion. A panel of blocking Abs to LFA-1, Mac-1, and
ICAM-3 was added to assess the relative contributions of these
molecules. We report that 1) LFA-1 binds ICAM-3 as its primary ligand
supporting homotypic adhesion, although the possibility of other
ligands was also detected. 2) Mac-1 binding to an unidentified ligand
supports homotypic adhesion with an efficiency comparable to LFA-1 at
low shear rates of 100 s-1. Above 300 s-1,
however, Mac-1 and not LFA-1 were the predominant molecules supporting
cell adhesion. This is in contrast to neutrophil adhesion to
ICAM-1-transfected cells, where LFA-1 binds with a higher avidity than
Mac-1 to ICAM-1. 3) Following stimulation, the capacity of LFA-1 to
support aggregate formation decreases with time at a rate 3-fold
faster than that of Mac-1. The results suggest that the relative
contributions of ß2 integrins and ICAM-3 to neutrophil
adhesion is regulated by the magnitude of fluid shear and time of
stimulus over a range of blood flow conditions typical of the venular
microcirculation.
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