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Blood, Vol. 92 No. 5 (September 1), 1998:
pp. 1626-1638
Hydrodynamic Shear Shows Distinct Roles for LFA-1 and Mac-1 in
Neutrophil Adhesion to Intercellular Adhesion Molecule-1
Sriram Neelamegham,
Andrew D. Taylor,
Alan R. Burns,
C. Wayne Smith, and
Scott I. Simon
From the Section of Leukocyte Biology, Baylor College of Medicine,
Houston; Institute of Biosciences and Bioengineering, Rice University,
Houston, TX; and the Department of Chemical Engineering, State
University of New York, Buffalo, NY.
The binding of neutrophil  2 integrin to intercellular
adhesion molecule-1 (ICAM-1) expressed on the inflamed endothelium is
critical for neutrophil arrest at sites of tissue inflammation. To
quantify the strength and kinetics of this interaction, we measured the
adhesion between chemotactically stimulated neutrophils and
ICAM-1-transfected mouse cells (E3-ICAM) in suspension in a cone-plate
viscometer at shear rates typical of venular blood flow (100 s 1 to 500 s1). The kinetics of
aggregation were fit with a mathematical model based on two-body
collision theory. This enabled estimation of adhesion efficiency,
defined as the probability with which collisions between cells resulted
in firm adhesion. The efficiency of
2-integrin-dependent adhesion was highest (~0.2) at
100 s1 and it decreased to approximately zero at 400 s1. Both LFA-1 and Mac-1 contributed equally to adhesion
efficiency over the initial 30 seconds of stimulation, but adhesion was
entirely Mac-1-dependent by 120 seconds. Two hydrodynamic parameters
were observed to influence integrin-dependent adhesion efficiency: the
level of shear stress and the intercellular contact duration. Below a
critical shear stress (<2 dyn/cm2), contact duration
predominantly limited adhesion efficiency. The estimated minimum
contact duration for 2-integrin binding was
approximately 6.5 ms. Above the critical shear stress (>2 dyn/cm2), the efficiency of neutrophil adhesion to E3-ICAM
was limited by both the contact duration and the tensile stress. We
conclude that at low shear, neutrophil adhesion is modulated
independently through either LFA-1 or Mac-1, which initially contribute
with equal efficiency, but differ over the duration of chemotactic stimulation.
© 1998 by The American Society of Hematology.
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