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Fibrinogen mediates leukocyte-endothelium bridging in vivo at low shear
forces
P Sriramarao, LR Languino and DC Altieri
Laboratory of Immunology and Vascular Biology, La Jolla Institute for
Experimental Medicine, CA, USA.
In addition to preserving hemostasis, fibrinogen assembly on leukocytes
mediates inflammatory responses and may aberrantly contribute to vascular
injury. In this study, we used real-time intravital video microscopy in
exposed rabbit mesentery to investigate the potential role of fibrinogen on
leukocyte adherence mechanisms, in vivo. At physiologic concentrations of
0.15 to 0.5 mg/mL, human fibrinogen dose- dependently enhanced by threefold
to fivefold the adhesion of chemoattractant-stimulated monocytic HL-60
cells to rabbit mesenteric endothelium, by acting as a bridging molecule
between the two types. Fibrinogen-dependent intercellular bridging occurred
in venules, but not in arterioles or capillaries (1), was optimal at
reduced flow shear forces (range: 0.77 to 2.79 dyne/cm2) (2), and produced
a firm attachment of monocytic cells to endothelium, rather than transient
rolling (3). Consistent with this model, rabbit fibrinogen failed to
support human leukocyte adhesion, while human fibrinogen enhanced monocytic
cell attachment to rabbit endothelial cells in vitro, in a reaction
indistinguishable from that observed with human endothelium. Antagonists of
the recently described association of fibrinogen with intercellular
adhesion molecule-1 (ICAM-1), including monoclonal antibodies (MoAbs) LB-2
or 2D5, or the fibrinogen gamma 3 peptide gamma Asn117-Ala133, blocked
fibrinogen-dependent leukocyte-endothelium interaction in vitro or in vivo,
respectively, while a control nonbinding antibody or the fibrinogen L10
peptide gamma Leu402-Val411 were ineffective. These data suggest that
simultaneous assembly of fibrinogen on leukocytes and endothelial ICAM-1
provides a pathway of intercellular adhesion which may act in concert with
beta 2 integrins to stabilize firm leukocyte attachment to endothelium, in
vivo. Given the recognized role of fibrinogen as a major risk factor for
atherosclerosis, this mechanism may directly contribute to thrombus
formation and endothelial cell damage in vascular diseases.
Volume 88,
Issue 9,
pp. 3416-3423,
11/01/1996
Copyright © 1996 by The American Society of Hematology
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