Introduction
The binding of neutrophils and mononuclear cells to vascular endothelium is an essential
prerequisite in maintaining effective immune-inflammatory responses. This process
has been unraveled as a regulated “adhesion cascade” that involves the expression
of multiple adhesion receptors of the integrin, selectin, and immunoglobulin gene
superfamilies on both cell types. These adhesive interactions are modulated by disparate
environmental signals, ranging from inflammatory and chemotactic cytokines to changes
in shear force at the vessel wall. Although of paramount importance in the preservation
of immune-inflammatory surveillance, dysregulation of leukocyte-endothelium interaction
also constitutes one of the earliest molecular events in the pathogenesis of such
vascular diseases as atherosclerosis. This dysregulation leads to the aberrant accumulation
of mononuclear cells in the damaged intima.
Recently, the interaction of fibrinogen with vascular cells has emerged as an alternate
mechanism for recruiting leukocytes at the site of vascular injury. Although the role
of fibrinogen as a risk factor for atherosclerosis has long been recognized, this
pathway has been associated with complex mechanisms of intercellular adhesion, signal
transduction, second-messenger generation, and modulation of gene expression in vascular
cells. These studies have revealed a multifaceted and far-reaching molecular link
between inflammation and hemostasis–a link that is of potential therapeutic relevance
for the pathogenesis of vascular diseases.