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Blood, Vol. 94 No. 10 (November 15), 1999:
pp. 3413-3420
Tissue Factor and Factor VIIa Receptor/Ligand Interactions Induce
Proinflammatory Effects in Macrophages
Malcolm A. Cunningham,
Pauline Romas,
Paul Hutchinson,
Stephen R. Holdsworth, and
Peter G. Tipping
From the Centre for Inflammatory Diseases, Monash University,
Department of Medicine, Monash Medical Centre, Clayton, Victoria,
Australia.
The potential for tissue factor (TF) to enhance inflammation by
factor VIIa-dependent induction of proinflammatory changes in
macrophages was explored. Purified recombinant human factor VIIa
enhanced reactive oxygen species production by human monocyte-derived macrophages expressing TF in vitro. This effect was dose- and time-dependent, ligand- and receptor-specific, and independent of other
coagulation proteins. This receptor/ligand binding induced phospholipase C-dependent intracellular calcium fluxes. Transfection studies using a human monocyte-derived cell line (U937) demonstrated that an intact intracytoplasmic domain of TF is required for factor VIIa-induced intracellular calcium fluxes. The capacity of TF to
enhance proinflammatory functions of rabbit peritoneal-elicited macrophages (production of reactive oxygen species and expression of
major histocompatibility complex class II and cell adhesion molecules)
was demonstrated in vivo by treatment with an anti-TF antibody. These
data demonstrate that, in addition to its role in activation of
coagulation, TF can directly augment macrophage activation. These
effects are initiated by binding factor VIIa and are independent of
other coagulation proteins. These studies provide the first
demonstration of a direct proinflammatory role for TF acting as a
cell-signaling receptor.
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