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,
*
Trudeau Institute, Saranac Lake, NY 12983;
Transplantation, Millennium Pharmaceuticals, Cambridge, MA 02139; and
Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215
Extravascular fibrin deposition is an early and persistent hallmark
of inflammatory responses. Fibrin is generated from plasma-derived
fibrinogen, which escapes the vasculature in response to endothelial
cell retraction at sites of inflammation. Our ongoing efforts to define
the physiologic functions of extravasated fibrin(ogen) have led to the
discovery, reported here, that fibrinogen stimulates macrophage
chemokine secretion. Differential mRNA expression analysis and RNase
protection assays revealed that macrophage inflammatory protein-1
(MIP-1), MIP-1
, MIP-2, and monocyte chemoattractant protein-1 are
fibrinogen inducible in the RAW264.7 mouse macrophage-like cell line,
and ELISA confirmed that both RAW264.7 cells and primary murine
thioglycolate-elicited peritoneal macrophages up-regulate the secretion
of monocyte chemoattractant protein-1 >100-fold upon exposure to
fibrinogen. Human U937 and THP-1 precursor-1 (THP-1) monocytic
cell lines also secreted chemokines in response to fibrinogen, upon
activation with IFN-
and differentiation with vitamin
D3, respectively. LPS contamination could not account for
our observations, as fibrinogen-induced chemokine secretion was
sensitive to heat denaturation and was unaffected by the pharmacologic
LPS antagonist polymyxin B. Nevertheless, fibrinogen- and LPS-induced
chemokine secretion both apparently required expression of functional
Toll-like receptor 4, as each was diminished in macrophages derived
from C3H/HeJ mice. Thus, innate responses to fibrinogen and bacterial
endotoxin may converge at the evolutionarily conserved Toll-like
recognition molecules. Our data suggest that extravascular fibrin(ogen)
induces macrophage chemokine expression, thereby promoting immune
surveillance at sites of inflammation.
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K. Kariko, H. Ni, J. Capodici, M. Lamphier, and D. Weissman mRNA |
