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Prepublished online as a Blood First Edition Paper on August 1, 2002; DOI 10.1182/blood-2002-01-0069.
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Blood, 15 December 2002, Vol. 100, No. 13, pp. 4470-4477
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Induction of platelet thrombi by bacteria and
antibodies
Ulf Sjöbring,
Ulrika Ringdahl, and
Zaverio M. Ruggeri
From the Section for Microbiology, Immunology and
Glycobiology, the Institute of Laboratory Medicine, University of Lund,
Lund, Sweden, and Roon Research Center for
Arteriosclerosis and Thrombosis, Division of Experimental Hemostasis
and Thrombosis, Departments of Molecular and Experimental Medicine and
of Vascular Biology, Scripps Research Institute, La Jolla, CA.
We have characterized 2 distinct mechanisms through which
infectious agents may promote platelet adhesion and thrombus formation in flowing blood, thus contributing to the progression of disease. In
one case, the process initiates when the integrin
 IIb 3 mediates platelet arrest onto
immobilized bacterial constituents that have bound plasma fibrinogen.
If blood contains antibodies against the bacteria, immunoglobulin (Ig)
G may cluster on the same surface and activate adherent platelets
through the Fc RIIA receptor, leading to thrombus growth. As an
alternative, bacteria that cannot bind fibrinogen may attach to
substrates, such as immobilized plasma proteins or components of the
extracellular matrix, which also support platelet adhesion. As a result
of this colocalization, IgG bound to bacteria can activate neighboring
platelets and induce thrombus growth regardless of their ability to
initiate platelet-surface contact. Our results demonstrate that
intrinsic constituents of infectious agents and host proteins play
distinct but complementary roles in recruiting platelets into thrombi,
possibly contributing to complications of acute and chronic infections.
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