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Prepublished online as a Blood First Edition Paper on August 1, 2002; DOI 10.1182/blood-2002-01-0069.
Submitted January 10, 2002
Accepted July 17, 2002
Induction of platelet thrombi by bacteria and antibodies
Ulf Sjobring, Ulrika Ringdahl, and Zaverio M Ruggeri*
Section for Microbiology, Immunology and Glycobiology, Institute of Laboratory Medicine, University of Lund, Lund, Sweden
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA, USA
* Corresponding author; email: ruggeri{at}scripps.edu.
We have characterized two 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  IIbß3 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, that also support platelet adhesion. As a result of this co-localization, 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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