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Induction of platelet thrombi by bacteria and antibodies.

Författare

  • Ulf Sjöbring
  • Ulrika Ringdahl
  • ZM Ruggieri

Summary, in English

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 alpha(IIb)beta(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(gamma)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

Publiceringsår

2002

Språk

Engelska

Sidor

4470-4477

Publikation/Tidskrift/Serie

Blood

Volym

100

Issue

13

Dokumenttyp

Artikel i tidskrift

Förlag

American Society of Hematology

Ämne

  • Clinical Medicine

Status

Published

ISBN/ISSN/Övrigt

  • ISSN: 1528-0020
  • 10.1182