Induction of platelet thrombi by bacteria and antibodies
(2002) In Blood 100(13). p.4470-4477- Abstract
- 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 FcgammaRIIA 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... (More)
- 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 FcgammaRIIA 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 regard-less 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/322072
- author
- Sjöbring, Ulf LU ; Ringdahl, Ulrika LU and Ruggeri, ZM
- organization
- publishing date
- 2002
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Blood
- volume
- 100
- issue
- 13
- pages
- 4470 - 4477
- publisher
- American Society of Hematology
- external identifiers
-
- pmid:12393652
- wos:000179759800033
- scopus:0037114630
- ISSN
- 1528-0020
- DOI
- 10.1182/blood-2002-01-0069
- language
- English
- LU publication?
- yes
- id
- f8c48ca3-e390-49c1-9f64-61b4fdc044c3 (old id 322072)
- date added to LUP
- 2016-04-01 12:14:03
- date last changed
- 2022-04-05 19:33:30
@article{f8c48ca3-e390-49c1-9f64-61b4fdc044c3,
abstract = {{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 FcgammaRIIA 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 regard-less 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.}},
author = {{Sjöbring, Ulf and Ringdahl, Ulrika and Ruggeri, ZM}},
issn = {{1528-0020}},
language = {{eng}},
number = {{13}},
pages = {{4470--4477}},
publisher = {{American Society of Hematology}},
series = {{Blood}},
title = {{Induction of platelet thrombi by bacteria and antibodies}},
url = {{http://dx.doi.org/10.1182/blood-2002-01-0069}},
doi = {{10.1182/blood-2002-01-0069}},
volume = {{100}},
year = {{2002}},
}