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Escherichia coli induces platelet aggregation in an Fcγ RII a‐dependent manner
Author(s) -
Moriarty R. D.,
Cox A.,
McCall M.,
Smith S. G. J.,
Cox D.
Publication year - 2016
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/jth.13226
Subject(s) - platelet , escherichia coli , platelet activation , microbiology and biotechnology , chemistry , receptor , biology , biochemistry , immunology , gene
EssentialsEscherichia coli (Ecoli) ‐mediated sepsis is a serious illness associated with thrombocytopenia. Gram‐positive bacteria‐induced platelet activation has been characterized, but not Gram‐negative bacteria. E. coli induces platelet aggregation in an α IIb β 3 , FcγRIIa and donor‐dependent manner. E. coli is a potent inducer of platelet activation, and the Fc receptor is a possible drug target for sepsis.Summary Background The discovery of pathogen‐recognition receptors such as Toll‐like receptors on platelets has led to the emergence of the concept of platelets as important components of the host response to infection. Escherichia coli (E. coli) ‐mediated sepsis is a serious illness characterized by the occurrence of thrombocytopenia. Whereas there has been a wealth of research on platelet activation by Gram‐positive bacteria, little is known about the mechanisms associated with Gram‐negative bacteria‐induced platelet activation with Gram‐negative bacteria. Objectives To determine the mechanisms by which Gram‐negative E. coli induces platelet aggregation. Methods Induction of platelet aggregation with E. coli strain O157:H7 was tested in platelet‐rich plasma ( PRP ), washed platelets, and serum depleted of complement factors. Platelet inhibitors (against α II b β 3 , glycoprotein Ibα and Fcγ RII a) were used. Platelet thromboxane synthesis was analyzed after E. coli stimulation. Cell binding assays were used to assess the ability of E. coli to support platelet adhesion. Trypsinization was used to determine the role of E. coli surface proteins. Results and conclusion E. coli ‐induced aggregation in PRP was donor‐dependent. E. coli O157:H7 induced aggregation with a lag time of 6.9 ± 1.3 min in an α II b β 3 ‐dependent and Fcγ RII a‐dependent manner. Furthermore, this interaction was enhanced by the presence of complement, and was dependent on thromboxane synthesis. These results show E. coli to be a potent inducer of platelet aggregation.