Amplification of bacteria-induced platelet activation is triggered by Fc?RIIA, integrin ?IIb?3, and platelet factor 4.

ABSTRACT: Bacterial adhesion to platelets is mediated via a range of strain-specific bacterial surface proteins that bind to a variety of platelet receptors. It is unclear how these interactions lead to platelet activation. We demonstrate a critical role for the immune receptor Fc?RIIA, ?IIb?3, and Src and Syk tyrosine kinases in platelet activation by Staphylococcus aureus, Streptococcus sanguinis, Streptococcus gordonii, Streptococcus oralis, and Streptococcus pneumoniae. Fc?RIIA activation is dependent on immunoglobulin G (IgG) and ?IIb?3 engagement. Moreover, feedback agonists adenosine 5'-diphosphate and thromboxane A2 are mandatory for platelet aggregation. Additionally, platelet factor 4 (PF4) binds to bacteria and reduces the lag time for aggregation, and gray platelet syndrome ?-granule-deficient platelets do not aggregate to 4 of 5 bacterial strains. We propose that Fc?RIIA-mediated activation is a common response mechanism used against a wide range of bacteria, and that release of secondary mediators and PF4 serve as a positive feedback mechanism for activation through an IgG-dependent pathway.

SUBMITTER: Arman M 

PROVIDER: S-EPMC4023422 | biostudies-literature | 2014 May

REPOSITORIES: biostudies-literature