
Ticagrelor Increases Platelet-Mediated Staphylococcus aureus Killing, Resulting in Clearance of Bacteremia
Author(s) -
Erlinda R. Ulloa,
Satoshi Uchiyama,
Robert L. Gillespie,
Victor Nizet,
George Sakoulas
Publication year - 2021
Publication title -
the journal of infectious diseases (online. university of chicago press)/the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1093/infdis/jiab146
Subject(s) - staphylococcus aureus , ticagrelor , bacteremia , platelet , medicine , sepsis , microbiology and biotechnology , platelet factor 4 , staphylococcal infections , immunology , biology , antibiotics , bacteria , myocardial infarction , acute coronary syndrome , genetics
Platelets are a critical immune defense against Staphylococcus aureus bloodstream infections. Staphylococcus aureus α-toxin is a virulence factor that decreases platelet viability and accelerates platelet clearance. It has been shown that ticagrelor blocks α-toxin-mediated platelet injury and resulting thrombocytopenia, protecting mice in a lethal S. aureus sepsis model. We now present the use of ticagrelor as adjunctive therapy in a patient with a S. aureus endovascular infection and thrombocytopenia, associated with restoration of platelet count and bacteremia clearance. Ticagrelor enhanced platelet killing of the S. aureus bloodstream isolate from the treated patient in vitro.