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. 2021 Oct 7;9:716302. doi: 10.3389/fcell.2021.716302

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Copyright © 2021 Leeten, Jacques, Lancellotti and Oury.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Hypothetical model of aspirin and ticagrelor action on S. aureus IE vegetation. (A) The antiplatelet drugs may exert direct effects on bacteria. (B) Ticagrelor and/or aspirin may inhibit bacteria–platelet interactions by acting on either platelet activation or bacteria toxins, which could also alter the adhesion of these hetero-aggregates on damaged or inflamed endothelia. The exact mechanisms of action of aspirin and ticagrelor on vegetation formation remain to be determined, as well as potential added value of ticagrelor compared to aspirin. FnbpA, fibronectin binding protein A; ClfA, clumping factor A; IsdB, iron regulated surface determinant B; Fn, fibronectin; Fg, fibrinogen; IgG, immunoglobulins; VWF, von Willebrand factor; VWbp, von Willebrand factor binding protein (Claes et al., 2017, 2018; Liesenborghs et al., 2018).