Abstract
Platelets are the cornerstone of hemostasis. However, their exaggerated aggregation induces deleterious consequences. In several diseases, such as infectious endocarditis and sepsis, the interaction between platelets and bacteria leads to platelet aggregation. Despite platelet involvement, no antiplatelet therapy is currently recommended in these infectious diseases. We aimed here, to evaluate, in vitro, the effect of antiplatelet drugs on platelet aggregation induced by two of the bacterial pathogens most involved in infectious endocarditis, Staphylococcus aureus and Streptococcus sanguinis. Blood samples were collected from healthy donors (n = 43). Treated platelet rich plasmas were incubated with three bacterial strains of each species tested. Platelet aggregation was evaluated by Light Transmission Aggregometry. CD62P surface exposure was evaluated by flow cytometry. Aggregate organizations were analyzed by scanning electron microscopy. All the strains tested induced a strong platelet aggregation. Antiplatelet drugs showed distinct effects depending on the bacterial species involved with different magnitude between strains of the same species. Ticagrelor exhibited the highest inhibitory effect on platelet activation (p <0.001) and aggregation (p <0.01) induced by S. aureus. In the case of S. sanguinis, platelet activation and aggregation were better inhibited using the combination of both aspirin and ticagrelor (p <0.05 and p <0.001 respectively). Aggregates ultrastructure and effect of antiplatelet drugs observed by scanning electron microscopy depended on the species involved. Our results highlighted that the effect of antiplatelet drugs depended on the bacterial species involved. We might recommend therefore to consider the germ involved before introduction of an optimal antiplatelet therapy.
Highlights
Platelet–bacteria interactions are a cornerstone of several infectious vascular damages such as Disseminated Intra-vascular Coagulation (DIC) following sepsis or embolic events following infectious endocarditis (IE) (Hamzeh-Cognasse et al, 2015).Staphylococci and streptococci represent the most incriminated germs in IE (Park et al, 2016; Habib et al, 2019)
We aimed to evaluate all types of oral antiplatelet drugs used currently in clinical practice on platelet aggregation induced by different strains of each bacterial species (S. aureus and S. sanguinis), looking for possible inter species and inter-strain variability
While pretreatment of Platelet-Rich Plasma (PRP) with aspirin decreased platelet aggregation compared to untreated PRP, whatever the strain, the greatest decrease has been observed when PRP was pretreated with ticagrelor (Figures 1A and 2B)
Summary
Platelet–bacteria interactions are a cornerstone of several infectious vascular damages such as Disseminated Intra-vascular Coagulation (DIC) following sepsis or embolic events following infectious endocarditis (IE) (Hamzeh-Cognasse et al, 2015).Staphylococci and streptococci represent the most incriminated germs in IE (Park et al, 2016; Habib et al, 2019). Platelet–bacteria interactions are a cornerstone of several infectious vascular damages such as Disseminated Intra-vascular Coagulation (DIC) following sepsis or embolic events following infectious endocarditis (IE) (Hamzeh-Cognasse et al, 2015). The presence of protein receptors at the surface of these bacteria allows them to interact with platelets thereby promoting their aggregation (Ford et al, 1993; Hamzeh-Cognasse et al, 2015; Hannachi et al, 2019b). These platelet–bacteria interactions seem to be diverted in favor of bacteria despite the recognized immune role of platelets. The formation of aggregates around the bacteria allows their protection against host immunity as well as their dissemination through bloodstream (Kahn et al, 2013; Paharik and Horswill, 2016)
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