Statins potentiate the antibacterial effect of platelets on Staphylococcus aureus

Platelets have largely demonstrated their implication in anti-infectious immunity. This effect is ensured by the secreted molecules stored mostly in platelet alpha granules. Previous studies have reported that Staphylococcus aureus showed sensitivity to this antibacterial effect of platelets. Statins, for their part, have shown a modulating effect on platelet activation. Furthermore, several studies have reported a protective effect of statins in staphylococcal endocarditis. The aim of this study was to investigate the influence of statins on the antibacterial effect of washed platelets. Blood samples were collected from healthy donors (n = 35). PRP was prepared according to the ISTH recommendation. Bacteria were incubated for four hours with untreated-washed platelets, or rather treated by statins and/or GPIIbIIIa antagonists. In order to evaluate the antibacterial effect, the platelet-bacteria mix was spread on the blood agar to count the number of colonies after 18 hours of incubation. Measurement of CD 41 and CD62P expression by flow cytometry was performed to evaluate the effect of statin on bacterial-induced platelet activation. Statins have shown a potentiation of the antibacterial effect of washed platelets (p < .01 for Atorvastatin and Rosuvastatin and p < .001 for Fluvastatin vs untreated washed platelets condition). This effect of statins was dose-dependent and was more significant at 20 μM. The addition of Fluvastatin to platelet-bacterial mix significantly increased the expression of platelet CD41 and CD62P (p < .05 and p < .01 vs resting washed platelets, respectively). Tirofiban, GPIIbIIIa antagonist, reversed the antibacterial effect of washed platelets and suppressed the potentiating effect of statins. Our study demonstrated that statins potentiate the anti-staphylococcal effect of washed platelets. This result may explain the beneficial effect of statins on Staphylococcus aureus infective endocarditis. Further studies are therefore required to explain this effect at the molecular level and to assess its impact in vivo.