Effect Of Streptococcus Sanguinis/ Porphyromonas Gingivalis On Platelet Aggregation

To elucidate molecular mechanisms underlying Streptococcus sanguinis (S.s) and Porphyromonas gingivalis (P.g) - mediated platelet activation/ aggregation, the temporal dynamics of S.s - P.g co-aggregation and its impact on platelet responsiveness were further investigated. Equal concentrations of S.s and P.g were prepared, and equal portions‌ of each were pre-mixed for 30 minutes. S.s was first added to platelet-rich plasma (PRP), followed by the addition of an equal volume of P.g after 3, 6, 9 or 12 minutes. Bacterial concentrations were standardized across groups, with PBS and 10 μM ADP as controls. Platelet activation (P-selectin expression) and aggregation (fibrinogen binding) were quantified via flow cytometry. S.s and P.g could significantly induce platelet activation/ aggregation either individually or at different intervals (p<0.05 vs PBS), while the pre-mixed bacteria showed relatively inapparent effects (p<0.05). Compared with S.s + P.g group, other experimental groups were upregulated significantly (all P<0.05) in P-selectin expression and fibrinogen binding. And there was no significant difference among S.s -3/6/9/12- P.g groups (all P>0.05). S.s and P.g induce platelet activation/ aggregation, potentially conducive to thrombus formation. However, their co-aggregation induces mutual antagonism, likely via competitive receptor binding or inhibitory metabolite secretion, indicating that while individual species enhance cardiovascular risk, their coexistence may paradoxically mitigate thrombogenesis through interspecies interference.