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Platelets enhance dendritic cell responses against S. aureus through CD40-CD40L interactions.

Staphylococcus aureus is a major human pathogen that can cause mild to severe life threatening infections in many tissues and organs. Platelets are known to participate in protection against S. aureus by directly killing and enhancing the activities of neutrophils and macrophages in clearing S. aureus infection. Platelets have also been shown to induce monocyte differentiation into dendritic cells and to enhance activation of dendritic cells. Therefore, in the present study, we explored the role of platelets in enhancing bone marrow derived dendritic cell (BMDC) function against S. aureus We observed a significant increase in dendritic cell phagocytosis and intracellular killing of methicillin-resistant Staphylococcus aureus (MRSA) strain (USA300) by thrombin-activated platelets or their releasates. Enhancement of bacteria uptake and killing by DCs are mediated by platelet derived CD40L. Co-culture of USA300 and BMDCs in presence of thrombin-activated platelet releasates invokes upregulation of maturation marker CD80 on DCs and enhanced production of pro-inflammatory cytokines TNFα, IL-12, and IL-6. Overall, these observations support our hypothesis that platelets play a critical role in the host defense against S. aureus infection. Platelets stimulate DCs leading to direct killing of S. aureus and enhanced DC maturation, potentially leading to adaptive immune responses against S. aureus .

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