Understanding how infection alters cell-cell interactions and release of MV from specific blood borne elements may help to identify new targets for reducing cardiovascular/thrombotic risk with infection. This study demonstrates the acute, immediate interaction of platelets and leukocytes after incubation of whole blood with a sentinel dose of LPS through TLR4 signaling. Exchange of antigens and associations of specific cell-derived MV among cells is a mechanism for the transfers signaling molecules to specific cells. For example, MV derived from neutrophils induced platelet activation by binding to platelets GP1ba (Glycoprotein 1b a) via activated a M b 2 on MV [38] , while platelet-derived MV mediate leukocyte-leukocyte aggregation, activate leukocyte phagocytic properties and amplify leukocyte-mediated tissue injury in thrombotic and inflammatory disorders [39] . Results from the present study demonstrate that the number of platelets positive for leukocyte antigen increased within 60 min of exposure to LPS. This increase was not accompanied by increased expression of PS on cell or MV surface. Because expression of the leukocyte antigen on platelets was defined using the platelet size gate and platelet specific marker CD41 on the flow cytometry, larger leukocytes would be excluded. Therefore, these leukocyte antigens may represent a membrane exchange during platelet-leukocyte adhesion or adhesion of leukocyte-derived MV to the platelets. The half-life of whole platelet-leukocyte aggregates may be shorter and therefore, we did not determine whole platelet-leukocyte aggregates in this study.