MV are cell membrane-derived vesicles ranging in size from 0.1 to 1 micron in diameter which are shed in response to cellular activation, cell-cell interaction and apoptosis [23, 24, 25, 26, 27] . These cell-derived vesicles are an interface of activation between cellular components of the blood with the vascular wall and between soluble components of the blood associated with immunity including response to infection [24, 28, 29] . For example, phosphatidylserine (PS) on the surface of MV provides catalytic sites for prothrombinase complex to generate thrombin needed for the conversion of fibrinogen to fibrin in formation of clots [25, 30, 31] . Furthermore, exposure of diluted blood to LPS in vitro increased production of platelet-derived as well as tissue factor positive MV within 3 to 6 hours [32, 33, 34] . While those experiments provide evidence that LPS modulates platelet activation, they do not provide any insight about the interactions of platelet with other blood elements within the earliest stages of activation especially at time points prior to the period when measurable changes in circulating cytokines are observed in vivo [14] . Therefore, the present study was designed to test the hypothesis that acute exposure to a sentinel dose of LPS would induce MV production and exchange of specific proteins/ receptors between platelets and leukocytes via TLR4 activation. MV transport of biologically active cell contents including cell surface receptors among cells were identified using antibodies specific for cell antigens (i.e. CD41 or CD45, which is platelet-or leukocyte-specific antigens respectively) [24] ; MV derived from platelets and/or leukocytes were distinguished by cell specific fluorescein conjugated antigen staining using calibrated flow cytometry.