A single TLR4 sentinel dose injection of LPS, such as used in this study, shortened platelet half-life and increased platelet production without increases in cytokine production within 3 hours of stimulation [14] . Although in vivo interaction of plateletand leukocyte-aggregates with the vascular wall could stimulate or exacerbate proinflammatory immune responses [43, 44] , the half-life of these cell aggregates is not known. A significant finding of the present in vivo study is that leukocytes sustain or retain platelet antigen seven days after an in vivo injection of LPS. This time point corresponds to turnover of the platelet pool and is consistent with observations that changes in platelet half-life and increases in platelet turnover are dependent on the concentration of agonist, i.e. LPS, activation [13, 14] . Quantification of dual-positive events is usually not considered in studies of cellular or MV quantification with LPS stimulation. Results from the present study, therefore, suggest that platelet-leukocyte antigen could be used as an additional biomarker of cellular activation for diagnostic or prognostic purposes in settings of sub-clinical or asymptomatic exposures to infective agents.