Mechanisms of the priming effect of low doses of lipopoly-saccharides on leukocyte-dependent XXXX in whole blood.

@entity1423 @entity5750 @entity1425 @entity26 @entity1426 @entity2823 @entity8729 @entity2939 @entity857
Several studies focused on the ability of bacterial lipopolysac-charides (LPS) in triggering platelet and/or leukocyte activation. The aim of this study was to investigate the molecular mechanisms involved in the aggregation of platelets and in their interaction with leukocytes in whole blood after stimulation with low doses of LPS. LPS did not directly induce @entity1423 in whole blood, but they primed the aggregation of platelets induced by @entity1425 , @entity857 and @entity1426 . As shown by cytofluorimetry, platelets neither bind @entity2823 -LPS, nor express the LPS-receptors @entity5750 and @entity2939 ( @entity2939 ). On the contrary, LPS primed monocytes and to a lesser extent polymorphonuclear neutrophils to adhere to platelets. Both platelet-leukocyte interaction and @entity1423 in whole blood were inhibited by blockade of @entity5750 and @entity2939 . Moreover, the interaction between platelets and leukocytes was inhibited by @entity8729 , and by blockade of PAF and reactive @entity26 species, suggesting a role of @entity8729 and of leukocyte-derived mediators. In conclusion, these results elucidate the mechanisms leading to platelet activation and interaction with leukocytes triggered by LPS. They suggest that the activation of platelets by LPS is mainly dependent on leukocytes and especially monocytes as a result of @entity5750 and @entity2939 engagement. Moreover, we found that leukocyte-platelet interaction was triggered by the synthesis of PAF and the generation of @entity26 radicals that induced upregulation of surface expression of @entity8729 .
