Abstract
Vascular endothelial cells play a pivotal mediatory role in many responses to systemic inflammation including the crosstalk between coagulation and inflammation in sepsis [1, 2]. Endothelial cells respond to the cytokines expressed and released by activated leukocytes but can also release cytokines themselves. Furthermore, endothelial cells are able to express adhesion molecules and growth factors that may not only promote the inflammatory response further but also affect a myriad of downstream responses. It has recently become clear that, in addition to these mostly indirect effects of the endothelium, injured endothelial cells directly interfere with platelet–vessel wall interaction, neutrophil entrapment through formation of extracellular nets, and activation of inflammation and coagulation mediated by microparticles (Fig. 1). Blood cell–vessel wall interaction in sepsis
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