Endothelial activation and dysfunction in sepsis

Abstract

Severe sepsis is a major cause of morbidity and mortality worldwide. Recent advances in our understanding of the pathophysiology of sepsis have emphasized the pivotal role of the innate immune system in the development of a deleterious host response to bacterial infection. It is now recognized that the endothelium is an important effector cell of the innate immune system. This review examines evidence for endothelial dysfunction in experimental sepsis as manifested by activation of coagulation and fibrinolytic systems, alterations in vasomotor tone, increased permeability, augmented leukocyte adhesion, and enhanced apoptosis. As discussed here, many of these perturbations are observed in patients with severe sepsis, suggesting that endothelial dysfunction is also important clinically and may be an important target for new therapeutic approaches.