Adhesion molecule and proinflammatory cytokine gene expression in hepatic sinusoidal endothelial cells following cecal ligation and puncture

Multiple organ dysfunction syndrome (MODS) is thought to be a frequent consequence of sepsis[1-3]. Despite substantial advances in our knowledge and understanding of the basic pathophysiologic mechanisms[4-7], in critically ill patients infections and sepsis are still associated with a high mortality[8,9]. There is evidence that the development of tissue damage in sepsis and shock is closely associated with the release of an ever increasing number of mediators and accumulation of neutrophils at the sites of infection or injury[10,11]. The endothelium is an intimal layer of simple squamous cells which provides a continuous, fluent surface for circulating blood. It is not the passive, metabolically inert barrier that it was once thought to be, and it is now known to be a metabolically and physiologically dynamic tissue with multiple functions. On the basis of recent discoveries in the field of endothelial cell biology (such as endothelium-derived mediators and the expression of adhesion molecules), end othelial cells are now thought to be not only target cells of injury, but also actively involved in inflammatory reactions and subsequent organ damage[12,13]. Polymicrobial sepsis induced by cecal ligation and puncture (CLP) is a model of sepsis which reproduces many of the inflammatory and pathological sequelae that are observed clinically. Following CLP, animals develop bacteremia,hypothermia,hypotension,anddamagetomultiple organ systems[14]. The present study was designed to observe the gene expression of adhesion molecules and proinflammatory cytokines in hepatic sinusoidal endothelial cells with a CLP model, in order to investigate the role of endothelial cells in tissue damage during sepsis.