Endothelial-platelet interaction in sepsis

Abstract

Introduction. Endothelial cells and platelets are actively involved in pathogenetic processes in sepsis — an unregulated reaction of the host organism in response to infection, leading, on the one hand, to the development of prothrombotic, and on the other hand, to hemorrhagic readiness.Aim — to summarize the current information on the mechanisms of intercellular interaction between endotheliocytes and platelets in sepsis.Main findings. The development of multiple organ failure, which increases the likelihood of an unfavorable outcome of sepsis, is partly due to endothelial dysfunction, as well as the involvement of platelets in the pathogenetic process. Under physiological conditions, an anatomically and functionally intact endothelium is important to prevent microvascular thrombosis. Although platelets are most associated with hemostasis, they perform many other functions, including participation in inflammatory processes through complement activation, interaction with leukocytes and monocytes, participation in host defense against infection, and regulation of vascular tone. There is also abundant evidence that suggests that the processes regulating hemostasis evolved as a component of the inflammatory response to infection. Many of these interaction points occur on the surface of endothelial cells, linking these two cell types, endotheliocytes and platelets, in initiating and regulating blood clotting and inflammation. Various mechanisms may contribute to direct and indirect platelet activation in sepsis, including pathogen-induced platelet activation, pathogen- and inflammation-induced endothelial and leukocyte activation, and complement-mediated platelet activation.