Molecular basis of endothelial dysfunction in sepsis.
Sepsis is one of the major causes of mortality in critically ill patients and develops as a result of the host response to infection. A complex network of events is set into motion in the body by the infection and results in the pathogenesis of sepsis. This review article focuses on the molecular mechanisms and components involved in the pathogenesis of sepsis with a major emphasis on the endothelium. This includes sepsis-inducing bacterial components (e.g. endotoxins), cellular targets of these molecules and their responses, host reactions, intracellular and cytokine networks, individual susceptibility and new therapeutic targets in sepsis treatment.
Peters
Kirsten
K
Institute of Pathology, Johannes Gutenberg University of Mainz, Langenbeckstr. 1, 55101, Mainz, Germany. kirkpatric@pathologie.klinik.uni-mainz.de
Unger
Ronald E
RE
Brunner
Joachim
J
Kirkpatrick
C James
CJ
D015815:Cell Adhesion Molecules / Q000378:metabolism; D016207:Cytokines / Q000276:immunology; D004198:Disease Susceptibility; D042783:Endothelial Cells / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D004731:Endotoxins / Q000378:metabolism; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000378:metabolism; D007375:Interleukin-1 / Q000235:genetics; D008297:Male; D008562:Membrane Glycoproteins / Q000235:genetics / Q000378:metabolism; D009154:Mutation; D009569:Nitric Oxide / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism; D018805:Sepsis / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D051193:Toll-Like Receptors
D015815:Cell Adhesion Molecules; D016207:Cytokines; D004731:Endotoxins; D007375:Interleukin-1; D008562:Membrane Glycoproteins; D017382:Reactive Oxygen Species; D011956:Receptors, Cell Surface; D051193:Toll-Like Receptors; D009569:Nitric Oxide