title: The molecular pathogenesis of endotoxic shock and organ failure.
abstract: Sepsis is still associated with a high mortality rate. Septic shock and sequential multiple organ failure have a strong correlation with poor outcome. Lipopolysaccharide (LPS) plays a pivotal role in the initiation of host responses to Gram-negative infection. A number of mediators, such as cytokines, nitric oxide and eicosanoids, are responsible for most of the manifestations caused by LPS, and circulatory failure, leukocyte-induced tissue injury and coagulation disorder appear to be critical determinants in the development of sequential organ failure. Although several anti-LPS or anti-cytokine clinical trials have been attempted, none of them has so far been successful.
authors: Dept of Molecular Preventive Medicine, Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyou-ku, Tokyo, 113-0033, Japan.
authors: R
authors: R
authors: Karima
authors: S
authors: S
authors: Matsumoto
authors: H
authors: H
authors: Higashi
authors: K
authors: K
authors: Matsushima
mesh_terms: D016905:Gram-Negative Bacterial Infections / Q000503:physiopathology; D006801:Humans; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism; D008070:Lipopolysaccharides / Q000276:immunology / Q000378:metabolism; D009102:Multiple Organ Failure / Q000235:genetics* / Q000503:physiopathology* / Q000628:therapy; D012772:Shock, Septic / Q000235:genetics* / Q000503:physiopathology* / Q000628:therapy; D015398:Signal Transduction
chemical_list: D018836:Inflammation Mediators; D008070:Lipopolysaccharides