title: [Protective role of high density lipoproteins in sepsis: basic issues and clinical implications].
abstract: High density lipoproteins (HDL) are responsible of reverse cholesterol transport and play an important antiatherogenic role. In recent years, several studies suggest that HDL have additional functions, including a possible anti-inflammatory activity in infectious conditions. Furthermore, available evidence indicates that the presence of lipopolysaccharide (LPS) within the circulation during infectious states induced by gram-negative bacteria may be involved in the decrease in HDL cholesterol levels and changes in lipoprotein composition, which have been associated with a higher mortality due to sepsis in animal models and in humans. In this article, we review this subject and also discuss possible mechanisms that explain the positive impact achieved by native HDL, reconstituted HDL, or HDL apolipoprotein peptides on the inflammatory response and mortality in models of endotoxemia. In this regard, it has been proposed that one of the mechanisms by which HDL protect against sepsis may be mediated by its binding ability and/or neutralizing capacity on LPS, avoiding an excessive response of the immune system. Thus, increasing blood levels of HDL and/or parenteral HDL administration may represent a new anti-inflammatory tool for managing septic states in humans.
authors.forename: Susana
authors.initials: S
authors.lastname: Contreras-Duarte
authors.forename: Pablo
authors.initials: P
authors.lastname: Varas
authors.forename: Fernanda
authors.initials: F
authors.lastname: Awad
authors.forename: Dolores
authors.initials: D
authors.lastname: Busso
authors.forename: Attilio
authors.initials: A
authors.lastname: Rigotti
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D016632:Apolipoprotein A-I / Q000032:analysis; D050197:Atherosclerosis / Q000517:prevention & control*; D002784:Cholesterol / Q000097:blood; D004195:Disease Models, Animal; D019446:Endotoxemia / Q000097:blood / Q000276:immunology*; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000276:immunology; D018836:Inflammation Mediators / Q000378:metabolism; D008070:Lipopolysaccharides / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood / Q000187:drug effects / Q000502:physiology*; D051379:Mice; D018384:Oxidative Stress / Q000502:physiology*; D018805:Sepsis / Q000097:blood / Q000276:immunology*; D013927:Thrombosis / Q000097:blood
chemical_list: D000893:Anti-Inflammatory Agents; D016632:Apolipoprotein A-I; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D008075:Lipoproteins, HDL; D002784:Cholesterol