Print Email Facebook Twitter Apolipoproteins modulate the inflammatory response to lipopolysaccharide Title Apolipoproteins modulate the inflammatory response to lipopolysaccharide Author Berbée, J.F.P. Havekes, L.M. Rensen, P.C.N. TNO Kwaliteit van Leven Publication year 2005 Abstract An increasing body of evidence demonstrates a close interplay between lipoprotein metabolism and sepsis. Sepsis results in an increase of plasma triglycerides within VLDL as a consequence of an enhanced hepatic VLDL production and/or inhibited peripheral and hepatic VLDL clearance. In contrast, sepsis decreases plasma cholesterol within LDL and mainly HDL. The decrease in HDL is accompanied by a loss of mainly apoAI-containing particles, an almost total loss of apoCI, and an increase in apoE-containing HDL, as related to the effect of LPS on a wide range of apolipoproteins, plasma enzymes, lipid transfer factors, and receptors that are involved in HDL metabolism. Reciprocally, all lipoprotein classes have been shown to bind LPS and to attenuate the biological response to LPS in vitro and in rodents. Moreover, triglyceride-rich lipoproteins protect rodents against death from LPS and bacterial sepsis. Accumulating evidence indicates that apolipoproteins such as apoE and apoAI, and not the lipid moieties of the particles, may be responsible for these protective effects of lipoproteins. Therefore, to increase our understanding of the complex interaction between lipoprotein metabolism and sepsis, further studies that address the specific roles of apolipoproteins in sepsis are warranted. © W. S. Maney & Son Ltd. Chemicals / CAS: cholesterol, 57-88-5; Apolipoproteins E; Apolipoproteins; Lipids; Lipopolysaccharides; Lipoproteins Subject BiologyBiomedical ResearchApolipoprotein EHepatocyteLipid metabolismLipopolysaccharideLipoproteinApolipoproteinApolipoprotein A1Apolipoprotein ECholesterolHigh density lipoproteinLipid transfer proteinLow density lipoproteinTriacylglycerolVery low density lipoproteinCholesterol blood levelDeathEnzyme blood levelIn vitro studyInflammationLipid analysisLipoprotein metabolismNonhumanProtein bindingRodentTriacylglycerol blood levelAnimalsApolipoproteinsApolipoproteins EHumansInflammationLipidsLipopolysaccharidesLipoproteinsSepsisBacteria (microorganisms)Rodentia To reference this document use: http://resolver.tudelft.nl/uuid:21ba360b-f602-46d6-b7ac-cb6fc743c50f DOI https://doi.org/10.1179/096805105x35215 TNO identifier 238545 ISSN 0968-0519 Source Journal of Endotoxin Research, 11 (2), 97-103 Document type article Files To receive the publication files, please send an e-mail request to TNO Library.