Repository hosted by TU Delft Library

Home · Contact · About · Disclaimer ·

Apolipoproteins modulate the inflammatory response to lipopolysaccharide

Publication files not online:

Author: Berbée, J.F.P. · Havekes, L.M. · Rensen, P.C.N.
Institution: TNO Kwaliteit van Leven
Source:Journal of Endotoxin Research, 2, 11, 97-103
Identifier: 238545
doi: doi:10.1179/096805105X35215
Keywords: Biology · Biomedical Research · Apolipoprotein E · Hepatocyte · Lipid metabolism · Lipopolysaccharide · Lipoprotein · Apolipoprotein · Apolipoprotein A1 · Apolipoprotein E · Cholesterol · High density lipoprotein · Lipid transfer protein · Low density lipoprotein · Triacylglycerol · Very low density lipoprotein · Cholesterol blood level · Death · Enzyme blood level · In vitro study · Inflammation · Lipid analysis · Lipoprotein metabolism · Nonhuman · Protein binding · Rodent · Triacylglycerol blood level · Animals · Apolipoproteins · Apolipoproteins E · Humans · Inflammation · Lipids · Lipopolysaccharides · Lipoproteins · Sepsis · Bacteria (microorganisms) · Rodentia


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