The lipemia of sepsis: triglyceride-rich lipoproteins as agents of innate immunity

Bacterial endotoxin (LPS) elicits dramatic responses in the host including elevated plasma lipid levels due to the increased synthesis and secretion of triglyceride (TG)-rich lipoproteins by the liver, and the inhibition of lipoprotein lipase. This cytokine-induced hyperlipoproteinemia, clinically t...

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Bibliographic Details
Published in:Journal of endotoxin research 2000, Vol.6 (6), p.421-430
Main Authors: Harris, H W, Gosnell, J E, Kumwenda, Z L
Format: Article
Language:English
Subjects:
Acute-Phase Reaction - etiology
Animals
Humans
lipemia
Lipopolysaccharides - toxicity
Lipoproteins - blood
Lipoproteins - immunology
Models, Biological
Protein Binding
Sepsis - blood
Sepsis - etiology
Sepsis - immunology
Triglycerides - blood
Triglycerides - immunology
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Summary:Bacterial endotoxin (LPS) elicits dramatic responses in the host including elevated plasma lipid levels due to the increased synthesis and secretion of triglyceride (TG)-rich lipoproteins by the liver, and the inhibition of lipoprotein lipase. This cytokine-induced hyperlipoproteinemia, clinically termed the "lipemia of sepsis", was customarily thought to represent the mobilization of lipid stores to fuel the host response to infection. However, since lipoproteins can also bind and neutralize LPS, we hypothesize that TG-rich lipoproteins (VLDL and chylomicrons) are also components of an innate, non-adaptive host immune response to infection. Herein we review data demonstrating the capacity of lipoproteins to bind LPS, protect against LPS-induced toxicity, and modulate the overall host response to this bacterial toxin. Lastly, we propose a pathway whereby lipoprotein-bound LPS may represent a novel, endogenous mechanism for regulating the hepatic acute phase response.
ISSN:0968-0519
1743-2839
DOI:10.1179/096805100101532351