Triglyceride-rich lipoproteins as agents of innate immunity.
Bacterial endotoxin (i.e., lipopolysaccharide [LPS]) elicits dramatic responses in the host, including elevated plasma lipid levels due to increased synthesis and secretion of triglyceride-rich lipoproteins by the liver and inhibition of lipoprotein lipase. This cytokine-induced hyperlipoproteinemia, clinically termed the "lipemia of sepsis," was customarily thought to involve the mobilization of lipid stores to fuel the host response to infection. However, because lipoproteins can also bind and neutralize LPS, we have long postulated that triglyceride-rich lipoproteins (very-low-density lipoproteins and chylomicrons) are also components of an innate, nonadaptive host immune response to infection. Recent research demonstrates the capacity of lipoproteins to bind LPS, protect against LPS-induced toxicity, and modulate the overall host response to this bacterial toxin.
Barcia
Anthony M
AM
Department of Surgery, University of California, San Francisco, CA 94143-0104, USA.
Harris
Hobart W
HW
D000209:Acute-Phase Proteins / Q000378:metabolism; D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism; D006801:Humans; D006951:Hyperlipoproteinemias / Q000097:blood / Q000276:immunology*; D007113:Immunity, Innate; D018950:Lipopolysaccharide Receptors / Q000276:immunology / Q000378:metabolism; D008070:Lipopolysaccharides / Q000276:immunology* / Q000378:metabolism; D008074:Lipoproteins / Q000097:blood / Q000737:chemistry / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000378:metabolism; D018805:Sepsis / Q000097:blood / Q000276:immunology* / Q000378:metabolism; D014280:Triglycerides / Q000032:analysis / Q000097:blood; D000099231:Lipopolysaccharide-Binding Protein
D000209:Acute-Phase Proteins; D002352:Carrier Proteins; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D008074:Lipoproteins; D008562:Membrane Glycoproteins; D014280:Triglycerides; D000099231:Lipopolysaccharide-Binding Protein