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A more recent version of this article appeared on August 1, 2003

Papers In Press, published online ahead of print May 16, 2003
J. Lipid Res., doi:10.1194/jlr.M200440-JLR200
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Submitted on November 13, 2002
Revised on May 2, 2003
Accepted on May 8, 2003

A single intravenous dose of endotoxin rapidly alters serum lipoproteins and lipid transfer proteins in normal volunteers

Lisa C. Hudgins, Thomas S. Parker, Daniel M. Levine, Bruce R. Gordon, Stuart S. Saal, Xian-cheng Jiang, Cindy E. Seidman, Jolanta D. Tremaroli, Julie Lai, and Albert L. Rubin

The Rogosin Institute, The Rockefeller University, New York, NY 10021

Corresponding Author: hudgins{at}mail.rockefeller.edu

Endotoxemia is associated with rapid and marked declines in serum levels of LDL and HDL by unknown mechanisms. To reproduce these lipoprotein changes in vivo, a single, small dose of endotoxin (E. Coli 0113, 2 ng/kg) or saline was administered intravenously in a random order, cross-over design to each of 6 normal volunteers after 4 days of a controlled diet. Shortly after endotoxin, subjects had mild flu-like symptoms and markedly increased serum levels of tumor necrosis factor and its soluble receptors, interleukin-6, cortisol, serum amyloid A and C- reactive protein. At 3-4 h, TG, VLDL TG and NEFA peaked without an increase in TG palmitate that would indicate an increase in fatty acid synthesis. TG then abruptly declined to a nadir at 9 h, followed at 12-24 h by nadirs in cholesterol, LDL cholesterol, apolipoprotein B, and phospholipid (all subclasses). At 12 h, there was also a 3-fold increase in lipopolysaccharide-binding protein (LBP), but much smaller and later decreases in the activities of phospholipid transfer protein and CETP. Unexpectedly, HDL cholesterol and apolipoprotein A-1 levels were not affected, but almost half of the decrease in phospholipid was HDL phospholipid. In conclusion, the decrease in LDL in many inflammatory states was rapidly induced in normal volunteers with a single intravenous dose of endotoxin. The direction of the effect on TG and VLDL depended on the time after endotoxin exposure (first increase, then decrease). The selective loss of phospholipid from HDL may have been mediated by LBP and, after more intense or prolonged inflammation, could result in increased HDL clearance and reduced HDL levels.


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