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Infection and Immunity, May 2001, p. 2821-2828, Vol. 69, No. 5
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.5.2821-2828.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Distribution and Kinetics of
Lipoprotein-Bound Endotoxin
J. H. M.
Levels,1,*
P. R.
Abraham,2
A.
van den
Ende,1 and
S. J. H.
van Deventer2
Department of Vascular
Medicine1 and Department of Experimental
Internal Medicine,2 Academic Medical Center,
Amsterdam, The Netherlands
Received 3 October 2000/Returned for modification 21 December
2000/Accepted 29 January 2001
Lipopolysaccharide (LPS), the major glycolipid component of
gram-negative bacterial outer membranes, is a potent endotoxin responsible for pathophysiological symptoms characteristic of infection. The observation that the majority of LPS is found in association with plasma lipoproteins has prompted the suggestion that
sequestering of LPS by lipid particles may form an integral part of a
humoral detoxification mechanism. Previous studies on the biological
properties of isolated lipoproteins used differential ultracentrifugation to separate the major subclasses. To preserve the
integrity of the lipoproteins, we have analyzed the LPS distribution, specificity, binding capacity, and kinetics of binding to lipoproteins in human whole blood or plasma by using high-performance gel permeation chromatography and fluorescent LPS of three different chemotypes. The
average distribution of O111:B4, J5, or Re595 LPS in whole blood from
10 human volunteers was 60% (±8%) high-density lipoprotein (HDL),
25% (±7%) low-density lipoprotein, and 12% (±5%) very low density
lipoprotein. The saturation capacity of lipoproteins for all three LPS
chemotypes was in excess of 200 µg/ml. Kinetic analysis however,
revealed a strict chemotype dependence. The binding of Re595 or J5 LPS
was essentially complete within 10 min, and subsequent redistribution
among the lipoprotein subclasses occurred to attain similar
distributions as O111:B4 LPS at 40 min. We conclude that under
simulated physiological conditions, the binding of LPS to lipoproteins
is highly specific, HDL has the highest binding capacity for LPS, the
saturation capacity of lipoproteins for endotoxin far exceeds the LPS
concentrations measured in clinical situations, and the kinetics of LPS
association with lipoproteins display chemotype-dependent differences.
*
Corresponding author. Mailing address: Academic Medical
Center, Department of Vascular Medicine, P.O. Box 22660, 1100 DD
Amsterdam, The Netherlands. Phone: 31-20-5663895. Fax: 31-20-5669232. E-mail: h.levels{at}amc.uva.nl.
Infection and Immunity, May 2001, p. 2821-2828, Vol. 69, No. 5
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.5.2821-2828.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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