This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Levels, J. H. M.
Right arrow Articles by Meijers, J. C. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Levels, J. H. M.
Right arrow Articles by Meijers, J. C. M.

 Previous Article  |  Next Article 

Infection and Immunity, April 2005, p. 2321-2326, Vol. 73, No. 4
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.4.2321-2326.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Lipopolysaccharide Is Transferred from High-Density to Low-Density Lipoproteins by Lipopolysaccharide-Binding Protein and Phospholipid Transfer Protein

J. H. M. Levels,1* J. A. Marquart,1 P. R. Abraham,2 A. E. van den Ende,1 H. O. F. Molhuizen,1 S. J. H. van Deventer,3 and J. C. M. Meijers1

Departments of Experimental Vascular Medicine,1 Experimental Internal Medicine,2 Gastroenterology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands3

Received 18 June 2004/ Returned for modification 15 September 2004/ Accepted 2 December 2004

Lipopolysaccharide (LPS), the major outer membrane component of gram-negative bacteria, is a potent endotoxin that triggers cytokine-mediated systemic inflammatory responses in the host. Plasma lipoproteins are capable of LPS sequestration, thereby attenuating the host response to infection, but ensuing dyslipidemia severely compromises this host defense mechanism. We have recently reported that Escherichia coli J5 and Re595 LPS chemotypes that contain relatively short O-antigen polysaccharide side chains are efficiently redistributed from high-density lipoproteins (HDL) to other lipoprotein subclasses in normal human whole blood (ex vivo). In this study, we examined the role of the acute-phase proteins LPS-binding protein (LBP) and phospholipid transfer protein (PLTP) in this process. By the use of isolated HDL containing fluorescent J5 LPS, the redistribution of endotoxin among the major lipoprotein subclasses in a model system was determined by gel permeation chromatography. The kinetics of LPS and lipid particle interactions were determined by using Biacore analysis. LBP and PLTP were found to transfer LPS from HDL predominantly to low-density lipoproteins (LDL), in a time- and dose-dependent manner, to induce remodeling of HDL into two subpopulations as a consequence of the LPS transfer and to enhance the steady-state association of LDL with HDL in a dose-dependent fashion. The presence of LPS on HDL further enhanced LBP-dependent interactions of LDL with HDL and increased the stability of the HDL-LDL complexes. We postulate that HDL remodeling induced by LBP- and PLTP-mediated LPS transfer may contribute to the plasma lipoprotein dyslipidemia characteristic of the acute-phase response to infection.

* Corresponding author. Mailing address: Academic Medical Center, Department of Experimental Vascular Medicine G1-114, P.O. Box 22660, 1100 DD Amsterdam, The Netherlands. Phone: 31205665899. Fax: 31205669232. E-mail: h.levels{at}amc.uva.nl.

Editor: J. T. Barbieri

Infection and Immunity, April 2005, p. 2321-2326, Vol. 73, No. 4
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.4.2321-2326.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Shibata, N., Glass, C. K. (2009). Regulation of macrophage function in inflammation and atherosclerosis. J. Lipid Res. 50: S277-S281 [Abstract] [Full Text]  
  • Calderon-Garciduenas, L., Macias-Parra, M., Hoffmann, H. J., Valencia-Salazar, G., Henriquez-Roldan, C., Osnaya, N., Monte, O. C.-d., Barragan-Mejia, G., Villarreal-Calderon, R., Romero, L., Granada-Macias, M., Torres-Jardon, R., Medina-Cortina, H., Maronpot, R. R. (2009). Immunotoxicity and Environment: Immunodysregulation and Systemic Inflammation in Children. Toxicol Pathol 37: 161-169 [Abstract] [Full Text]  
  • Samyn, H., Moerland, M., van Gent, T., van Haperen, R., Metso, J., Grosveld, F., Jauhiainen, M., van Tol, A., de Crom, R. (2008). Plasma phospholipid transfer activity is essential for increased atherogenesis in PLTP transgenic mice: a mutation-inactivation study. J. Lipid Res. 49: 2504-2512 [Abstract] [Full Text]  
  • Gautier, T., Klein, A., Deckert, V., Desrumaux, C., Ogier, N., Sberna, A.-L., Paul, C., Le Guern, N., Athias, A., Montange, T., Monier, S., Piard, F., Jiang, X.-C., Masson, D., Lagrost, L. (2008). Effect of Plasma Phospholipid Transfer Protein Deficiency on Lethal Endotoxemia in Mice. J. Biol. Chem. 283: 18702-18710 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»