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Infection and Immunity, June 2002, p. 2995-3003, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.2995-3003.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Lipopolysaccharide Down Regulates Both Scavenger Receptor B1 and ATP Binding Cassette Transporter A1 in RAW Cells

Irina Baranova,1 Tatyana Vishnyakova,1 Alexander Bocharov,2 Zhigang Chen,1 Alan T. Remaley,1 John Stonik,1 Thomas L. Eggerman,2,3 and Amy P. Patterson1*

National Heart, Lung and Blood Institute,1 National Institute of Diabetes and Digestive and Kidney Diseases,3 Division of Cellular and Gene Therapies, Center for Biologics Evaluation and Research, U.S. Food and Drug Administration, Bethesda, Maryland 208922

Received 29 October 2001/ Returned for modification 19 December 2001/ Accepted 1 March 2002

Lipopolysaccharide (LPS) has recently been shown to facilitate macrophage foam cell formation and has been suggested to be a proatherogenic factor. The mechanism of LPS induced cholesterol accumulation, however, is unclear. In this report, using the macrophage-like RAW 264.7 cell line, we provide experimental evidence that LPS's proatherogenic effects may at least in part reflect altered cholesterol metabolism. Data presented demonstrate that in a dose-dependent manner, LPS is able to down regulate the mRNA expression of the two primary high-density lipoprotein (HDL) receptors, scavenger receptor B1 (SR-B1) and ATP binding cassette A1 (ABCA1), with a 50% inhibitory concentration of less than 0.2 ng/ml, as well as to decrease SR-B1 protein expression by 80%. We also found that LPS treatment resulted in a significant decrease (to 20% of the control level) of the specific 125I-HDL binding as well as in 50% inhibition of the HDL-mediated cholesterol efflux compared to untreated cells. In addition, we compared the potencies of various modified LPS preparations and demonstrated that the phosphorylated lipid A portion of LPS, which is highly conserved among gram-negative microorganisms, including Chlamydia, is primarily responsible for the effects of LPS on SR-B1 and ABCA1 expression. Inhibitors of NF-{kappa}B activation were observed to efficiently block the suppressive effect of LPS on SR-B1 and ABCA1, suggesting a mechanism involving NF-{kappa}B. These data indicate that the LPS effects on cholesterol metabolism may contribute to the proatherogenic properties of LPS.

* Corresponding author. Present address: Office of the Director, National Institutes of Health, 6705 Rockledge Dr., Suite 750, Bethesda, MD 20892. Phone: (301) 496-9838. Fax: (301) 496-9839. E-mail: pattersa{at}od.nih.gov.

Editor: B. B. Finlay

Infection and Immunity, June 2002, p. 2995-3003, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.2995-3003.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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