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Originally published In Press as doi:10.1074/jbc.M009915200 on January 2, 2001

J. Biol. Chem., Vol. 276, Issue 12, 8820-8824, March 23, 2001
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Apolipoprotein E Protects Against Bacterial Lipopolysaccharide-induced Lethality
A NEW THERAPEUTIC APPROACH TO TREAT GRAM-NEGATIVE SEPSIS*

Marijke Van OostenDagger §, Patrick C. N. RensenDagger §, Edwin S. Van AmersfoortDagger , Miranda Van EckDagger , Anne-Marie Van Dam||, John J. P. Brevé||, Tikva Vogel**, Amos Panet**, Theo J. C. Van BerkelDagger , and Johan KuiperDagger Dagger Dagger

From the Dagger  Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, University of Leiden, Sylvius Laboratories, P. O. Box 9503, 2300 RA Leiden, The Netherlands; the || Research Institute Neurosciences Vrije Universiteit, Faculty of Medicine, Department of Pharmacology, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands; and ** Bio-Technology General Ltd., Kiryat Weizmann, Rehovot 76326, Israel

Septic shock is the most common cause of death in intensive care units and no effective treatment is available at present. Lipopolysaccharide (LPS) is the primary mediator of Gram-negative sepsis by inducing the production of macrophage-derived cytokines. Previously, we showed that apolipoprotein E (apoE), an established modulator of lipid metabolism, can bind LPS, thereby redirecting LPS from macrophages to hepatocytes in vivo. We now report that intravenously administered LPS strongly increases the serum levels of apoE. In addition, apoE can prevent the LPS-induced production of cytokines and subsequent death in rodents. Finally, apoE-deficient mice show a significantly higher sensitivity toward LPS than control wild-type mice. These findings indicate that apoE may have a physiological role in the protection against sepsis, and recombinant apoE may be used therapeutically to protect against LPS-induced endotoxemia.

* This work was supported by Medical Sciences Grant 902-23-139 from The Netherlands Organization for Scientific Research, Council for Medical Research.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ These authors contributed equally to this work.

Present address: Radiation Genetics and Chemical Mutagenesis, University of Leiden, Sylvius Laboratories, P. O. Box 9503, 2300 RA Leiden, The Netherlands.

Dagger Dagger To whom correspondence should be addressed. Tel.: 31 715276040; Fax: 31 715276032; E-mail: j.kuiper@lacdr.leidenuniv.nl.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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