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Originally published In Press as doi:10.1194/jlr.M700446-JLR200 on May 5, 2008

Papers In Press, published online ahead of print August 1, 2008
J. Lipid Res., doi:10.1194/jlr.M700446-JLR200
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Journal of Lipid Research, Vol. 49, 1640-1645, August 2008
Copyright © 2008 by American Society for Biochemistry and Molecular Biology

Effect of lipid-bound apoA-I cysteine mutants on lipopolysaccharide-induced endotoxemia in miceboxs

Yunlong Wang, Xuewei Zhu, Gang Wu, Le Shen and Baosheng Chen1

National Laboratory of Medical Molecular Biology, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100005, China

boxs The online version of this article (available at http://www.jlr.org) contains supplementary data in the form of two tables and one figure.

This work was supported by Chinese National Basic Research Grant 973 (2006CB503801).

Published, JLR Papers in Press, May 5, 2008.

1 To whom correspondence should be addressed. e-mail: bschen{at}ibms.pumc.edu.cn

HDL has been shown to be able to neutralize the toxicity of lipopolysaccharide (LPS). Our previous study (J. Lipid Res. 2005. 46: 1303–1311) characterized the properties of secondary structure and in vitro functions of different cysteine mutants of apolipoprotein A-I. Here, we reconstituted recombinant HDLs (named rHDLwt, rHDL52, rHDL74, rHDL107, rHDL129, rHDL173, rHDL195, and rHDL228) by mixing wild type or those mutants with dipalmitoyl phosphatidylcholine and examined their in vivo effects on LPS-induced endotoxemia in mice. Our results showed that 24 h after injection, mice receiving rHDL74 or rHDL52 had a significant decrease of plasma tumor necrosis factor {alpha} (TNF-{alpha}) and interleukin-1β (IL-1β), compared with control mice receiving either saline or rHDLwt (P < 0.05). Administration of rHDL74 to mice injected with LPS also led to a decrease of plasma IL-6, protection of lung against acute injury, and attenuation of endotoxin-induced clinical symptoms in mice, compared with controls injected with LPS only. However, injection of rHDL228 significantly increased plasma concentration of TNF-{alpha} and exacerbated LPS-induced lung injury. In summary, compared with rHDLwt, rHDL74 and rHDL52 exhibit higher anti-inflammation capabilities, whereas rHDL228 shows hyper-proinflammation by exacerbating LPS-induced endotoxemia in mice.

Supplementary key words apolipoprotein A-I • cysteine mutant • rHDL • inflammatory cytokines • lung injury


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