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J. Lipid Res.
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A more recent version of this article appeared on April 1, 2005

Papers In Press, published online ahead of print February 1, 2005
J. Lipid Res., doi:10.1194/jlr.C400018-JLR200
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Submitted on December 20, 2004
Revised on January 14, 2005
Accepted on January 20, 2005

Suppression of HMGB1 release by stearoyl lysophosphatidylcholine: An additional mechanism for its therapeutic effects in experimental sepsis

Guoqian Chen, Jianhua Li, Xiaoling Qiang, Christopher J. Czura, Mahendar Ochani, Kanta Ochani, Luis Ulloa, Huan Yang, Kevin J. Tracey, Ping Wang, Andrew E. Sama, and Haichao Wang

Department of Emergency Medicine, North Shore University Hospital, Manhasset, NY 11030

Corresponding Author: hwang{at}nshs.edu

Stearoyl lysophosphatidylcholine (LPC) has recently been proven protective against lethal sepsis by stimulating neutrophils to eliminate invading pathogens through an H2O2-dependent mechanism. Here we demonstrate that stearoyl, but not caproyl LPC, significantly attenuates circulating HMGB1 levels in endotoxemia and sepsis by suppressing endotoxin-induced HMGB1 release from macrophages/monocytes. Neutralizing antibodies against G2A, a cell surface receptor preferably binding LPC species with longer fatty acid acyl chains, dose-dependently abrogated stearoyl LPC-mediated suppression of HMGB1 release. Thus, stearoyl LPC confers protection against lethal experimental sepsis partly by facilitating the elimination of the invading pathogens, and partly by inhibiting endotoxin-induced HMGB1 release through a cell surface receptor (G2A)-dependent mechanism.


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