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Am J Physiol Lung Cell Mol Physiol (November 26, 2003). doi:10.1152/ajplung.00220.2003
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Submitted on July 9, 2003
Accepted on November 20, 2003

Inhibition of LPS- and CpG DNA-induced TNF-{alpha} Response by Oxidized Phospholipids

Zheng Ma1, Jiang Li1, Lijuan Yang1, Ying Mu1, Wen Xie1, Bruce Pitt2, and Song Li1*

1 Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University pf Pittsburgh, Pittsburgh, PA, USA
2 Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA, USA

* To whom correspondence should be addressed. E-mail: sol4{at}pitt.edu.

Lipid oxidation is commonly seen in innate immune response in which reactive oxygen intermediates (ROIs) are generated to kill pathogenic microorganisms. Although oxidation products of phospholipids have generally been regarded to play a role in a number of chronic inflammatory processes several studies have shown that oxidized phospholipids inhibit lipopolysaccharide (LPS)-induced acute proinflammatory response in cultured macrophages and endothelial cells. We report in this study that oxidized 1- palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (PAPC) but not non-oxidized PAPC significantly inhibits the LPS-induced TNF-{alpha} response in intact mice. Oxidized PAPC also inhibits the CpG DNA-induced TNF-{alpha} response in cultured macrophages and in intact mice. To elucidate the mechanisms of action we show that oxidized PAPC but not non-oxidized PAPC inhibits the LPS- and CpG- induced activation of p38 MAPK and NF-{kappa}B cascade. These results suggest a role of oxidized lipids as a negative regulator in controlling the magnitude of innate immune response. Further studies on the mechanisms of action may lead to the development of a new type of anti-inflammatory drug for the treatment of acute inflammatory diseases such as sepsis.




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