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Published ahead of print on July 15, 2004, doi:10.1165/rcmb.2004-0057OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 4, October 2004, 432-439

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Submitted on February 17, 2004
Revised on July 14, 2004

Extracellular superoxide dismutase attenuates lipopolysaccharide-induced neutrophilic inflammation

Russell P Bowler1*, Mike Nicks1, Karen Tran1, Grant Tanner1, Ling-Yi Chang1, Scott K Young1, and G. Scott Worthen1

1 Department of Medicine, National Jewish Medical and Research Center, Denver, CO, USA

* To whom correspondence should be addressed. E-mail: bowlerr{at}njc.org.

Extracellular superoxide dismutase (EC-SOD) is an abundant antioxidant in the lung and vascular walls. Previous studies have shown that EC-SOD attenuates lung injury in a diverse variety of lung injury models. In this study we examined the role of EC-SOD in mediating lipopolysaccharide (LPS)-induced lung inflammation. We found that LPS-induced neutrophilic lung inflammation was exaggerated in EC-SOD deficient mice and diminished in mice that overexpressed EC-SOD specifically in the lung. Similar patterns were seen for BAL cytokines such as tumor necrosis factor-{alpha}, KC, and macrophage inflammatory protein-2 as well as expression of lung intercellular adhesion molecule-1, vascular cell adhesion molecule-1, endothelial cell selectin, and platelet selectin . In a macrophage cell line EC-SOD inhibited LPS-induced macrophage cytokine release, but did not alter expression of intercellular adhesion molecules in endothelial cells. These results suggest that EC-SOD plays an important role in attenuating the inflammatory response in the lung most likely by decreasing release of proinflammatory cytokines from phagocytes.




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