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Am J Physiol Lung Cell Mol Physiol 280: L69-L78, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 1, L69-L78, January 2001

Prevention of influenza-induced lung injury in mice overexpressing extracellular superoxide dismutase

Hagir B. Suliman1, Lisa K. Ryan2, Lisa Bishop2, and Rodney J. Folz1,3

Departments of 1 Medicine and 3 Cell Biology, Division of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham 27710; and 2 Immunotoxicology Branch, Experimental Toxicology Division, National Health and Environmental Effects Research Laboratory, United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711

Reactive oxygen and nitrogen species such as superoxide and nitric oxide are released into the extracellular spaces by inflammatory and airway epithelial cells. These molecules may exacerbate lung injury after influenza virus pneumonia. We hypothesized that enhanced expression of extracellular superoxide dismutase (EC SOD) in mouse airways would attenuate the pathological effects of influenza pneumonia. We compared the pathogenic effects of a nonlethal primary infection with mouse-adapted Hong Kong influenza A/68 virus in transgenic (TG) EC SOD mice versus non-TG (wild-type) littermates. Compared with wild-type mice, EC SOD TG mice showed less lung injury and inflammation as measured by significant blunting of interferon-gamma induction, reduced cell count and total protein in bronchoalveolar lavage fluid, reduced levels of lung nitrite/nitrate nitrotyrosine, and markedly reduced lung pathology. These results demonstrate that enhancing EC SOD in the conducting and distal airways of the lung minimizes influenza-induced lung injury by both ameliorating inflammation and attenuating oxidative stress.

transgenic mice; antioxidants; nitric oxide synthase


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