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1 Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
2 Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
3 Department of Immunobiology, Yale University School of Medicine, New Haven, CT, USA
4 Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, Worcester, MA, USA
* To whom correspondence should be addressed. E-mail: choiam{at}msx.upmc.edu.
Hyperoxia generates an oxidative stress in the mouse lung, which activates the major stress inducible kinase pathways, including c-Jun-NH2-terminal kinase (JNK). We examined the effect of Jnk1 gene deletion on in vivo responses to hyperoxia in mice. The survival of Jnk1-/- mice was reduced relative to wild-type mice after exposure to continuous hyperoxia. Jnk1-/- mice displayed higher protein concentration in bronchoalveolar lavage (BAL) fluid and increased expression of heme oxygenase-1, a stress-inducible gene, after 65 hours of hyperoxia. Contrary to other markers of injury, the leukocyte count in BAL fluid of Jnk1-/- mice was markedly diminished relative to that of wild-type mice. The decrease in BAL leukocyte count was not associated with any decrease in lung myeloperoxidase activity at baseline or after hyperoxia treatment. Pretreatment with inhaled lipopolysaccharide increased BAL neutrophil content and extended hyperoxia survival time to a similar extent in Jnk1-/- and wild type mice. Associated with increased mortality, Jnk1-/- mice had increased pulmonary epithelial cell apoptosis after exposure to hyperoxia compared to wild-type mice. These results indicate that JNK pathways participate in adaptive responses to hyperoxia in mice.
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