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Am J Physiol Lung Cell Mol Physiol 285: L250-L257, 2003. First published March 21, 2003; doi:10.1152/ajplung.00387.2002
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Deficiency in the c-Jun NH2-terminal kinase signaling pathway confers susceptibility to hyperoxic lung injury in mice

Danielle Morse,1 Leo E. Otterbein,1 Simon Watkins,2 Sean Alber,2 Zhihong Zhou,1 Richard A. Flavell,3 Roger J. Davis,4 and Augustine M. K. Choi1

1Division of Pulmonary, Allergy and Critical Care Medicine, 2Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213; 3Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520; and 4Howard Hughes Medical Institute and Program in Molecular Medicine, Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01605

Submitted 14 November 2002 ; accepted in final form 17 March 2003

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 h 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 with wild-type mice. These results indicate that JNK pathways participate in adaptive responses to hyperoxia in mice.

hyperoxia; mitogen-activated protein kinase; oxidative stress; stress response; oxygen toxicity; apoptosis


Address for reprint requests and other correspondence: A. M. K. Choi, Div. of Pulmonary, Allergy and Critical Care Medicine, NW 628 UPMC Montefiore, 3459 5th Ave., Pittsburgh, PA 15213 (E-mail: choiam{at}msx.upmc.edu).




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