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Infection and Immunity, October 2001, p. 5991-5996, Vol. 69, No. 10
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.10.5991-5996.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Impaired Pulmonary NF-kappa B Activation in Response to Lipopolysaccharide in NADPH Oxidase-Deficient Mice

M. Audrey Koay,1 John W. Christman,1,2,* Brahm H. Segal,3 Annapurna Venkatakrishnan,1 Thomas R. Blackwell,2 Steven M. Holland,3 and Timothy S. Blackwell1,2

Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 272321; Department of Veterans Affairs, Nashville, Tennessee 372432; and Laboratory of Host Defenses, National Institutes of Health, Bethesda, Maryland 208923

Received 19 March 2001/Returned for modification 24 May 2001/Accepted 12 July 2001

Reactive oxygen species (ROS) are thought to be involved in intracellular signaling, including activation of the transcription factor NF-kappa B. We investigated the role of NADPH oxidase in the NF-kappa B activation pathway by utilizing knockout mice (p47phox-/-) lacking the p47phox component of NADPH oxidase. Wild-type (WT) controls and p47phox-/- mice were treated with intraperitoneal (i.p.) Escherichia coli lipopolysaccharide (LPS) (5 or 20 µg/g of body weight). LPS-induced NF-kappa B binding activity and accumulation of RelA in nuclear protein extracts of lung tissue were markedly increased in WT compared to p47phox-/- mice 90 min after treatment with 20 but not 5 µg of i.p. LPS per g. In another model of lung inflammation, RelA nuclear translocation was reduced in p47phox-/- mice compared to WT mice following treatment with aerosolized LPS. In contrast to NF-kappa B activation in p47phox-/- mice, LPS-induced production of macrophage inflammatory protein 2 in the lungs and neutrophilic lung inflammation were not diminished in these mice compared to WT mice. We conclude that LPS-induced NF-kappa B activation is deficient in the lungs of p47phox-/- mice compared to WT mice, but this abnormality does not result in overt alteration in the acute inflammatory response.

* Corresponding author. Mailing address: Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University School of Medicine, T-1217 MCN, Nashville, TN 27232-2650. Phone: (615) 327-4751, ext 7928. Fax: (615) 340-2347. E-mail: john.christman{at}mcmail.vanderbilt.edu.

Infection and Immunity, October 2001, p. 5991-5996, Vol. 69, No. 10
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.10.5991-5996.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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