This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow E-mail this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ASM journals
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Koay, M. A.
Right arrow Articles by Blackwell, T. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Koay, M. A.
Right arrow Articles by Blackwell, T. S.

 Previous Article  |  Next Article 

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.


This article has been cited by other articles:

  • Yao, H., Edirisinghe, I., Yang, S.-R., Rajendrasozhan, S., Kode, A., Caito, S., Adenuga, D., Rahman, I. (2008). Genetic Ablation of NADPH Oxidase Enhances Susceptibility to Cigarette Smoke-Induced Lung Inflammation and Emphysema in Mice. Am. J. Pathol. 172: 1222-1237 [Abstract] [Full Text]  
  • Li, L., Frei, B. (2006). Iron Chelation Inhibits NF-{kappa}B-Mediated Adhesion Molecule Expression by Inhibiting p22phox Protein Expression and NADPH Oxidase Activity. Arterioscler. Thromb. Vasc. Bio. 26: 2638-2643 [Abstract] [Full Text]  
  • Lee, Y.C. G., Knight, D. A., Lane, K. B., Cheng, D. S., Koay, M. A., Teixeira, L. R., Nesbitt, J. C., Chambers, R. C., Thompson, P. J., Light, R. W. (2005). Activation of proteinase-activated receptor-2 in mesothelial cells induces pleural inflammation. Am. J. Physiol. Lung Cell. Mol. Physiol. 288: L734-L740 [Abstract] [Full Text]  
  • Balish, E., Warner, T. F., Nicholas, P. J., Paulling, E. E., Westwater, C., Schofield, D. A. (2005). Susceptibility of Germfree Phagocyte Oxidase- and Nitric Oxide Synthase 2-Deficient Mice, Defective in the Production of Reactive Metabolites of Both Oxygen and Nitrogen, to Mucosal and Systemic Candidiasis of Endogenous Origin. Infect. Immun. 73: 1313-1320 [Abstract] [Full Text]  
  • Chatterjee, S., Fisher, A. B. (2004). ROS to the rescue. Am. J. Physiol. Lung Cell. Mol. Physiol. 287: L704-L705 [Full Text]  
  • Mizgerd, J. P., Lupa, M. M., Hjoberg, J., Vallone, J. C., Warren, H. B., Butler, J. P., Silverman, E. S. (2004). Roles for early response cytokines during Escherichia coli pneumonia revealed by mice with combined deficiencies of all signaling receptors for TNF and IL-1. Am. J. Physiol. Lung Cell. Mol. Physiol. 286: L1302-L1310 [Abstract] [Full Text]  
  • Sadikot, R. T., Zeng, H., Yull, F. E., Li, B., Cheng, D.-s., Kernodle, D. S., Jansen, E. D., Contag, C. H., Segal, B. H., Holland, S. M., Blackwell, T. S., Christman, J. W. (2004). p47phox Deficiency Impairs NF-{kappa}B Activation and Host Defense in Pseudomonas Pneumonia. J. Immunol. 172: 1801-1808 [Abstract] [Full Text]  
  • Brown, J. R., Goldblatt, D., Buddle, J., Morton, L., Thrasher, A. J. (2003). Diminished production of anti-inflammatory mediators during neutrophil apoptosis and macrophage phagocytosis in chronic granulomatous disease (CGD). J. Leukoc. Biol. 73: 591-599 [Abstract] [Full Text]  
  • Forman, H. J., Torres, M. (2002). Reactive Oxygen Species and Cell Signaling: Respiratory Burst in Macrophage Signaling. Am. J. Respir. Crit. Care Med. 166: S4-8 [Abstract] [Full Text]  
  • Hsu, H.-Y., Wen, M.-H. (2002). Lipopolysaccharide-mediated Reactive Oxygen Species and Signal Transduction in the Regulation of Interleukin-1 Gene Expression. J. Biol. Chem. 277: 22131-22139 [Abstract] [Full Text]  
  • Yang, S., Panoskaltsis-Mortari, A., Shukla, M., Blazar, B. R., Haddad, I. Y. (2002). Exuberant Inflammation in Nicotinamide Adenine Dinucleotide Phosphate-Oxidase-Deficient Mice After Allogeneic Marrow Transplantation. J. Immunol. 168: 5840-5847 [Abstract] [Full Text]  
  • Gao, X.-p., Standiford, T. J., Rahman, A., Newstead, M., Holland, S. M., Dinauer, M. C., Liu, Q.-h., Malik, A. B. (2002). Role of NADPH Oxidase in the Mechanism of Lung Neutrophil Sequestration and Microvessel Injury Induced by Gram-Negative Sepsis: Studies in p47phox-/- and gp91phox-/- Mice. J. Immunol. 168: 3974-3982 [Abstract] [Full Text]  


Copyright © 2010 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»