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American Journal of Respiratory Cell and Molecular Biology. Vol. 31, pp. 377-381, 2004
© 2004 American Thoracic Society
DOI: 10.1165/rcmb.2004-0124TR

Translational Review

Lung Inflammation as a Therapeutic Target in Cystic Fibrosis

David R. Koehler, Gregory P. Downey, Neil B. Sweezey, A. Keith Tanswell and Jim Hu

Programme in Lung Biology Research and the Canadian Institutes of Health Research Group in Lung Development, Hospital for Sick Children, Toronto; Toronto General Hospital Research Institute, University Health Network, Toronto; and Departments of Medicine, Paediatrics, Physiology, and Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada

Address correspondence to: Jim Hu, Programme in Lung Biology Research, Hospital for Sick Children, 555 University Ave., Toronto, ON, Canada M5G 1X8. E-mail: jhu{at}sickkids.ca

Cystic fibrosis (CF) lung disease is characterized by chronic neutrophilic inflammation and infection. Effective management of airway inflammation could complement other therapies for the treatment of CF. Recent progress has been made in understanding the signaling pathways regulating inflammatory cytokines in the lung. Here we examine the mechanisms responsible for inflammation in the CF lung, and discuss potential therapeutic strategies targeting inflammation.

Abbreviations: cystic fibrosis, CF • cystic fibrosis transmembrane conductance regulator, CFTR • inhibitor of nuclear factor {kappa}B, I{kappa}B • I{kappa}B kinase, IKK • interleukin, IL • nuclear factor {kappa}B, NF-{kappa}B • signal transducer and activator of transcription-1, STAT1 • Toll-like receptor, TLR • tumor necrosis factor {alpha}, TNF-{alpha}




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