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A more recent version of this article appeared on October 28, 2005
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M507977200v1
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Papers In Press, published online ahead of print August 25, 2005
J. Biol. Chem, 10.1074/jbc.M507977200
Submitted on July 21, 2005
Accepted on August 25, 2005

TNF-alpha triggers mucus production in airway epithelium through an IKKbeta dependent mechanism

Jose M. Lora, Dong Mei Zhang, Sha Mei Liao, Timothy Burwell, Anne Marie King, Philip A. Barker, Latika Singh, Marie Keaveney, Jay Morgenstern, Jose Carlos Gutierrez-Ramos, Anthony J. Coyle, and Christopher C. Fraser

Inflammation, Millennium Pharmaceuticals, Cambridge, MA 02139

Corresponding Author: fraser{at}mpi.com

Excessive mucus production by airway epithelium is a major characteristic of a number of respiratory diseases, including asthma, chronic bronchitis and cystic fibrosis. However, the signal transduction pathways leading to mucus production are poorly understood. Here we examine the potential role of IKKbeta in mucus synthesis in vitro and in vivo. TNF-alpha or TGF-beta stimulation of human epithelial cells resulted in mucus secretion as measured by MUC5AC mRNA and protein. TNF-alpha stimulation induced Ikappa B kinase beta (IKKbeta )-dependent p65 nuclear translocation, mucus synthesis and production of cytokines from epithelial cells. TNF-alpha , but not TGF-alpha induced mucus production dependent of IKKbeta -mediated NF-kappa B activation. In vivo, TNF-alpha induced NF-kappa B as determined by whole mouse body bioluminescence. This activation was localized to the epithelium as revealed by LacZ staining in NF-kappa B- LacZ transgenic mice. TNF-alpha -induced mucus production in vivo could also be inhibited by administration into the epithelium of an IKKbeta dominant negative adenovirus. Taken together, our results demonstrate the important role of IKKbeta in TNF-alpha mediated mucus production in airway epithelium in vitro and in vivo.


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