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Articles in PresS, published online ahead of print September 27, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00086.2002
Submitted on March 22, 2002
Accepted on September 20, 2002
B activation and IL-8 expression in CF bronchial epithelial cells
1 Department of Pediatrics, University of Chicago, Chicago, IL, USA
2 Ben May Institute for Cancer Research, University of Chicago, Chicago, IL, USA
* To whom correspondence should be addressed. E-mail: mhershen{at}midway.uchicago.edu.
Ligation of the asialoGM1 Pseudomonas aeruginosa pilin receptor has been demonstrated to induce IL-8 expression in airway epithelial cells via a nuclear factor (NF)-
B-dependent pathway. We examined the signaling pathways required for asialoGM1-mediated NF-B activation in IB3 cells, a human bronchial epithelial cell line derived from a cystic fibrosis (CF) patient, and C-38 cells, the rescued cell line which expresses a functional CFTR. Ligation of the asialoGM1 receptor with specific antibody induced greater IL-8 expression in IB3 cells than C-38 cells, consistent with the greater density of asialoGM1 receptors in CF phenotype cells. AsialoGM1-mediated activation of NF-B, IB kinase (IKK) and extracellular signal regulated kinase (ERK) were also greater in IB3 cells. Using genetic inhibitors, we found that IKKß and NF-B inducing kinase (NIK) are required for maximal NF-B transactivation and transcription from the IL-8 promoter. Finally, while ERK activation was required for maximal asialoGM1-mediated IL-8 expression, inhibition of ERK signaling had no effect on IKK or NF-B activation, suggesting that ERK regulates IL-8 expression in a NF-B-independent manner.
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