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B activation and
IL-8 expression in CF bronchial epithelial cells
Department of Pediatrics and Ben May Institute for Cancer Research, University of Chicago, Chicago, Illinois 60637
Ligation of the
asialoGM1 Pseudomonas aeruginosa pilin receptor has been
demonstrated to induce IL-8 expression in airway epithelial cells via
an 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 that expresses a
functional CF transmembrane regulator. 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 ERK
was also greater in IB3 cells. With the use of genetic inhibitors, we
found that IKK-
and NF-B-inducing kinase are required for maximal
NF-B transactivation and transcription from the IL-8 promoter.
Finally, although 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 an NF-B-independent manner.
asialoGM1; extracellular signal-regulated kinase; IB kinase; mitogen-activated protein kinase; mitogen-activated protein
kinase/extracellular signal-regulated kinase kinase kinase; nuclear
factor-B-inducing kinase; tumor necrosis factor-
; cystic fibrosis
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