Signaling intermediates required for NF-κB activation and IL-8 expression in CF bronchial epithelial cells

• DOI: 10.1152/ajplung.00086.2002
• Publication Date: 2015-03-03T20:20:04Z
• Authors: Jing Li; Xa Dwight Johnson; Svetlana Iazvovskaia; Alan Tan; Anning Lin; Marc B. Hershenson
• Keywords: Transcriptional Activation; 0301 basic medicine; Cystic Fibrosis; Transcription, Genetic; Tumor Necrosis Factor-alpha; Interleukin-8; NF-kappa B; Bronchi; Epithelial Cells; G(M1) Ganglioside; Protein Serine-Threonine Kinases; Antibodies; Cell Line; I-kappa B Kinase; Enzyme Activation; 03 medical and health sciences; Humans; Mitogen-Activated Protein Kinases; Promoter Regions, Genetic; Signal Transduction

Ligation of the asialoGM1 Pseudomonas aeruginosa pilin receptor has been demonstrated to induce IL-8 expression in airway epithelial cells via an NF-κB-dependent pathway. We examined signaling pathways required for asialoGM1-mediated NF-κB activation IB3 cells, a human bronchial cell line derived from cystic fibrosis (CF) patient, and C-38 rescued that expresses functional CF transmembrane regulator. with specific antibody induced greater than consistent density receptors phenotype cells. AsialoGM1-mediated NF-κB, IκB kinase (IKK), ERK was also With use genetic inhibitors, we found IKK-β NF-κB-inducing are maximal transactivation transcription promoter. Finally, although expression, inhibition had no effect on IKK or activation, suggesting regulates NF-κB-independent manner.