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Effects of cystic fibrosis transmembrane conductance regulator and DeltaF508CFTR on inflammatory response, ER stress, and Ca2+ of airway epithelia Hybiske K; Fu Z; Schwarzer C; Tseng J; Do J; Huang N; Machen TEAm J Physiol Lung Cell Mol Physiol 2007[Nov]; 293 (5): L1250-60We tested whether cystic fibrosis (CF) airway epithelia have larger innate immune responses than non-CF or cystic fibrosis transmembrane conductance regulator (CFTR)-corrected cells, perhaps resulting from ER stress due to retention of DeltaF508CFTR in the endoplasmic reticulum (ER) and activation of cytosolic Ca(2+) (Ca(i)) and nuclear factor (NF)-kappaB signaling. Adenovirus infections of a human CF (DeltaF508/DeltaF508) nasal cell line (CF15) provided isogenic comparisons of wild-type (wt) CFTR and DeltaF508CFTR. In the absence of bacteria, there were no or only small differences among CF15, CF15-lacZ (beta-galactosidase-expressing), CF15-wtCFTR (wtCFTR-corrected), and CF15-DeltaF508CFTR (to test ER retention of DeltaF508CFTR) cells in NF-kappaB activity, interleukin (IL)-8 secretion, Ca(i) responses, and ER stress. Non-CF and CF primary cultures of human bronchial epithelial cells (HBE) secreted IL-8 equivalently. Upon infection with Pseudomonas aeruginosa (PA) or flagellin (key activator for airway epithelia), CF15, CF15-lacZ, CF15-wtCFTR, and CF15DeltaF508CFTR cells exhibited equal PA binding, NF-kappaB activity, and IL-8 secretion; cells also responded similarly to flagellin when both CFTR (forskolin) and Ca(i) signaling (ATP) were activated. CF and non-CF HBE responded similarly to flagellin + ATP. Thapsigargin (Tg, releases ER Ca(2+)) increased flagellin-stimulated NF-kappaB and ER stress similarly in all cells. We conclude that ER stress, Ca(i), and NF-kappaB signaling and IL-8 secretion were unaffected by wt- or DeltaF508CFTR in control and during exposure to PA, flagellin, flagellin + ATP, or flagellin + ATP + forskolin. Tg, but not wt- or DeltaF508CFTR, triggered ER stress. Previous measurements showing hyperinflammatory responses in CF airway epithelia may have resulted from cell-specific, rather than CFTR- or DeltaF508CFTR-specific effects.|Bronchi/cytology/metabolism[MESH]|Calcium Signaling[MESH]|Calcium/*metabolism[MESH]|Cells, Cultured[MESH]|Cystic Fibrosis Transmembrane Conductance Regulator/*pharmacology[MESH]|Cystic Fibrosis/*metabolism/microbiology/pathology[MESH]|Endoplasmic Reticulum/*drug effects/metabolism[MESH]|Enzyme-Linked Immunosorbent Assay[MESH]|Flagellin/pharmacology[MESH]|Humans[MESH]|Inflammation[MESH]|Interleukin-8/metabolism[MESH]|Microscopy, Confocal[MESH]|Mutation/genetics[MESH]|NF-kappa B/metabolism[MESH]|Pseudomonas Infections/metabolism/microbiology/pathology[MESH]|Pseudomonas aeruginosa/pathogenicity[MESH]|Respiratory Mucosa/*drug effects/metabolism[MESH] |
