Fig 3. In human bronchial epithelial cells, PGE₂ stimulated Cl^- secretion is completely CFTR dependent.

A. Representative I_sc trace with vertical deflections indicating the change in I_sc after a 1 mV pulse was applied (every 1 minute). Bronchial epithelial cells were exposed to serosal to mucosal Cl^- gradient with equivalent bilateral HCO₃^-. PGE₂ (1 μM, serosal) was added to HBE41 WT cells after a baseline period of ≥ 10 minutes, with CFTR_inh-172 (20 μM, mucosal) added afterwards. To verify cell viability, ATP (500 μM, mucosal) was added. B. Representative I_sc trace from a similar experiment with CFBE41 CF cells. C. Change in PGE₂-stimulated I_sc (mean ± SEM, n ≥ 4) in CFBE41 WT and CF cells. Asterisks denote significance by Student’s t-test (***, P < 0.001). Mean percent inhibition compared to CFBE41 WT noted. D-F. PGE₂ stimulated Cl^- secretion in 16HBE14o- cells (D), primary cultures of human bronchial epithelial cells (E), and primary cultures from CF nasal polyp extract (F). Experiments were performed in the same manner as Fig 3A and representative I_sc traces are shown. N ≥ 3 experiments were performed for each set of cells with similar responses.