Fig. 2.
TNFα+IL-17 increase CFTR activity and expression. After TNFα+IL-17 treatment for 24 h, human airway epithelia were mounted in modified Ussing chambers with symmetric Krebs-Ringer solution gassed with 5% CO2. Epithelia were voltage clamped followed by continuous recording of short-circuit current (ISC) and transepithelial conductance (Gt) as pharmacologic agents were sequentially added to the apical chamber. A–D: ISC, ΔISC, Gt, and ΔGt in control and TNFα+IL-17-treated epithelia. E: TNFα+IL-17-induced changes in SCNN1A, TMEM16A, and CFTR transcript abundance. F: estimate of paracellular conductance (Gp) obtained from residual Gt after inhibition of epithelial Na+ channel (ENaC), calcium-activated anion channel (CaCC), and CFTR. For A–D, n = 5 different donors; for E and F, n = 6 different donors. Bars indicate means and SD. Statistical significance between control and TNFα+IL-17-treated epithelia was tested using paired Student’s t test. *P < 0.05, **P < 0.01.