Fig. 3.
Effects of forskolin, ATP, and flagellin on ICl across Calu-3 monolayers. A: typical experiment (of 4 similar) showing effects of forskolin (20 μM, serosal solution) followed by P. aeruginosa flagellin (10−7 g/ml, apical) and then glibenclamide (1 mM, apical and basolateral) on ICl. B: typical experiment (of 5 similar) showing effects of P. aeruginosa flagellin (10−7 g/ml, apical) followed by forskolin (1 μM, arrow). Flagellin caused a characteristic, slow increase in ICl, and subsequent forskolin addition caused rapid increases in ICl. GlyH101 (20 μM, arrow) inhibited ICl to the control levels. C: typical experiment (of 6 similar) showing effects of ATP (100 μM) added to the apical and then basolateral solution. There was a rapid increase followed by a decrease to plateau. Adding P. aeruginosa flagellin (10−7 g/ml, apical) caused a further increase of ICl. ICl was inhibited by CFTRinh172 (20 μM, apical). D: averages ±SD steady-state increases of ICl (ΔICl) of Calu-3 cells in response to flagellin, forskolin, and ATP each added individually and also in response to flagellin added in the presence of forskolin (flagellin+forskolin) and flagellin added in presence of ATP (flagellin+ATP). All treatments except flagellin+forskolin yielded significant increases in ICl. P < 0.05, n = 5–6 in each case.