Fig. 1.
Cytokine-induced neutrophil chemokine (CINC)-1 and transforming growth factor (TGF)-β1 cause a synergistic inhibition of β2AR agonist–stimulated cystic fibrosis transmembrane conductance regulator (CFTR)-specific Cl− transport across rat type II alveolar (ATII) cell monolayers. (A) Coexposure of rat ATII cell monolayers to a small dose (1 ng/ml for 6 h) of CINC-1 and TGF-β1 causes a synergistic inhibition of the epinephrine-stimulated CFTR-specific Cl− absorption across the apical membrane of these cells while single exposure to 1 ng/ml of CINC-1 or TGF-β1 has no effect. (B) Coexposure of rat ATII cell monolayers to a dose (10 ng/ml for 6 h) of CINC-1 and TGF-β1 does not increase the inhibitory effect of single exposure of the same dose of CINC-1 and TGF-β1 on the epinephrine-stimulated CFTR-specific Cl− absorption across the apical membrane of rat ATII cell monolayers. For all experiments, mean basal short-circuit current was −7 ± 1.8 μA, mean epinephrine-treated short-circuit current was −24 ± 2.4 μA. The results are means ± SD (n = 12); *P < 0.05 from controls.

Cytokine-induced neutrophil chemokine (CINC)-1 and transforming growth factor (TGF)-β1 cause a synergistic inhibition of β2AR agonist–stimulated cystic fibrosis transmembrane conductance regulator (CFTR)-specific Cl transport across rat type II alveolar (ATII) cell monolayers. (A) Coexposure of rat ATII cell monolayers to a small dose (1 ng/ml for 6 h) of CINC-1 and TGF-β1 causes a synergistic inhibition of the epinephrine-stimulated CFTR-specific Cl absorption across the apical membrane of these cells while single exposure to 1 ng/ml of CINC-1 or TGF-β1 has no effect. (B) Coexposure of rat ATII cell monolayers to a dose (10 ng/ml for 6 h) of CINC-1 and TGF-β1 does not increase the inhibitory effect of single exposure of the same dose of CINC-1 and TGF-β1 on the epinephrine-stimulated CFTR-specific Cl absorption across the apical membrane of rat ATII cell monolayers. For all experiments, mean basal short-circuit current was −7 ± 1.8 μA, mean epinephrine-treated short-circuit current was −24 ± 2.4 μA. The results are means ± SD (n = 12); *P < 0.05 from controls.

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