The apical mucus layer alters the pharmacological properties of the airway epithelium

Electrogenic transepithelial ion transport can be measured with the short-circuit current technique. Such experiments are frequently used to evaluate the activity of the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated chloride channel that is defective in cystic fibrosis, one of the most frequent genetic diseases. Typically, CFTR activity is estimated from the effect of CFTR<sub>inh</sub>-172, a selective CFTR inhibitor. Unexpectedly, we found that CFTR<sub>inh</sub>-172, in addition to PPQ-102, another CFTR inhibitor, caused only partial inhibition of CFTR function, particularly in epithelia in pro-inflammatory conditions, which are characterized by abundant mucus secretion. We hypothesized that the mucus layer was responsible for the poor activity of CFTR inhibitors. Therefore, we treated the epithelial surface with the reducing agent dithiothreitol to remove mucus. Removal of mucus, confirmed by immunofluorescence, resulted in highly enhanced sensitivity of CFTR to pharmacological inhibition. Our results show that the mucus layer represents an important barrier whose presence limits the activity of pharmacological agents. This is particularly relevant for CFTR and the evaluation of therapeutic approaches for correction of the basic defect in cystic fibrosis. KEY POINTS: Activity of the cAMP-activated cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel can be evaluated by measuring the inhibition elicited by the selective blockers CFTR<sub>inh</sub>-172 and PPQ-102. In short-circuit current recordings on human airway epithelia, CFTR inhibitors had only a partial effect on cAMP-dependent chloride secretion, suggesting the possible contribution of other ion channels. The mucus layer covering the epithelial surface was removed with the reducing agent dithiothreitol. Treatment of epithelia with dithiothreitol markedly improved the efficacy of CFTR inhibitors. The partial effect of CFTR inhibitors might be explained by the presence of the mucus layer acting as a barrier.

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Publication Details

Journal
The Journal of Physiology
Published
2025-03-06
DOI
https://doi.org/10.1113/jp287891
Citations
2
Primary Topic
Cystic Fibrosis Research Advances
Type
article
Field-Weighted Citation Impact
3.04
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article

The apical mucus layer alters the pharmacological properties of the airway epithelium

Emanuela Pesce, Daniela Guidone, Martina De Santis, Nicoletta Pedemonte et al.
2 citations
The Journal of Physiology
Cystic Fibrosis Research Advances
3.04
article

The apical mucus layer alters the pharmacological properties of the airway epithelium

Emanuela Pesce, Daniela Guidone, Martina De Santis, Nicoletta Pedemonte, Luis J. V. Galietta, Valeria Capurro
article en
2 citations

Abstract

Electrogenic transepithelial ion transport can be measured with the short-circuit current technique. Such experiments are frequently used to evaluate the activity of the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated chloride channel that is defective in cystic fibrosis, one of the most frequent genetic diseases. Typically, CFTR activity is estimated from the effect of CFTR<sub>inh</sub>-172, a selective CFTR inhibitor. Unexpectedly, we found that CFTR<sub>inh</sub>-172, in addition to PPQ-102, another CFTR inhibitor, caused only partial inhibition of CFTR function, particularly in epithelia in pro-inflammatory conditions, which are characterized by abundant mucus secretion. We hypothesized that the mucus layer was responsible for the poor activity of CFTR inhibitors. Therefore, we treated the epithelial surface with the reducing agent dithiothreitol to remove mucus. Removal of mucus, confirmed by immunofluorescence, resulted in highly enhanced sensitivity of CFTR to pharmacological inhibition. Our results show that the mucus layer represents an important barrier whose presence limits the activity of pharmacological agents. This is particularly relevant for CFTR and the evaluation of therapeutic approaches for correction of the basic defect in cystic fibrosis. KEY POINTS: Activity of the cAMP-activated cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel can be evaluated by measuring the inhibition elicited by the selective blockers CFTR<sub>inh</sub>-172 and PPQ-102. In short-circuit current recordings on human airway epithelia, CFTR inhibitors had only a partial effect on cAMP-dependent chloride secretion, suggesting the possible contribution of other ion channels. The mucus layer covering the epithelial surface was removed with the reducing agent dithiothreitol. Treatment of epithelia with dithiothreitol markedly improved the efficacy of CFTR inhibitors. The partial effect of CFTR inhibitors might be explained by the presence of the mucus layer acting as a barrier.

The Journal of PhysiologyVol. 603(9)
Istituto Giannina Gaslini (IT), Telethon Institute Of Genetics And Medicine (IT)
Good health and well-being
Openalex Percentile: Top 11%
Cystic Fibrosis Research Advances
3.04
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