Ivacaftor restores delayed mucociliary transport caused by Pseudomonas aeruginosa–induced acquired cystic fibrosis transmembrane conductance regulator dysfunction in rabbit nasal epithelia
Background Abnormal chloride (Cl–) transport dehydrates airway surface liquid (ASL) in sinonasal epithelium leading to mucus stasis and chronic rhinosinusitis. As an experimental epithelium, rabbit tissue provides an excellent representation of human sinus disease, and the rabbit sinusitis model is...
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Published in | International forum of allergy & rhinology Vol. 12; no. 5; pp. 690 - 698 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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01.05.2022
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Abstract | Background
Abnormal chloride (Cl–) transport dehydrates airway surface liquid (ASL) in sinonasal epithelium leading to mucus stasis and chronic rhinosinusitis. As an experimental epithelium, rabbit tissue provides an excellent representation of human sinus disease, and the rabbit sinusitis model is both established and well suited for therapeutic interventions in vivo. Our objective in this study was to evaluate whether ivacaftor reverses the consequences of Pseudomonas aeruginosa–induced acquired cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction.
Methods
Rabbit nasal cavities were assessed for responsiveness to ivacaftor in vivo (by nasal potential difference [NPD] assay). Rabbit nasal epithelial (RNE) cultures were incubated with an ultrafiltrate of P aeruginosa (PAO1 strain) for 4 hours and tested for acquired CFTR dysfunction. Markers of mucociliary function, including airway surface liquid depth (ASL), periciliary liquid depth (PCL), ciliary beat frequency (CBF), and mucociliary transport (MCT), were measured by micro‐optical coherence tomography (μOCT) after PAO1 and/or ivacaftor incubation.
Results
Ivacaftor resulted in a significant mean NPD polarization of 21.8 ± 2.1 mV, which was significantly greater than that seen in the low Cl− control (12.9 ± 1.3; p = 0.01). PAO1 exposure induced a state of acquired CFTR dysfunction in rabbit nasal epithelium as measured by forskolin‐stimulated short‐circuit current (ISC) (control, 37.0 ± 1.1 μA/cm2; PAO1, 24.4 ± 1.1 μA/cm2; p < 0.001). RNE cultures exposed to PAO1 had inhibited mucociliary function, whereas coincubation with ivacaftor restored mucociliary clearance, as measured by μOCT.
Conclusion
In rabbit nasal epithelium, ivacaftor robustly stimulates CFTR‐mediated Cl− secretion and normalizes ASL and CBF in PAO1‐induced acquired CFTR dysfunction. Preclinical testing of CFTR potentiators as therapy for P aeruginosa rabbit sinusitis is planned. |
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AbstractList | BackgroundAbnormal chloride (Cl–) transport dehydrates airway surface liquid (ASL) in sinonasal epithelium leading to mucus stasis and chronic rhinosinusitis. As an experimental epithelium, rabbit tissue provides an excellent representation of human sinus disease, and the rabbit sinusitis model is both established and well suited for therapeutic interventions in vivo. Our objective in this study was to evaluate whether ivacaftor reverses the consequences of Pseudomonas aeruginosa–induced acquired cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction.MethodsRabbit nasal cavities were assessed for responsiveness to ivacaftor in vivo (by nasal potential difference [NPD] assay). Rabbit nasal epithelial (RNE) cultures were incubated with an ultrafiltrate of P aeruginosa (PAO1 strain) for 4 hours and tested for acquired CFTR dysfunction. Markers of mucociliary function, including airway surface liquid depth (ASL), periciliary liquid depth (PCL), ciliary beat frequency (CBF), and mucociliary transport (MCT), were measured by micro‐optical coherence tomography (μOCT) after PAO1 and/or ivacaftor incubation.ResultsIvacaftor resulted in a significant mean NPD polarization of 21.8 ± 2.1 mV, which was significantly greater than that seen in the low Cl− control (12.9 ± 1.3; p = 0.01). PAO1 exposure induced a state of acquired CFTR dysfunction in rabbit nasal epithelium as measured by forskolin‐stimulated short‐circuit current (ISC) (control, 37.0 ± 1.1 μA/cm2; PAO1, 24.4 ± 1.1 μA/cm2; p < 0.001). RNE cultures exposed to PAO1 had inhibited mucociliary function, whereas coincubation with ivacaftor restored mucociliary clearance, as measured by μOCT.ConclusionIn rabbit nasal epithelium, ivacaftor robustly stimulates CFTR‐mediated Cl− secretion and normalizes ASL and CBF in PAO1‐induced acquired CFTR dysfunction. Preclinical testing of CFTR potentiators as therapy for P aeruginosa rabbit sinusitis is planned. Background Abnormal chloride (Cl – ) transport dehydrates airway surface liquid (ASL) in sinonasal epithelium leading to mucus stasis and chronic rhinosinusitis. As an experimental epithelium, rabbit tissue provides an excellent representation of human sinus disease, and the rabbit sinusitis model is both established and well suited for therapeutic interventions in vivo. Our objective in this study was to evaluate whether ivacaftor reverses the consequences of Pseudomonas aeruginosa– induced acquired cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction. Methods Rabbit nasal cavities were assessed for responsiveness to ivacaftor in vivo (by nasal potential difference [NPD] assay). Rabbit nasal epithelial (RNE) cultures were incubated with an ultrafiltrate of P aeruginosa (PAO1 strain) for 4 hours and tested for acquired CFTR dysfunction. Markers of mucociliary function, including airway surface liquid depth (ASL), periciliary liquid depth (PCL), ciliary beat frequency (CBF), and mucociliary transport (MCT), were measured by micro‐optical coherence tomography (μOCT) after PAO1 and/or ivacaftor incubation. Results Ivacaftor resulted in a significant mean NPD polarization of 21.8 ± 2.1 mV, which was significantly greater than that seen in the low Cl − control (12.9 ± 1.3; p = 0.01). PAO1 exposure induced a state of acquired CFTR dysfunction in rabbit nasal epithelium as measured by forskolin‐stimulated short‐circuit current (I SC ) (control, 37.0 ± 1.1 μA/cm 2 ; PAO1, 24.4 ± 1.1 μA/cm 2 ; p < 0.001). RNE cultures exposed to PAO1 had inhibited mucociliary function, whereas coincubation with ivacaftor restored mucociliary clearance, as measured by μOCT. Conclusion In rabbit nasal epithelium, ivacaftor robustly stimulates CFTR‐mediated Cl − secretion and normalizes ASL and CBF in PAO1‐induced acquired CFTR dysfunction. Preclinical testing of CFTR potentiators as therapy for P aeruginosa rabbit sinusitis is planned. Abnormal chloride (Cl ) transport dehydrates airway surface liquid (ASL) in sinonasal epithelium leading to mucus stasis and chronic rhinosinusitis. As an experimental epithelium, rabbit tissue provides an excellent representation of human sinus disease, and the rabbit sinusitis model is both established and well suited for therapeutic interventions in vivo. Our objective in this study was to evaluate whether ivacaftor reverses the consequences of Pseudomonas aeruginosa-induced acquired cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction. Rabbit nasal cavities were assessed for responsiveness to ivacaftor in vivo (by nasal potential difference [NPD] assay). Rabbit nasal epithelial (RNE) cultures were incubated with an ultrafiltrate of P aeruginosa (PAO1 strain) for 4 hours and tested for acquired CFTR dysfunction. Markers of mucociliary function, including airway surface liquid depth (ASL), periciliary liquid depth (PCL), ciliary beat frequency (CBF), and mucociliary transport (MCT), were measured by micro-optical coherence tomography (μOCT) after PAO1 and/or ivacaftor incubation. Ivacaftor resulted in a significant mean NPD polarization of 21.8 ± 2.1 mV, which was significantly greater than that seen in the low Cl control (12.9 ± 1.3; p = 0.01). PAO1 exposure induced a state of acquired CFTR dysfunction in rabbit nasal epithelium as measured by forskolin-stimulated short-circuit current (I ) (control, 37.0 ± 1.1 μA/cm ; PAO1, 24.4 ± 1.1 μA/cm ; p < 0.001). RNE cultures exposed to PAO1 had inhibited mucociliary function, whereas coincubation with ivacaftor restored mucociliary clearance, as measured by μOCT. In rabbit nasal epithelium, ivacaftor robustly stimulates CFTR-mediated Cl secretion and normalizes ASL and CBF in PAO1-induced acquired CFTR dysfunction. Preclinical testing of CFTR potentiators as therapy for P aeruginosa rabbit sinusitis is planned. Background Abnormal chloride (Cl–) transport dehydrates airway surface liquid (ASL) in sinonasal epithelium leading to mucus stasis and chronic rhinosinusitis. As an experimental epithelium, rabbit tissue provides an excellent representation of human sinus disease, and the rabbit sinusitis model is both established and well suited for therapeutic interventions in vivo. Our objective in this study was to evaluate whether ivacaftor reverses the consequences of Pseudomonas aeruginosa–induced acquired cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction. Methods Rabbit nasal cavities were assessed for responsiveness to ivacaftor in vivo (by nasal potential difference [NPD] assay). Rabbit nasal epithelial (RNE) cultures were incubated with an ultrafiltrate of P aeruginosa (PAO1 strain) for 4 hours and tested for acquired CFTR dysfunction. Markers of mucociliary function, including airway surface liquid depth (ASL), periciliary liquid depth (PCL), ciliary beat frequency (CBF), and mucociliary transport (MCT), were measured by micro‐optical coherence tomography (μOCT) after PAO1 and/or ivacaftor incubation. Results Ivacaftor resulted in a significant mean NPD polarization of 21.8 ± 2.1 mV, which was significantly greater than that seen in the low Cl− control (12.9 ± 1.3; p = 0.01). PAO1 exposure induced a state of acquired CFTR dysfunction in rabbit nasal epithelium as measured by forskolin‐stimulated short‐circuit current (ISC) (control, 37.0 ± 1.1 μA/cm2; PAO1, 24.4 ± 1.1 μA/cm2; p < 0.001). RNE cultures exposed to PAO1 had inhibited mucociliary function, whereas coincubation with ivacaftor restored mucociliary clearance, as measured by μOCT. Conclusion In rabbit nasal epithelium, ivacaftor robustly stimulates CFTR‐mediated Cl− secretion and normalizes ASL and CBF in PAO1‐induced acquired CFTR dysfunction. Preclinical testing of CFTR potentiators as therapy for P aeruginosa rabbit sinusitis is planned. BACKGROUNDAbnormal chloride (Cl- ) transport dehydrates airway surface liquid (ASL) in sinonasal epithelium leading to mucus stasis and chronic rhinosinusitis. As an experimental epithelium, rabbit tissue provides an excellent representation of human sinus disease, and the rabbit sinusitis model is both established and well suited for therapeutic interventions in vivo. Our objective in this study was to evaluate whether ivacaftor reverses the consequences of Pseudomonas aeruginosa-induced acquired cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction. METHODSRabbit nasal cavities were assessed for responsiveness to ivacaftor in vivo (by nasal potential difference [NPD] assay). Rabbit nasal epithelial (RNE) cultures were incubated with an ultrafiltrate of P aeruginosa (PAO1 strain) for 4 hours and tested for acquired CFTR dysfunction. Markers of mucociliary function, including airway surface liquid depth (ASL), periciliary liquid depth (PCL), ciliary beat frequency (CBF), and mucociliary transport (MCT), were measured by micro-optical coherence tomography (μOCT) after PAO1 and/or ivacaftor incubation. RESULTSIvacaftor resulted in a significant mean NPD polarization of 21.8 ± 2.1 mV, which was significantly greater than that seen in the low Cl- control (12.9 ± 1.3; p = 0.01). PAO1 exposure induced a state of acquired CFTR dysfunction in rabbit nasal epithelium as measured by forskolin-stimulated short-circuit current (ISC ) (control, 37.0 ± 1.1 μA/cm2 ; PAO1, 24.4 ± 1.1 μA/cm2 ; p < 0.001). RNE cultures exposed to PAO1 had inhibited mucociliary function, whereas coincubation with ivacaftor restored mucociliary clearance, as measured by μOCT. CONCLUSIONIn rabbit nasal epithelium, ivacaftor robustly stimulates CFTR-mediated Cl- secretion and normalizes ASL and CBF in PAO1-induced acquired CFTR dysfunction. Preclinical testing of CFTR potentiators as therapy for P aeruginosa rabbit sinusitis is planned. |
Author | Lim, Dong Jin Banks, Catherine Cho, Do‐Yeon Zhang, Shaoyan Grayson, Jessica W. Tearney, Guillermo J. Woodworth, Bradford A. Skinner, Daniel F. Rowe, Steven M. |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34704673$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1002_alr_23301 crossref_primary_10_1016_j_otc_2022_09_009 crossref_primary_10_1002_alr_23309 crossref_primary_10_1177_01455613231214622 crossref_primary_10_1186_s12931_024_02889_w crossref_primary_10_1002_lary_31431 crossref_primary_10_1016_j_jcf_2023_09_002 |
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Keywords | micro-optical coherence tomography cystic fibrosis chronic rhinosinusitis sinusitis mucociliary clearance ivacaftor CFTR chronic sinusitis mucociliary transport |
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Notes | Funding information National Institutes of Health (NIH)/National Institutes of Allergy and Infectious Disease (grant K08AI146220‐02 to D.Y.C.); NIH/National Institute of Diabetes and Digestive and Kidney Diseases (grant 5P30DK072482‐03 to S.M.R.); NIH/NHLBI (grants R01 HL133006‐05 and K08HL107142‐05 to B.A.W.). Potential conflict of interest: B.A.W: consultant for Cook Medical and Smith and Nephew. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
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Abnormal chloride (Cl–) transport dehydrates airway surface liquid (ASL) in sinonasal epithelium leading to mucus stasis and chronic rhinosinusitis.... Abnormal chloride (Cl ) transport dehydrates airway surface liquid (ASL) in sinonasal epithelium leading to mucus stasis and chronic rhinosinusitis. As an... Background Abnormal chloride (Cl – ) transport dehydrates airway surface liquid (ASL) in sinonasal epithelium leading to mucus stasis and chronic... BackgroundAbnormal chloride (Cl–) transport dehydrates airway surface liquid (ASL) in sinonasal epithelium leading to mucus stasis and chronic rhinosinusitis.... BACKGROUNDAbnormal chloride (Cl- ) transport dehydrates airway surface liquid (ASL) in sinonasal epithelium leading to mucus stasis and chronic rhinosinusitis.... |
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SubjectTerms | Aminophenols Animals CFTR Chloride transport Chlorides - metabolism chronic rhinosinusitis chronic sinusitis Cystic fibrosis Cystic Fibrosis Transmembrane Conductance Regulator Epithelium Forskolin Humans ivacaftor micro‐optical coherence tomography Mucociliary Clearance mucociliary transport Mucus Nasal Mucosa - metabolism Pseudomonas aeruginosa Quinolones Rabbits Respiratory tract Rhinitis Rhinosinusitis Sinus Sinusitis Sinusitis - drug therapy Therapeutic applications |
Title | Ivacaftor restores delayed mucociliary transport caused by Pseudomonas aeruginosa–induced acquired cystic fibrosis transmembrane conductance regulator dysfunction in rabbit nasal epithelia |
URI | https://onlinelibrary.wiley.com/doi/abs/10.1002%2Falr.22907 https://www.ncbi.nlm.nih.gov/pubmed/34704673 https://www.proquest.com/docview/2654501903/abstract/ https://search.proquest.com/docview/2587000624 |
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