Literature DB >> 31734731

Chloride Conductance, Nasal Potential Difference and Cystic Fibrosis Pathophysiology.

Elenara da Fonseca Andrade Procianoy1,2, Fernando Antônio de Abreu E Silva3,4, Paulo José Cauduro Maróstica3,5, Paul M Quinton6.   

Abstract

PURPOSE: Cystic fibrosis (CF) is a multisystem genetic disease caused by dysfunction of the epithelial anionic channel Cystic Fibrosis Transmembrane conductance Regulator (CFTR). Decreased mucociliary clearance because of thickened mucus is part of the pulmonary disease pathophysiology. It is controversial if the thickened airway surface liquid (ASL) is caused by the deficient chloride secretion and excessive sodium (through ENaC) and water hyperabsorption from the periciliar fluid or by the lack of bicarbonate secretion with relative acidification of the ASL. Correlations between the magnitude of in vivo chloride conductance with phenotypic characteristics and CF genotype can help to elucidate these mechanisms and direct to new treatments.
METHODS: Nasal potential difference was measured in 28 CF patients (age from 0.3 to 28 year) and correlated with pulmonary function, pancreatic phenotype, pulmonary colonization and genotype severity.
RESULTS: The CFTR-chloride conductance was better in older patients (r = 0.40; P = 0.03), in patients with better pulmonary function (r = 0.48; P = 0.01), and was associated with genotype severity. Higher chloride diffusion in the presence of a favorable chemical gradient was associated with Pseudomonas aeruginosa negativity (P < 0.05). More negative NPDmax was associated with pancreatic insufficiency (P < 0.01) as well with genotype severity, but not with the pulmonary function.
CONCLUSIONS: The anion permeability through CFTR, mainly chloride, but bicarbonate as well, is the most critical factor in CF airway pathophysiology. Treatments primarily directed to correct CFTR function and/or airway acidity are clearly a priority.

Entities:  

Keywords:  Bicarbonate; CFTR; Cystic fibrosis; Genetic disease; Pseudomonas aeruginosa

Mesh:

Substances:

Year:  2019        PMID: 31734731     DOI: 10.1007/s00408-019-00293-6

Source DB:  PubMed          Journal:  Lung        ISSN: 0341-2040            Impact factor:   2.584


  29 in total

1.  Pulmonary disease severity in men with deltaF508 cystic fibrosis and residual chloride secretion.

Authors:  S R Thomas; A Jaffe; D M Geddes; M E Hodson; E W Alton
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Review 2.  Role of epithelial HCO3⁻ transport in mucin secretion: lessons from cystic fibrosis.

Authors:  Paul M Quinton
Journal:  Am J Physiol Cell Physiol       Date:  2010-10-06       Impact factor: 4.249

Review 3.  ENaC inhibitors and airway re-hydration in cystic fibrosis: state of the art.

Authors:  Mike Althaus
Journal:  Curr Mol Pharmacol       Date:  2013-03       Impact factor: 3.339

4.  Physiology of epithelial chloride and fluid secretion.

Authors:  Raymond A Frizzell; John W Hanrahan
Journal:  Cold Spring Harb Perspect Med       Date:  2012-06       Impact factor: 6.915

5.  Protocols for in vivo measurement of the ion transport defects in cystic fibrosis nasal epithelium.

Authors:  P G Middleton; D M Geddes; E W Alton
Journal:  Eur Respir J       Date:  1994-11       Impact factor: 16.671

Review 6.  The Clinical Biology of Cystic Fibrosis Transmembrane Regulator Protein: Its Role and Function in Extrapulmonary Disease.

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Review 7.  CFTR, bicarbonate, and the pathophysiology of cystic fibrosis.

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Authors:  Teresinha Leal; Isabelle Fajac; Helen L Wallace; Patrick Lebecque; Jean Lebacq; Dominique Hubert; Josette Dall'Ava; Daniel Dusser; Anusha P Ganesan; Christiane Knoop; Jean Cumps; Pierre Wallemacq; Kevin W Southern
Journal:  Clin Biochem       Date:  2008-04-08       Impact factor: 3.281

Review 9.  Cystic fibrosis.

Authors:  J Stuart Elborn
Journal:  Lancet       Date:  2016-04-29       Impact factor: 79.321

10.  Modified method to measure nasal potential difference.

Authors:  Teresinha Leal; Jean Lebacq; Patrick Lebecque; Jean Cumps; Pierre Wallemacq
Journal:  Clin Chem Lab Med       Date:  2003-01       Impact factor: 3.694

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