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Differential effects of cyclic and constant stress on ATP release and mucociliary transport by human airway epithelia.

Differential effects of cyclic and constant stress on ATP release and mucociliary transport by human airway epithelia. Research Abstract Details 

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  • Differential effects of cyclic and constant stress on ATP release and mucociliary transport by human airway epithelia. Abstract Text:

    In the lungs, the first line of defence against bacterial infection is the thin layer of airway surface liquid (ASL) lining the airway surface. The superficial airway epithelium exhibits complex regulatory pathways that blend ion transport to adjust ASL volume to maintain proper mucociliary clearance (MCC). We hypothesized that stresses generated by airflow and transmural pressures during breathing govern ASL volume by regulating the rate of epithelial ATP release. Luminal ATP, via interactions with apical membrane P2-purinoceptors, regulates the balance of active ion secretion versus absorption to maintain ASL volume at optimal levels for MCC. In this study we tested the hypothesis that cyclic compressive stress (CCS), mimicking normal tidal breathing, regulates ASL volume in airway epithelia. Polarized tracheobronchial epithelial cultures from normal and cystic fibrosis (CF) subjects responded to a range of CCS by increasing the rate of ATP release. In normal airway epithelia, the CCS-induced increase in ASL ATP concentration was sufficient to induce purinoceptor-mediated increases in ASL height and MCC, via inhibition of epithelial Na(+)-channel-mediated Na(+) absorption and stimulation of Cl(-) secretion through CFTR and the Ca(2+)-activated chloride channels. In contrast, static, non-oscillatory stress did not stimulate ATP release, ion transport or MCC, emphasizing the importance of rhythmic mechanical stress for airway defence. In CF airway cultures, which exhibit basal ASL depletion, CCS was partially effective, producing less ASL volume secretion than in normal cultures, but a level sufficient to restore MCC. The present data suggest that CCS may (1) regulate ASL volume in the normal lung and (2) improve clearance in the lungs of CF patients, potentially explaining the beneficial role of exercise in lung defence.

    Differential effects of cyclic and constant stress on ATP release and mucociliary transport by human airway epithelia. Publishing Authors By Initials

    For similar biomechanics: stress, mechanical research abstracts see: biomechanics: stress, mechanical research

    PUBMED ID PMID:

    MEDLINE DATE:

    Differential effects of cyclic and constant stress on ATP release and mucociliary transport by human airway epithelia. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: The Journal of physiology

    VOLUME: 580

    Page Numbers: 577-92

    Journal Abbreviation:

    ISSN: 0022-3751

    DAY: 22

    MONTH: 02

    YEAR: 2007

    Differential effects of cyclic and constant stress on ATP release and mucociliary transport by human airway epithelia. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 266262

    Differential effects of cyclic and constant stress on ATP release and mucociliary transport by human airway epithelia. Keywords Mesh Terms:

    KEYWORDS: Stress, Mechanical

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Differential effects of cyclic and constant stress on ATP release and mucociliary transport by human airway epithelia. Information

    Substance Name: Adenosine Triphosphate

    Registry Number: 56-65-5

    Grant and Affiliation Information for Differential effects of cyclic and constant stress on ATP release and mucociliary transport by human airway epithelia.

    AFFILIATION: Cystic Fibrosis Research and Treatment Center, University of North Carolna, Chapel Hill, NC 27599-7248, USA. bbutton@med.unc.edu

    Country: England

    England Research PublicationEngland Research Publication

    AGENCY: United States NHLBI

    GRANT: HL060280

    ACRONYM: HL

    MEDLINETA: J Physiol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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