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Abnormal cilia in Polynesians with bronchiectasis

S Wakefield, D Waite

    The American Review of Respiratory Disease
    |June 1, 1980
    PubMed
    Summary
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    Patients with bronchiectasis often have abnormal cilia lacking dynein arms, leading to impaired mucociliary transport. This suggests a genetic cause for the condition, potentially a mutation affecting ciliary structure and function.

    Area of Science:

    • Respiratory Medicine
    • Cell Biology
    • Genetics

    Background:

    • Bronchiectasis is a chronic respiratory condition characterized by permanent enlargement of the airways.
    • Ciliary dysfunction is implicated in the pathogenesis of various respiratory diseases.
    • Mucociliary transport is crucial for clearing mucus and pathogens from the airways.

    Purpose of the Study:

    • To investigate the ultrastructural abnormalities of cilia in patients with bronchiectasis.
    • To correlate ciliary structure with pulmonary mucociliary transport rates.
    • To explore the potential genetic basis of these ciliary defects in bronchiectasis.

    Main Methods:

    • Electron microscopy was used to examine bronchial and nasal ciliated epithelium from 13 bronchiectasis patients.

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  • Ciliary ultrastructure was analyzed for the presence of dynein arms and other structural anomalies.
  • Pulmonary mucociliary transport rates were assessed in the study participants.

    • Main Results:

    • All examined cilia lacked dynein arms, a key component for ciliary movement.
    • Additional ciliary abnormalities were observed, including missing, extra, or misplaced tubules, compound cilia, and vesiculated cilia.
    • Pulmonary mucociliary transport was absent or significantly reduced in all patients.

    Conclusions:

    • The absence of dynein arms and other ciliary defects are consistently found in bronchiectasis patients.
    • These structural abnormalities directly correlate with impaired mucociliary transport.
    • A genetic mutation or mutations are strongly suggested as the underlying cause of bronchiectasis and associated ciliary dysfunction.