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Related Experiment Videos

Epithelium-derived inhibitory factor in human bronchus.

L B Fernandes1, J M Preuss, J W Paterson

  • 1Department of Pharmacology, University of Western Australia, Perth.

European Journal of Pharmacology
|October 23, 1990
PubMed
Summary

Removing the bronchial epithelium increased airway sensitivity to histamine and methacholine in non-diseased lungs, but not in asthmatic lungs. This suggests asthma may damage the epithelium, reducing an inhibitory factor that normally protects airways.

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Area of Science:

  • Pulmonary Medicine
  • Respiratory Physiology
  • Pharmacology

Background:

  • The human bronchial epithelium plays a role in regulating airway smooth muscle tone.
  • Epithelium-derived inhibitory factors (EpDIF) may influence bronchial reactivity.
  • Epithelial damage in asthma could alter the release of these factors.

Purpose of the Study:

  • To investigate the role of the bronchial epithelium in modulating airway sensitivity to spasmogens.
  • To determine if epithelium removal affects bronchial reactivity differently in non-diseased versus asthmatic human lungs.
  • To characterize an epithelium-derived inhibitory factor (EpDIF) using a bioassay system.

Main Methods:

  • Isolated human bronchi (non-diseased and asthmatic) were used to assess changes in sensitivity to histamine and methacholine after epithelial removal.

Related Experiment Videos

  • A co-axial bioassay with endothelium-denuded rat aorta was employed to detect vasorelaxant EpDIF released from human bronchial tissue.
  • Phenylephrine-induced contraction was used as a baseline to measure the effects of EpDIF.

    • Main Results:

    • Epithelium removal increased the potency of histamine and methacholine 2- and 5-fold, respectively, in non-diseased bronchi.
    • No significant increase in spasmogen potency was observed in asthmatic bronchi after epithelium removal.
    • The bioassay confirmed the release of a vasorelaxant EpDIF from bronchial tissue, which was abolished by epithelium removal.

    Conclusions:

    • The bronchial epithelium normally releases an inhibitory factor (EpDIF) that modulates airway smooth muscle responsiveness.
    • Disease-induced epithelial damage in asthma may impair EpDIF release, potentially contributing to increased bronchial hyperresponsiveness.
    • Human airway smooth muscle may be sensitive to this EpDIF, and its absence can lead to increased sensitivity to spasmogens.