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Inflammation and asthma.

J A Nadel

    The Journal of Allergy and Clinical Immunology
    |May 1, 1984
    PubMed
    Summary
    This summary is machine-generated.

    Asthma involves airway hyperresponsiveness triggered by stimuli. Cell-to-cell interactions and inflammation, involving epithelial cells and neutrophils, are key in experimental and clinical asthma.

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    Area of Science:

    • Pulmonary Medicine
    • Immunology
    • Cell Biology

    Background:

    • Asthma is characterized by extreme airway sensitivity to various stimuli.
    • Experimental models demonstrate that inflammatory damage can induce airway hyperresponsiveness.
    • Cell-to-cell interactions are implicated in both experimental and potentially clinical asthma.

    Purpose of the Study:

    • To investigate the role of cell-to-cell interactions in experimental airway hyperreactivity.
    • To explore the inflammatory cascades involved in asthma.
    • To understand the mechanisms of exercise-induced bronchospasm.

    Main Methods:

    • Induction of airway hyperresponsiveness in experimental models.
    • Analysis of inflammatory cell involvement, including epithelial cells and neutrophils.

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  • Examination of stimuli like cooling, osmolality changes, and environmental irritants (ozone).

    • Main Results:

    • Cell-to-cell interactions were found to be important in experimental airway hyperreactivity.
    • Epithelial cells and neutrophils were identified as significant contributors to inflammation.
    • Mechanisms for exercise-induced bronchospasm involving mediator release and smooth muscle contraction were proposed.

    Conclusions:

    • Inflammatory cascades and cell-to-cell interactions play a crucial role in asthma pathogenesis.
    • Multiple inflammatory mechanisms, including sensory nerve involvement and other immune cells, may contribute to asthma.
    • Environmental factors can exacerbate asthma symptoms through inflammation.