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Steroid-unresponsive asthma.

Donald Y M Leung1, Joseph D Spahn, Stanley J Szefler

  • 1Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado 80262, USA. leungd@njc.org

Seminars in Respiratory and Critical Care Medicine
|August 10, 2005
PubMed
Summary
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A subset of asthma patients are resistant to corticosteroids, with two types identified: Type I (cytokine-induced, reversible receptor defect) and Type II (low receptor numbers). Understanding these differences is key for effective treatment.

Area of Science:

  • Pulmonology
  • Immunology
  • Pharmacology

Background:

  • Corticosteroids are standard treatment for chronic asthma.
  • A small percentage of asthma patients exhibit steroid resistance, showing persistent airway inflammation and obstruction.
  • Steroid-resistant asthma presents distinct challenges in patient management.

Purpose of the Study:

  • To differentiate between the two main types of steroid-resistant asthma.
  • To elucidate the underlying mechanisms of Type I and Type II steroid-resistant asthma.
  • To inform systematic approaches for managing steroid-resistant asthma.

Main Methods:

  • Classification of steroid-resistant asthma into Type I and Type II based on glucocorticoid receptor expression and function.
  • Investigation of cytokine involvement and interleukin (IL)-2 and IL-4 effects in Type I steroid-resistant asthma.

Related Experiment Videos

  • In vitro culture studies to assess reversibility of glucocorticoid receptor defects.

    • Main Results:

    • Type I steroid-resistant asthma is characterized by increased expression of the less active glucocorticoid receptor beta isoform, influenced by cytokines.
    • Type II steroid-resistant asthma is associated with reduced numbers of functional glucocorticoid receptors.
    • The glucocorticoid receptor defect in Type I SR asthma is reversible in culture and sustained by IL-2 and IL-4, unlike Type II.

    Conclusions:

    • Steroid-resistant asthma comprises at least two distinct subtypes with different molecular mechanisms.
    • Type I SR asthma's reversible glucocorticoid receptor defect offers potential therapeutic targets.
    • Effective management necessitates identifying the specific type of steroid resistance and considering alternative anti-inflammatory strategies.