Relationship between IL-4 and IL-5 mRNA expression and disease severity in atopic asthma

Am J Respir Crit Care Med. 1997 Sep;156(3 Pt 1):704-8. doi: 10.1164/ajrccm.156.3.9610033.


Atopic asthma is characterized by chronic inflammation of the bronchial mucosa in which eosinophil- and immunoglobulin E (IgE)-dependent mechanisms are believed to be prominent. Therefore, specific proeosinophilic mediators such as interleukin (IL)-5 and essential cofactors for IgE switching in B-lymphocytes such as IL-4 could play a pivotal role in asthma. However, the exact role that individual inflammatory mediators play in the development of the disease in humans is still unknown. Using semiquantitative reverse transcriptase-polymerase chain reaction amplification in bronchial biopsies from 10 atopic asthmatics, we have tested the hypothesis that IL-4 and IL-5 mRNA expression relative to beta-actin mRNA correlates with validated indicators of disease severity. IL-4 and IL-5 mRNA copies relative to beta-actin mRNA were detected in bronchial biopsies from atopic asthmatics. The numbers of IL-5 mRNA copies relative to beta-actin mRNA correlated with disease severity assessed by the Aas asthma score (r = 0.70, p = 0.01), baseline FEV1 (r = -0.94, p = 0.001), baseline peak expiratory flow rate (r = -0.77, p = 0.01), peak expiratory flow rate variability over 2 wk (r = 0.69, p = 0.028), and the histamine PC20 (r = -0.72, p = 0.018). Conversely, the numbers of IL-4 mRNA copies relative to beta-actin mRNA did not correlate with asthma severity, but they positively correlated with total serum IgE concentrations (r = -0.90, p = 0.001). Our present results support the concept that IL-5 may determine asthma clinical expression and severity, and by inference they support the development of IL-5 targeted therapies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Asthma / immunology*
  • Asthma / pathology*
  • Biopsy
  • Bronchi / chemistry*
  • Case-Control Studies
  • Forced Expiratory Volume
  • Gene Expression / immunology*
  • Humans
  • Hypersensitivity, Immediate / complications*
  • Immunoglobulin E / immunology
  • Interleukin-4 / analysis*
  • Interleukin-5 / analysis*
  • Mucous Membrane
  • Peak Expiratory Flow Rate
  • Polymerase Chain Reaction
  • RNA, Messenger / analysis*
  • Reproducibility of Results
  • Severity of Illness Index*


  • Interleukin-5
  • RNA, Messenger
  • Interleukin-4
  • Immunoglobulin E