Relationship between IL-4 and IL-5 mRNA expression and disease severity in atopic asthma
American journal of respiratory and critical care medicine, 1997•atsjournals.org
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 …
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 …
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 β -actin mRNA correlates with validated indicators of disease severity. IL-4 and IL-5 mRNA copies relative to β -actin mRNA were detected in bronchial biopsies from atopic asthmatics. The numbers of IL-5 mRNA copies relative to β -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 β -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.
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