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Published on: August 7, 2017
Interleukin-5 messenger RNA expression in peripheral blood CD4+ cells in asthma
1Department of Medicine, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, N.T., Hong Kong.
Background:
IL-5 has been implicated in the pathogenesis of asthma through its regulatory role on eosinophil survival, proliferation, and effector function.
Objective:
The study was designed to investigate the relationships between IL-5 messenger RNA expression in circulating CD4+ cells and serum concentrations of eosinophil cationic protein (ECP), a marker of eosinophil activation, and disease activity in asthma.
Methods:
IL-5 gene expression was assessed semiquantitatively in ex vivo stimulated CD4+ cells by reverse transcription-polymerase chain reaction and serum ECP concentration measured from venous blood samples collected from patients with acute severe asthma before the commencement of systemic steroid therapy (day 1) and on day 7 and from patients with stable asthma and healthy volunteers.
Results:
IL-5 gene expression was significantly higher in patients with acute asthma before steroid treatment than in those with stable disease and healthy subjects (p < 0.0001). Similar results were obtained with serum ECP levels: levels in patients with acute asthma were highest (20.30 +/- 5.31 micrograms/L), followed by levels in patients with stable asthma (2.76 +/- 0.65 micrograms/L) and levels in normal control subjects (1.37 +/- 0.06 micrograms/L; p < 0.01 for all comparisons). Significant falls in both IL-5 expression and serum ECP level were seen on day 7 (p < 0.001) and coincided with a significant improvement in peak expiratory flow (p < 0.0001). Significant correlations were observed between IL-5 expression and ECP level (rho = 0.39, p < 0.01), IL-5 expression and peak expiratory flow (rho = -0.55, p < 0.0002), and peak expiratory flow and ECP level (rho = -0.32, p < 0.04).
Conclusion:
Our data therefore support an important regulatory role of IL-5 on eosinophil function in human asthma in vivo.
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