Background: Little is known about airway inflammation in childhood asthma. The aims of this study were to analyze the expression of a wide range of mediators of airway inflammation in childhood asthma.
Methods: Eight asthmatic children with acute exacerbations were recruited for the study. Peripheral blood was drawn from the patients at the time of exacerbation and after improvement. Total RNA was extracted from the isolated T lymphocytes. The differential display (DD) RT-PCR method was used to detect expressed genes, and the quantification of candidate gene expression was performed using real-time quantitative RT-PCR.
Results: The only gene for which significant expression differences were detected in both DD analysis and quantitative RT-PCR was lipocortin II (annexin II) (exacerbation > remission, p < 0.05). In quantitative RT-PCR of interleukin-4 (IL-4), IL-5, interferon-gamma, IL-12 receptor-beta and integrin alpha6, a significant difference was found only in the expression of IL-4 mRNA (exacerbation > remission, p < 0.05). The IL-4 plasma concentration tended to be higher in exacerbation than in remission.
Conclusions: Our findings suggest activation of T cells and IL-4 production may be involved not only in the basic pathogenesis of childhood asthma but also in its acute exacerbation, and that lipocortin II may be a marker or contribute to asthma exacerbation.
Copyright 2004 S. Karger AG, Basel