Mediators of Inflammation (Jan 2012)

Inflammatory Mediators in Induced Sputum and Airway Hyperresponsiveness in Cough Variant Asthma during Long-Term Inhaled Corticosteroid Treatment

  • Meixuan Liu,
  • Kaixiong Liu,
  • Ning Zhu,
  • Jingwen Xia,
  • Xiaodong Chen

DOI
https://doi.org/10.1155/2012/403868
Journal volume & issue
Vol. 2012

Abstract

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Objective. This study aimed to investigate improvements in inflammatory mediator levels in induced sputum and airway hyperresponsiveness (AHR) in cough variant asthma (CVA) during long-term inhaled corticosteroid (ICS) treatment. Patients and Methods. Patients with CVA (𝑁=35) and classic asthma (𝑁=26) and healthy subjects (𝑁=24) were recruited into this study. All patients were treated with budesonide (400 μg/day). Measurement of inflammatory mediators in induced sputum and PD20-FEV1 (the accumulated provocative dose resulting in a 20% decrease in FEV1) in histamine-challenged subjects was performed every three months after the start of medication. Interleukin- (IL-) 5 and IL-10 were assayed by ELISA, and the percentage of eosinophils was detected with Giemsa stain. Trends during the follow-up period were analyzed using a general linear model. Results. Inflammatory mediator levels in induced sputum and PD20-FEV1 in patients with CVA and classic asthma differed from those in the control group, although no differences were found in the two asthmatic groups. PD20-FEV1 significantly increased in CVA patients after ICS treatment for 3 months, while classic asthma patients exhibited a delayed change in AHR. After ICS treatment, levels of IL-5 and IL-10 as well as the percentage of eosinophils in the CVA group were altered at 3 months and 6 months, respectively. Accordingly, the level of inflammatory mediators in classic asthma changed more slowly. Conclusion. CVA has a greater improvement in airway inflammation and airway hyperresponsiveness (AHR) than classic asthma with respect to inhaled corticosteroid (ICS). Short-term ICS considerably reduces AHR although longer treatment is required for complete control of airway inflammation.