Prostaglandin I2 enhances cough reflex sensitivity to capsaicin in the asthmatic airway

Yoshihisa Ishiura,Masaki Fujimura,Miki Abo,Shigeharu Myou,Kouichi Nobata,Yoshitaka Oribe

doi:10.1186/1745-9974-3-2

Yoshihisa Ishiura, Masaki Fujimura + Show 4 more

Open Access

https://doi.org/10.1186/1745-9974-3-2

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Journal: Cough	Publication Date: Jan 12, 2007
Citations: 37	License type: cc-by

Affiliation: Toyama City Hospital, Kanazawa University

Abstract

Inflammatory mediators are involved in the pathogenesis of airway inflammation, but the role of prostaglandin I2 (PGI2) remains obscure. This study was designed to investigate the role of PGI2 in cough reflex sensitivity of the asthmatic airway, which is characterized by chronic eosinophilic airway inflammation. The effect of beraprost, a chemically and biologically stable analogue of PGI2, on cough response to inhaled capsaicin was examined in 21 patients with stable asthma in a randomized, placebo-controlled cross over study. Capsaicin cough threshold, defined as the lowest concentration of capsaicin eliciting five or more coughs, was measured as an index of airway cough reflex sensitivity. The cough threshold was significantly (p < 0.05) decreased after two weeks of treatment with beraprost [17.8 (GSEM 1.20) μM] compared with placebo [30.3 (GSEM 1.21) μM]. PGI2 increases cough reflex sensitivity of the asthmatic airway, suggesting that inhibition of PGI2 may be a novel therapeutic option for patients with asthma, especially cough predominant asthma.

Highlights

Chronic cough is one of the commonest respiratory symptoms
The present study showed that two-week treatment with a stable prostaglandin I2 (PGI2) analogue, beraprost, decreased the cough threshold to inhaled capsaicin in asthmatic patients
No difference could be found in the baseline pulmonary function, IgE production or peripheral eosinophil count between beraprost and placebo treatments. These findings suggest that PGI2 enhances the cough reflex sensitivity in the asthmatic airway

Summary

Introduction

Cough has been considered to be a defense mechanism of the airway to remove irritant particles or excess mucus, whereas non-productive cough, which is not associated with the clearance of the tracheobronchial mucus, may occur via increased cough reflex sensitivity. Inflammatory mediators such as prostaglandins may adjust the cough reflex sensitivity. Others reported that alveolar macrophages are able to synthesize large amount of PGI2 [4] These findings indicate that PGI2 may play some role in the asthmatic airway and can affect airway cough reflex sensitivity. We investigated the effect of oral administration of beraprost, a chemically and biologically stable analog of PGI2

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Results

Conclusion