Mechanisms of heightened airway cough receptor sensitivity in eosinophilic bronchitis (atopic cough : eosinophilic bronchitis without asthma).

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1.Clinical study on chronic nonproductive cough(1) A new clinical entity named as "ATOPIC COUGH" has been proposed, which is different from cough variant asthma.(2) Bronchodilator therapy is ineffective, bronchial responsiveness to methacholine is within normal range, and airway cough receptor sensitivity to inhaled capsaicin is heightened in atopic cough.(3) The histologic feature is considered to be large airway eosinophilic inflammation according to the following findings : no eosinophils in bronchoalveolar lavage fluid or bronchial lavage fluid, small number of eosinophils in biopsied bronchial specimens, and almost same number of eosinophils in hypertonic saline-induced sputum as bronchial asthma.(4) Histamine Hl-antagonists and steroids are effective for the treatment of atopic cough.2.Animal experiment on eosinophilic bronchitis(1) Eosinophilic bronchitis model of guinea pigs was successfully developed by intranasal administration of polymycin B twice a week for 3 weeks.(2) Airway cough receptor sensitivity to inhaled capsaicin was heightened but bronchial responsiveness to inhaled histamine was not increased in this model.(3) A neuropeptide inhibitor (FK-224) and a thromboxane receptor antagonist (S-1452) but not a beta2-agonist (procaterol) significantly reduced the heightened airway cough receptor sensitivity.(4) A histamine Hl-antagonist (azelastin) significantly suppressed the heightened airway cough receptor sensitivity.3.ConclusionFrom these results, it is suggested that there are at least 2 different mechanisms for the pathophysiology of persistent nonproductive cough (pathological cough) : heightened airway cough receptor sensitivity induced by eosinophilic inflammation of the large airway in atopic cough and bronchoconstriction based on bronchial hyperresponsiveness induced by eosinophilic inflammation of the central to peripheral airways in cough variant asthma.