摘要
Bronchial asthma is characterized by chronic recruitment of eosinophils in the airways. It has been reported that bronchial eosinophil recruitment and activation may even occur in mild-moderate stable asthma and that bronchial epithelium damage and airway responsiveness may be partially associated with the eosinophilic inflammatory reaction.1 There is increasing evidence that the eosinophil-rich bronchial inflammation characteristic of asthma is orchestrated, at least partly,
Bronchial asthma is characterized by chronic recruitment of eosinophils in the airways. It has been reported that bronchial eosinophil recruitment and activation may even occur in mild-moderate stable asthma and that bronchial epithelium damage and airway responsiveness may be partially associated with the eosinophilic inflammatory reaction.1 There is increasing evidence that the eosinophil-rich bronchial inflammation characteristic of asthma is orchestrated, at least partly,
