We read with interest the study by Park et al¹ published recently in Thorax. We agree that non-asthmatic eosinophilic bronchitis (EB), a condition characterised by eosinophilic inflammation without evidence of variable airflow obstruction, is a powerful disease control group to study the mechanisms involved in the development of airway hyperresponsiveness in asthma. Previous comparative studies have shown that asthma and EB are immunopathologically similar but that there are key differences—namely, mast cell localisation to the airway smooth muscle bundle² and increased IL-13 expression in asthma. Park et al¹ have proposed in their recent study that this list needs to be extended to include increased airway wall area as a feature confined to asthma. This is an important observation as other HRCT studies in asthma have suggested that increased airway wall area may, in fact, protect against airway hyperresponsiveness.³ However, the observed absence of increased airway wall …