Research into the pathogenetic mechanisms and clinical monitoring of inflammatory diseases of any system is complete only if it involves the study of both the underlying pathological features and the physiological consequences that result from what are always complex inflammatory processes. Respiratory diseases, including those of the airways, are no exception in this respect. It is, therefore, not surprising that the development over the last 25 years of techniques enabling the study of inflammatory processes in the airways has revolutionised understanding of the commonest pulmonary diseases, asthma and chronic obstructive pulmonary disease (COPD). Airways inflammation is now an established feature and a central consideration of any treatment strategy for both of these conditions.
Most of the initial observations made in asthma, documenting the involvement of eosinophils, mast cells, T‐cells and more recently structural cells, fibroblasts, endothelial cells and epithelial cells, were made in studies using fibreoptic bronchoscopy in conjunction with bronchoalveolar lavage and bronchial biopsy. However, the relative invasiveness of this technique restricted the use of bronchoscopy to a research setting that was available in a limited number of specialised centres. This did not allow …