Dear Editor,

We read with interest the study by Park et al(1). 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 demonstrated that asthma and EB are immunopathologically similar, but that there are key differences namely mast cell localisation to the airway smooth muscle bundle(2) and increased IL-13 expression in asthma. Park et al(1) 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 area in the EB group study may not reflect distinct differences between this disease and asthma, but may simply reflect duration of disease.

The subjects with EB had participated in an earlier study(4) .In this study duration of disease was on average about 7 months and very few subjects had symptoms or evidence of inflammation for more than one year. It is not clear from the current study the duration of disease in the asthma group, but this is likely to be years in many cases. This point needs to be clarified as conclusions made about possible differences in remodelling between asthma and EB are undermined if the disease duration is markedly different.

In our experience some patients with EB and prolonged eosinophilic airway inflammation have a progressive decline in their lung function (5) suggesting that airway wall remodelling is a feature in some patients with this condition. Therefore whether airway remodelling and increased airway wall thickness are features shared by asthma and EB or specific to the asthma phenotype remains to be fully addressed.

References

1. Park SW, Park JS, Lee YM, Lee JH, Jang AS, Kim DJ et al. Differences in radiological/HRCT findings in eosinophilic bronchitis compared to asthma: implication for bronchial responsiveness. Thorax 2005.

2. Brightling CE, Bradding P, Symon FA, Holgate ST, Wardlaw AJ, Pavord ID. Mast-cell infiltration of airway smooth muscle in asthma. New England Journal of Medicine 2002;346(22):1699-705.

3. Niimi A, Matsumoto H, Takemura M, Ueda T, Chin K, Mishima M. Relationship of airway wall thickness to airway sensitivity and airway reactivity in asthma. American Journal of Respiratory and Critical Care Medicine 2003;168(8):983-8.

4. Park SW, Lee YM, Jang AS, Lee JH, Hwangbo Y, Kim dJ et al. Development of chronic airway obstruction in patients with eosinophilic bronchitis: a prospective follow-up study. Chest 2004;125(6):1998-2004.

5. Berry MA, Brightling CE, Hargadon B, McKenna S, Wardlaw AJ, Pavord ID. Observational study of the natural history of eosinophilic bronchitis. Thorax 2003;58:46.