Abstract
The rising trends in asthma over the past 30 years are likely to be a consequence of changes in the environment acting on a susceptible genotype. Recognising that environmental agents impact on the bronchial epithelium, this structure is in a key position to translate and coordinate these gene-environment interactions. In asthma, the bronchial epithelium is stressed and damaged, with shedding of the columnar cells into the airway lumen. The aim of this review is to consider recent advances in our understanding of why the epithelium is damaged and how the ensuing repair responses orchestrate airway inflammation and remodelling leading to the development and maintenance of the asthmatic state.

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