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BackgroundAllergic airway inflammation contributes to the airway remodelling that has been linked to increased obstruction and morbidity in asthma. However, the mechanisms by which allergens contribute to airway remodelling in humans are not fully established. CCL18, chitotriosidase (CHIT1) and YKL‐40 are readily detectable in the lungs and contribute to remodelling in other fibrotic diseases, but...