Remodelling of the airways is a major feature of chronic persistent asthma,
resulting in epithelial goblet cell metaplasia, subepithelial and mucosal
fibrosis, smooth muscle hypertrophy and increased microvasculature, The epi
thelium is a major source of cytokines, chemokines and growth factors that
control remodelling in the adjacent myofibroblasts, microvasculature and ne
rves. Indeed, activation of the epithelial mesenchymal trophic unit is a fu
ndamental abnormality in chronic asthma. There are shortfalls in small anim
al models of relatively acute allergen-driven airway inflammatory responses
, since they do not identify effects on airway remodelling.