Airway epithelial dysfunction contributes to the pathogenesis of asthma

growth factor (VEGF), angiopoietin, and angiogenin in the airways, which promote neovascularization, expansion of the airway vascular bed, oedema, and airway narrowing. 19 These changes are inevitably associated with thickening and shedding of the airway epithelium in both atopic and non-atopic asthmatic patients. 20,21 Additionally, there is goblet cell, and submucous gland hyperplasia resulting in mucus hypersecretion. 22 This is accompanied by hyperplasia and hypertrophy of ASM cells, which acquire a highly proliferative, secretory, and contractile phenotype. 15,18,22 These structural changes are associated with more severe fixed airflow obstruction, which may be unresponsive to high dose inhaled corticosteroids (ICS), and to