Induction of human airway epithelial to mesenchymal transition upon rhinovirus infection

Background Structural changes of the airway, collectively referred to as airway remodeling are believed to be the underlying cause of the airway hyperresponsiveness that is characteristic of asthma. Airway remodeling is characterized by thickening of the subepithelial membrane, goblet cell hyperplasia, angiogenesis, increased smooth muscle mass, and epithelial fragility. Thickening of the subepithelial membrane, due to increased deposition of matrix proteins by fibroblasts/myofibroblasts, has been observed in children even prior to the formal diagnosis of asthma. Recent data have shown that young children who experience episodes of human rhinovirus (HRV)-induced wheezing in early childhood are at increased risk of subsequently developing asthma. The primary site of infection of HRV is the airway epithelium. Recent evidence suggests that the molecular reprogramming of epithelial cells through a process called epithelial to mesenchymal transition (EMT) may contribute to increases in fibroblast/myofibroblast in the asthmatic airway. Therefore, we hypothesize that HRV infection plays a role in early airway remodeling by triggering EMT to produce fibroblasts/myofibroblasts that cause thickening of the subepithelial membrane by depositing matrix proteins.