ABSTRACT
Airway remodeling encompasses a number of changes to the airway structure, found in asthma. This includes goblet cell hyperplasia, pseudothickening of the basement membrane due to subepithelial fibrosis, neovascularization, changes in the composition of the extracellular matrix, and smooth muscle hyperplasia and/or hypertrophy (1-7). What exactly causes these structural changes to occur is unclear. The amount of mediators present in asthmatic airway that can activate and induce or enhance proliferation of fibroblasts and smooth muscle cells is seemingly endless (8-11), ranging from mediators such as leukotrienes, or proinflammatory cytokines including TNFa and IL-lp, to a variety of growth factors. These can be divided in nonfibrogenic mediators, such as GM-CSF, and fibrogenic ones, including epidermal growth factor (EGF), insulin-like growth factor (IGF), and transforming growth factor p (TGF-p). The exact functional importance of each of these mediators in the pathogenesis of remodeling is unknown. This is a first area to which data derived from in vivo models can contribute valuable information.
