Airway Remodelling. The term remodelling describes the structural changes seen in the airways of patients with respiratory disease. The structural changes in the airway include angiogenesis (Xxxxx et al. 1999), deposition of fibrous and other extracellular matrix (ECM) proteins, elevated smooth muscle mass and proliferation, myofibroblast differentiation and proliferation, goblet cell hyperplasia and neovascularisation, subepithelial fibrosis, smooth muscle hypertrophy (Okayama, Xx, & Xxxxx 2007) (Figure 1.1). Ongoing inflammation, airway injury, and healing are also part of the remodelling process in asthma (Xxxxx et al. 2007). The changes of remodelling also include thickening of the reticular sub- basement membrane (rbm), a significant feature of established asthmatic remodelling, increased numbers of submucosal glands and increased airway wall collagen (Xxxx 2008). Thickening of the epithelial rbm has been reported in both adults and school-aged children. However, it is not known at what age rbm thickening begins (Xxxxxxx et al. 2006). Nevertheless the extent of airway remodelling correlates with severity of asthma, at least in cross-sectional studies. Airway remodelling is often considered to contribute to the element of irreversible airflow obstruction, which is a feature of some patients with asthma (Xxxxxxx et al. 2006). It has been suggested that reversibility in asthma is associated with mild disease but with disease progression, varying degrees of remodelling of the airways might lead to irreversibility (Xxxx et al. 2005). Overall, it can be seen that airway remodelling indicates changes in the composition, quantity as well as organisation of both the cellular and molecular components of the airway wall; alterations considered secondary to chronic injury and repair of the airway epithelial-mesenchymal trophic (EMT) unit (Xxxxx et al. 1999). Nevertheless much of the literature on airway remodelling is speculative in the sense that any observed histological change are not proven to correlate with changes in physiology and do not correlate with clinical phenotype (Bai & Knight 2005). Many mediators derived from various inflammatory cells (including mast cells, eosinophils, neutrophils and others) are implicated in the pathogenesis of airway remodelling, and consequently in the process of asthma. These mediators could be working in an autocrine or paracrine fashion. Although the mode of mechanism or signalling has not been investigated here, it is believed that the var...
