ABSTRACT
Airway wall remodeling in asthma is now recognized to be the product of long-standing bronchial inflammation. Inflammatory mediators and growth factors produced by this process have the capacity to cause cell infiltration, epithelial injury, collagen deposition, matrix restructuring, smooth muscle hypertrophy/hyperplasia, and increased bronchial vascularity. The bronchial vasculature may contribute to an increase in wall thickness and change in bronchial wall compliance through increased vessel caliber (vasodilatation), increased vessel numbers (angioneogenesis), and the formation of interstitial edema within the airway wall (microvascular leakage). Indirectly, vessels in crease airway wall thickness by acting as portals of entry for inflammatory cells, by local upregulation of adhesion glycoproteins. Major advances in the study of vascular function and revascularization after tissue injury, combined with recent observations concerning the immunology of the asthmatic airway,
have highlighted the importance of the vasculature in airway remodeling, now identifiable with specific stains (see Fig. 1).
