Airway inflammation is a hallmark of asthma. The inflammatory infiltrate comprises eosinophils, activated lymphocytes, activated macrophages and partly degranulated mast cells and basophils. Several studies have shown an association between the numbers of eosinophils and activated lymphocytes in the airways and clinical indices of disease severity. Eosinophils are thought to be important effector cells involved in bronchial mucosal damage by the release of cationic proteins, reactive oxygen species and proinflammatory and profibrotic cytokines. Much emphasis has been placed on CD4+ T cells as these cells orchestrate the events leading to the development of allergic airway responses mainly through the production of Th2-type cytokines that promote the eosinophil-rich infiltrate characterising asthma. Abundant evidence also points to a proinflammatory role for structural cells, including epithelial and endothelial cells, airway smooth muscle cells and fibroblasts. This review will discuss the potential contribution of structural cells to the inflammatory events in asthma specifically focusing on their ability to produce cytokines and chemokines involved in the recruitment and the activation of inflammatory cells in the airways.
