Airway fibrosis and angiogenesis due to eosinophil trafficking in chronic asthma.
Asthma is characterized by the presence of increased numbers of inflammatory cells in the airway in particular eosinophils and Th2 lymphocytes. In addition to the presence of inflammatory cells, the airways of patients with asthma exhibit varying levels of structural changes termed airway remodeling. These structural changes include subepithelial fibrosis, smooth muscle hypertrophy/hyperplasia, epithelial cell mucus metaplasia, and increased angiogenesis. This review focuses on the potential role of the eosinophil in promoting features of airway remodeling including fibrosis and neovascularization in chronic asthma. Eosinophils may potentially contribute to airway remodeling through release of eosinophil derived mediators such as TGFbeta which act directly upon target fibroblasts to promote fibrosis. In addition to the potential importance of the eosinophil to remodeling in asthma, eosinophilic esophagitis (EE) is another eosinophil associated disease that is associated with increased levels of esophageal eosinophils, increased levels of TGFbeta expression, and increased levels of fibrosis, suggesting that a similar mechanism of remodeling may contribute to both of these eosinophil associated diseases. However, remodeling in both asthma and EE is likely complex involving both eosinophil dependent and eosinophil independent pathways. Further studies in both humans and animal models will help to increase our knowledge of the contribution of the eosinophil to remodeling in asthma as well as EE.
Aceves
Seema S
SS
Department of Medicine, University of California San Diego, Biomedical Sciences Building, Room 5090, 9500 Gilman Drive, La Jolla, CA 92093-0635, USA.
Broide
David H
DH
D000818:Animals; D001249:Asthma / Q000378:metabolism*; D002908:Chronic Disease; D004804:Eosinophils / Q000502:physiology*; D006801:Humans; D008168:Lung / Q000098:blood supply*; D009389:Neovascularization, Pathologic / Q000209:etiology*; D011658:Pulmonary Fibrosis / Q000209:etiology*