The chronic inflammation experienced by asthmatics leads to irreversible airway remodeling. Airway remodeling is characterized by increased mucus secretion, epithelial damage, basement membrane fibrosis, fibroblast and smooth muscle cell hypertrophy, and hyperplasia. However, the most commonly described attribute of asthmatic airways is eosinophilia.
Eosinophils expressing the CCR3 chemokine receptor are drawn from pulmonary circulation primarily by Eotaxin/CCL11, which is overexpressed in asthmatic respiratory membrane epithelial cells, fibroblasts, and smooth muscle cells. It is known that eosinophils infiltrate the respiratory membranes of asthmatics and contribute significantly to the inflammatory component of asthma. Furthermore, several lines of evidence suggest an association between eosinophils and fibrosis. For example, eosinophils release cytotoxic mediators, pro-inflammatory cytokines, and TGF-beta, which has well-known fibrotic effects. Since eosinophils are rarely observed in healthy airways and the number of eosinophils present in asthmatic airways correlates with increasing disease severity.