Abstract
Airway epithelial cells are the front-line barrier to outer world, and abnormal response to environmental agents can cause asthma. Large numbers of recent studies support the evidence that airway epithelial cells play a crucial role in the development of airway inflammation and remodeling. Defective barrier function of airway epithelium facilitates allergic sensitization and initiation of allergic inflammation. Airway epithelial cells contribute to the development of type 2 immune response by secreting key cytokines, such as interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin and the interactions between various innate immune cells, including innate lymphoid cells, granulocytes, and macrophages. Furthermore, airway remodeling can be induced by epithelial cell-derived mediators even independently of airway inflammation. Aberrant repair of airway injury or distinct biophysical/biochemical characteristics of airway epithelial cells in asthmatics may be involved in the pathophysiologic mechanism of airway remodeling. Therapeutic approaches targeting airway epithelial cells are warranted.
References
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