Abstract
In asthma, bronchial mucosal tissues are chronically infiltrated by activated inflammatory cells (mainly lymphocytes and eosinophils) that have the capacity to produce a wide range of cytokines (IL-4, IL-5) and mediators (leucotrienes, prostaglandins, etc.). These molecules may significantly change the functional and phenotypic behavior of resident cells (epithelial cells, fibroblasts, smooth muscle cells, etc.) In addition to their role in tissue repair, resident cells are an important source of cytokines. They play an active role in modulating the immune response, suggesting that they may be involved in the maintenance and chronicity of the inflammatory response. These cells are also involved in structural changes observed in asthma, such as subepithelial fibrosis [3]. The alteration in the structure of the bronchial tree appears to be one of the factors involved in the persistence of bronchial hyperreactivity [4]. This review will focus on the role of structural cells on airway remodeling and their response to asthma medication.
Keywords: Asthma, airway remodeling, epithelium repair, fibroblasts, asthma medication
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