Bronchial epithelium as a key regulator of airway allergen sensitization and remodeling in asthma.

摘要: Asthma is a chronic inflammatory disorder of the airways manifesting as intermittent airflow limitation, which over time may become progressive (1). Both in allergic and nonallergic forms disease there evidence an altered local T cell response favor Th2 cytokine release resulting B isotype switching to IgE; mast cell, eosinophil, basophil recruitment; activation wide range mediators (2). However, it has clear that, by itself, inflammation not able explain many features characteristic asthma that restructuring airway wall also required (3). This “remodeling” presumably accounts for incomplete therapeutic efficacy corticosteroids, with persistence bronchial hyperresponsiveness (BHR), decline pulmonary function occurs those asthmatic individuals more severe Although atopy, propensity generate allergen-specific IgE, one strongest risk factors asthma, especially children young adults, only 10% atopics develop and, absence most notably disease. It seems plausible rather than IgE-mediated being initiator disordered function, epithelium itself abnormal this predisposes individual toward allergen sensitization, injurious effects respiratory viruses air pollutants (including tobacco smoke). A could provide basis remodeling asthma.