Pathophysiology of airway mucosa

Abstract

The lungs and airways are mucosal surfaces, which are a common site encountering foreign protein, viruses, and microorganisms. Most of the mammalians have the common mucosal immune system, including airway epithelium, submucosal glands, and bronchus-associated lymphoid tissue, to protect against infection and airway inflammation. Bronchial asthma is one of diseases in the airways, which is characterized by airway obstruction, eosinophilic inflammation, and airway hyperresponsiveness (AHR). Recent studies demonstrated the involvement of T helper type 2 (Th2) cytokines, chemokines, and costimulatory molecules in IgE synthesis and airway eosinophilia; however, the mechanism of AHR is still obscure. Among the candidates, Th2 cytokines, eicosanoids, and transcriptional factors are thought to play an important role in the development of allergen-induced AHR. In addition, recent observations have shown structural changes, “airway remodeling”, which is characterized by epithelial thickening, goblet cells hyperplasia/hypertrophy, subepithelial fibrosis, and smooth muscle hyperplasia/hypertrophy. These structural changes may be involved in the inefficacy of the response to β2 agonists and AHR. It is a better strategy for control of the disease to inhibit or suppress multi-functional molecules rather than to inhibit a sole factor, because so many factors (genetical and environmental) are involved in the pathophysiology of the disease.