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Asthma affects about 330 million individuals worldwide while 10% of asthmatic patients develop the severe type. The two main phenotypes of severe asthma are allergic and non-allergic. Notably, remodeling and mucus overexpression are hallmarks of severe asthma upon dysregulation of MUC5AC and MUC5B. In severe allergic asthma due to the initiation of the allergic cascade, immune cells are recruited and a large number of inflammatory mediators will be produced leading to the overexpression of MUC5AC and MUC5B in the airways. Moreover, the production of mediators including tumor necrosis factor α (TNF-α) and interleukin 13 (IL-13) will cause airways’ muscle proliferation. Both overproductions of mucin and muscle proliferation will lead to remodeling progression. On the other hand, in severe non-allergic asthma, fewer immune cells are involved but still, the expression of MUC5AC is enhanced. However, MUC5B might increase less than the amount of its expression in allergic phenotype due to the lower number of involved immune cells and mediators. In the non-allergic phenotype mediators such as interleukin 17 (IL-17) and transforming growth factor β (TGF-β) are responsible for muscle proliferation. The result of mucus overexpression and muscle proliferation is remodeling progression in the non-allergic severe asthma. Therefore, we hypothesize that MUC5AC and MUC5B overexpression in severe allergic asthma is greater than in severe non-allergic asthma. Hence, remodeling progression is more intensive in severe allergic asthma. In conclusion, given the central roles of MUC5AC and MUC5B in mediating the asthma …