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Mucus in chronic airway diseases: sorting out the sticky details.

机译:慢性气道疾病中的粘液:整理粘性细节。

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摘要

Mucous hypersecretion is a major cause of airway obstruction in asthma, chronic obstructive pulmonary disease, and cystic fibrosis. EGFR ligands and IL-13 are known to stimulate mucous induction, but the detailed mechanisms of epithelial mucous regulation have not been well defined. In this issue of the JCI, Tyner et al. show, in a mouse model of chronic mucous hypersecretion, that ciliated epithelial cell apoptosis is inhibited by EGFR activation, allowing IL-13 to stimulate the differentiation of these cells into goblet cells, which secrete mucus. In defining this coordinated, 2-step process, we can consider the therapeutic effects of blocking mucous production. This begs the question, Is it possible to reduce airway obstruction in chronic lung disease by inhibiting EGFR activation and/or by inhibiting IL-13?
机译:黏液分泌过多是哮喘、慢性阻塞性肺疾病和囊性纤维化中气道阻塞的主要原因。已知 EGFR 配体和 IL-13 可刺激粘液诱导,但上皮粘液调节的详细机制尚未明确。在本期JCI中,Tyner等人在慢性粘液分泌过多的小鼠模型中表明,纤毛上皮细胞凋亡受到EGFR激活的抑制,使IL-13能够刺激这些细胞分化为杯状细胞,从而分泌粘液。在定义这个协调的两步过程时,我们可以考虑阻断粘液产生的治疗效果。这就引出了一个问题,是否有可能通过抑制EGFR激活和/或抑制IL-13来减少慢性肺病的气道阻塞?

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