Mucociliary Defense: Emerging Cellular, Molecular, and Animal Models
Mucociliary Defense: Emerging Cellular, Molecular, and Animal Models
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DOI：
10.1513/annalsats.201806-439aw
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发表时间：
2018-11-01
影响因子：
8.3
通讯作者：
Evans, Christopher M.
中科院分区：
文献类型：
--
作者：
Benam, Kambez H.;Vladar, Eszter K.;Evans, Christopher M.
呼吸组织每天受到数十亿颗粒的轰击。如果任其积聚，这些颗粒可能会导致受伤、炎症或感染，从而可能会严重扰乱气流和气体交换。粘液纤毛防御是保护宿主组织的主要机制，通过粘液和纤毛的协调功能发挥作用，捕获和消除吸入的物质。粘膜纤毛功能对于消除内源性细胞和碎片也是必需的。尽管防御必然是强大的，但它也受到严格调节，以尽量减少对宿主的生理破坏。事实上，粘液纤毛功能障碍导致许多肺部疾病的发病机制，包括哮喘、慢性阻塞性肺病、肺纤维化和囊性纤维化，其中会发生气流受限、炎症、持续性组织损伤和结构重塑。在这里，我们重点介绍纤毛和粘蛋白生物学的最新进展、良好控制的粘膜纤毛相互作用的重要性，以及更好地了解它们如何调节先天屏障和免疫防御的必要性。
Respiratory tissues are bombarded by billions of particles daily. If allowed to accumulate, these particles can cause injury, inflammation, or infection, and thus may significantly disrupt airflow and gas exchange. Mucociliary defense, a primary mechanism for protecting host tissues, operates through the coordinated functions of mucus and cilia that trap and eliminate inhaled materials. Mucociliary function is also required for the elimination of endogenous cells and debris. Although defense is necessarily robust, it is also tightly regulated to minimize physiologic disruption of the host. Indeed, mucociliary dysfunction contributes to the pathogenesis of many lung diseases-including asthma, chronic obstructive pulmonary disease, pulmonary fibrosis, and cystic fibrosis-in which airflow limitation, inflammation, persistent tissue injury, and structural remodeling occur. Here, we highlight recent advances in cilia and mucin biology, the importance of well-controlled mucociliary interactions, and the need to better understand how these regulate innate barrier and immune defense.