Chronic obstructive pulmonary disease (COPD) is a highly prevalent chronic lung disease that is expected to become the third most common cause of death globally by 2030.1 It is characterised by extensive, detrimental structural and functional changes termed ‘remodelling’ in the airway epithelium in response to noxious inhaled contaminants. Cigarette smoke is traditionally considered the chief culprit, but environmental pollutants are now recognised as a critically important, if not as the major inhaled threat.2 The airway epithelium is a patchwork of luminal multiciliated and secretory cells and an underlying population of basal stem cells. Remodelling is evidenced by the expansion of secretory cells at the expense of multiciliated cells, which disrupts mucociliary clearance, a vital respiratory host defence mechanism.3 4 The resulting vicious cycles of infection, inflammation and injury fuel further remodelling phenotypes including diminished epithelial barrier and regenerative capacity. Basal stem cell depletion and dysfunction are thought to be critical underlying drivers of remodelling.5–8 However, detailed molecular mechanisms are lacking, and how remodelling changes during COPD progression, and whether it can be reversed remain key gaps in knowledge. In this issue of the journal, Stoleriu and colleagues use primary cultured human bronchial epithelial cells (pHBECs) to investigate remodelling by aerosolised zinc oxide nanoparticles as a model of environmental pollutants implicated in COPD pathogenesis. Consistent …

中文翻译：

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严重慢性阻塞性肺病的广泛气道重塑赋予了对环境压力源的弹性

慢性阻塞性肺疾病 (COPD) 是一种非常普遍的慢性肺部疾病，预计到 2030 年将成为全球第三大常见死亡原因。1 其特点是气道上皮发生广泛、有害的结构和功能变化，称为“重塑”。有毒的吸入污染物。传统上，香烟烟雾被认为是罪魁祸首，但现在环境污染物即使不是主要的吸入威胁，也被认为是一个至关重要的因素。2气道上皮是管腔多纤毛和分泌细胞以及基础干细胞群的拼凑而成。重塑的证据是分泌细胞的扩张以多纤毛细胞为代价，这破坏了粘膜纤毛清除，这是一种重要的呼吸道宿主防御机制。 3 4 由此产生的感染、炎症和损伤的恶性循环进一步加剧了表型的重塑，包括上皮屏障的减弱和再生容量。基底干细胞耗竭和功能障碍被认为是重塑的关键潜在驱动因素。5-8 然而，缺乏详细的分子机制，并且重塑在 COPD 进展过程中如何变化以及是否可以逆转仍然是关键的知识空白。在本期杂志中，Stoleriu 及其同事使用原代培养的人支气管上皮细胞 (pHBEC) 来研究雾化氧化锌纳米粒子的重塑，作为与慢性阻塞性肺病发病机制有关的环境污染物模型。持续的 …