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Inhalable Textile Microplastic Fibers Impair Airway Epithelial Differentiation.
American Journal of Respiratory and Critical Care Medicine ( IF 24.7 ) Pub Date : 2023-11-16 , DOI: 10.1164/rccm.202211-2099oc
Shanshan Song 1, 2 , Fransien van Dijk 1, 2 , Gwenda F Vasse 1, 2 , Qiongliang Liu 3 , Irene F Gosselink 4 , Ellen Weltjens 4 , Alex H V Remels 4 , Marina H de Jager 1 , Sophie Bos 1 , Chenxi Li 3 , Tobias Stoeger 3 , Markus Rehberg 3 , David Kutschke 3 , Gail W A van Eck 1 , Xinhui Wu 1, 2 , Suzanne H Willems 1 , Devin H A Boom 5 , Ingeborg M Kooter 4, 5 , Diana Spierings 6 , René Wardenaar 6 , Matthew Cole 7 , Martijn C Nawijn 2, 8 , Anna Salvati 9 , Reinoud Gosens 1, 2 , Barbro N Melgert 1, 2
Affiliation  

RATIONALE Microplastics are a pressing global concern and inhalation of microplastic fibers has been associated with interstitial and bronchial inflammation in flock workers. However, how microplastic fibers affect the lungs is unknown. OBJECTIVES Our aim was to assess the effects of 12x31 µm nylon 6,6 (nylon) and 15x52 µm polyethylene terephthalate (polyester) textile microplastic fibers on lung epithelial growth and differentiation. METHODS We used human and murine alveolar and airway-type organoids as well as air-liquid interface cultures derived from primary lung epithelial progenitor cells and incubated these with either nylon or polyester fibers or nylon leachate. In addition, mice received one dose of nylon fibers or nylon leachate and 7 days later organoid-forming capacity of isolated epithelial cells was investigated. MEASUREMENTS AND MAIN RESULTS We observed that nylon microfibers, more than polyester, inhibited developing airway organoids and not established ones. This effect was mediated by components leaching from nylon. Epithelial cells isolated from mice exposed to nylon fibers or leachate, also formed fewer airway organoids, suggesting long-lasting effects of nylon components on epithelial cells. Part of these effects were recapitulated in human air-liquid interface cultures. Transcriptome analysis revealed upregulation of Hoxa5 post-exposure to nylon fibers. Inhibiting Hoxa5 during nylon exposure restored airway organoid formation, confirming Hoxa5's pivotal role in the effects of nylon. CONCLUSIONS These results suggest that components leaching from nylon 6,6 may especially harm developing airways and/or airways undergoing repair and we strongly encourage to characterize both hazard of and exposure to microplastic fibers in more detail.

中文翻译:

可吸入纺织微塑料纤维会损害气道上皮分化。

基本原理 微塑料是全球紧迫的问题,吸入微塑料纤维与羊群工人的间质和支气管炎症有关。然而,微塑料纤维如何影响肺部尚不清楚。目的 我们的目的是评估 12x31 µm 尼龙 6,6(尼龙)和 15x52 µm 聚对苯二甲酸乙二醇酯(聚酯)纺织微塑料纤维对肺上皮生长和分化的影响。方法我们使用人和鼠的肺泡和气道类器官以及源自原代肺上皮祖细胞的气液界面培养物,并将它们与尼龙或聚酯纤维或尼龙浸出液一起孵育。此外,小鼠接受一剂尼龙纤维或尼龙浸出液,7天后研究了分离的上皮细胞的类器官形成能力。测量和主要结果 我们观察到,尼龙微纤维比聚酯更能抑制气道类器官的发育,而不是已形成的气道类器官。这种效应是由尼龙中浸出的成分介导的。从暴露于尼龙纤维或渗滤液的小鼠中分离出的上皮细胞也形成了较少的气道类器官,这表明尼龙成分对上皮细胞具有持久的影响。这些效应的一部分在人体气液界面培养物中得到了再现。转录组分析显示接触尼龙纤维后 Hoxa5 上调。在尼龙暴露期间抑制 Hoxa5 可恢复气道类器官的形成,证实了 Hoxa5 在尼龙作用中的关键作用。结论 这些结果表明,从尼龙 6,6 中浸出的成分可能特别损害正在发育的气道和/或正在修复的气道,我们强烈鼓励更详细地描述微塑料纤维的危害和暴露情况。
更新日期:2023-11-16
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