Lung Cell Biology, National Heart and Lung Institute, Imperial College London, UK.
Nanotoxicology. 2012 Feb;6(1):94-108. doi: 10.3109/17435390.2011.558643. Epub 2011 Feb 28.
The respiratory epithelium is a significant target of inhaled, nano-sized particles, the biological reactivity of which will depend on its physicochemical properties. Surface-modified, 50 and 100 nm, polystyrene latex nanoparticles (NPs) were used as model particles to examine the effect of particle size and surface chemistry on transformed human alveolar epithelial type 1-like cells (TT1). Live images of TT1 exposed to amine-modified NPs taken by hopping probe ion conductance microscopy revealed severe damage and holes on cell membranes that were not observed with other types of NPs. This paralleled induction of cell detachment, cytotoxicity and apoptotic (caspase-3/7 and caspase-9) cell death, and increased release of CXCL8 (IL-8). In contrast, unmodified, carboxyl-modified 50 nm NPs and the 100 nm NPs did not cause membrane damage, and were less reactive. Thus, the susceptibility and membrane damage to respiratory epithelium following inhalation of NPs will depend on both surface chemistry (e.g., cationic) and nano-size.
呼吸道上皮细胞是吸入的纳米级颗粒的重要靶标，其生物反应性将取决于其物理化学性质。本文使用表面改性的 50nm 和 100nm 聚苯乙烯乳胶纳米颗粒（NPs）作为模型颗粒，研究了粒径和表面化学性质对转化的人肺泡上皮 1 型样细胞（TT1）的影响。 hopping 探针离子电导显微镜拍摄的暴露于胺改性 NPs 的 TT1 的实时图像显示，细胞膜上出现了严重的损伤和孔，而其他类型的 NPs 则没有观察到这种情况。这与细胞脱离、细胞毒性和凋亡（caspase-3/7 和 caspase-9）细胞死亡的诱导以及 CXCL8（IL-8）的释放增加相平行。相比之下，未改性、羧基改性的 50nm NPs 和 100nm NPs 不会引起细胞膜损伤，反应性也较低。因此，吸入 NPs 后呼吸道上皮细胞的易感性和膜损伤将取决于表面化学性质（例如阳离子）和纳米尺寸。
