The increasing use of metal oxide nanoparticles (MONPs) as TiO₂ NPs or ZnO NPs has led to environmental release and human exposure. The respiratory system, effects on lamellar bodies and surfactant protein A (SP-A) of pneumocytes, can be importantly affected. Exposure of human alveolar epithelial cells (A549) induced differential responses; a higher persistence of TiO₂ in cell surface and uptake (measured by Atomic Force Microscopy) and sustained inflammatory response (by means of TNF-α, IL-10, and IL-6 release) and ROS generation were observed, whereas ZnO showed a modest response and low numbers in cell surface. A reduction in SP-A levels at 24 h of exposure to TiO₂ NPs (concentration-dependent) or ZnO NPs (the higher concentration) was also observed, reversed by blocking the inflammatory response (by the inhibition of IL-6). Loss of SP-A represents a relevant target of MONPs-induced inflammatory response that could contribute to cellular damage and loss of lung function.

越来越多地使用金属氧化物纳米粒子 (MONPs) 作为 TiO ₂ NPs 或 ZnO NPs 导致环境释放和人类暴露。呼吸系统、对肺细胞的层状体和表面活性蛋白 A (SP-A) 的影响可能会受到重要影响。暴露于人肺泡上皮细胞 (A549) 诱导差异反应；观察到 TiO ₂在细胞表面的持久性和吸收（通过原子力显微镜测量）和持续的炎症反应（通过 TNF-α、IL-10 和 IL-6 释放）和 ROS 生成，而 ZnO 显示出适度的反应和细胞表面的低数量。暴露于 TiO ₂ 24 小时时 SP-A 水平降低还观察到 NPs（浓度依赖性）或 ZnO NPs（较高浓度），通过阻断炎症反应（通过抑制 IL-6）来逆转。SP-A 的缺失代表 MONPs 诱导的炎症反应的相关靶点，可能导致细胞损伤和肺功能丧失。