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Polystyrene nanoparticles affect ultrastructure and surfactant proteins production in A549 cells grown under air-liquid interface conditions.
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This study examined how polystyrene nanoparticles affect the ultrastructure and surfactant protein production of lung cells, addressing occupational and environmental inhalation exposure risks. Nanoparticles disrupted cellular architecture and altered production of pulmonary surfactants critical for lung function, indicating potential respiratory harm from inhaled nanoplastics.
Micro- and nanoplastics are released into the environment through the degradation of plastic objects or can be intentionally synthesised for a specific product. Humans can be exposed to MNPs through inhalation and studies have already proven that the particles can cause occupational diseases. Therefore, it is of utmost importance to test their effects on lung models. The aim of this study was to investigate the effects of model polystyrene nanoparticles (PS) on the integrity and functionality of the lung barrier in terms of viability, permeability/translocation, resistance, and surfactant production. After thoroughly characterizing our particles and performing cytotoxicity tests on A549 cells grown under standard submerged conditions, showing that PS can affect acidic organelle activity, we investigated their effects on cells grown under more realistic conditions by combining transwells with an air-liquid interface (ALI) setup. For comparison, we also tested their effects on cells grown in submerged settings. These experiments showed that PS did not affect epithelial permeability, electrical resistance and did not induce cytotoxicity or translocate towards the barrier. However, a dose-dependent decrease in surface tension was observed together with an increase in mitochondrial activity which suggests stress induction. Quantification of surfactant proteins (SPs) revealed that the extracellular surfactant pool remained mostly unchanged, while the intracellular one decreased in a dose-dependent manner in treated samples. Accordingly, using TEM, we found, especially in ALI samples, that the particles were entrapped in autophagic vacuoles together with lamellar bodies and presented a lower number of mitochondria-ER contacts, which are structures crucially involved in surfactant production. Taken together, these results may indicate that PS may cause dysregulation of SPs leading to lung dysfunction without affecting barrier permeability or cell viability. Acknowledgements: this project (PlasticsFatE) has received funding from the European Union's Horizon 2020 Research and Innovation programme, under the Grant Agreement number 965367 Also see: https://micro2024.sciencesconf.org/559339/document
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