The effect of microplastics on the nasal epithelial cells in obstructive lung diseases

The goal of this study was to evaluate the biological effect of microplastic fibres on nasal epithelium from healthy subjects, as well as asthma and COPD pateients. We demonstrated the distinct biological response of asthmatic and COPD epithelial cells to microplastic fibers stimulation compared to healthy epithelial cells. ANKRD36, BCL2L15, C15orf48, CAPN14, FCGBP, FST, IL-19, MAFF, PGBD5, PKP1 and PTPRH are important markers of epithelial response after microplastic stimulation in obstructive lung disaeses. These mediators are linked to Th2 inflammation, alleviation of stress response, and, most notably, carcinogenesis. We demonstrated the distinct biological response of asthmatic and COPD epithelial cells to microplastic fibers stimulation compared to healthy epithelial cells. ANKRD36, BCL2L15, C15orf48, CAPN14, FCGBP, FST, IL-19, MAFF, PGBD5, PKP1 and PTPRH are important markers of epithelial response after microplastic stimulation in obstructive lung disaeses. These mediators are linked to Th2 inflammation, alleviation of stress response, and, most notably, carcinogenesis. Microplastic stimulation differently modified the response of airway epithelial cells in obstructive lung diseases than in controls. Asthmatic and COPD epithelial cells are more prone to damage after microplastic fibre exposure. A co-culture model (4 controls, 4 asthma, and 4 patients with COPD) employed nasal epithelial cells, was exposed to polyamide fibres for 48h. The cells were cultured at an air-liquid interface (ALI) for 21 days in PneumaCult medium (StemCell) within a two-chamber system (Greiner Bio-One). Cells were then stimulated with microplastic fibres (200 µg/cm2).