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Isolating Bronchial Epithelial Cells from Resected Lung Tissue for Biobanking and Establishing Well-Differentiated Air-Liquid Interface Cultures
Published on: May 26, 2023
Polyamide and polyvinyl chloride microplastics induce cytotoxicity and cytokine release in primary normal human
Yvonne C M Staal1, Irene F Gosselink2, Y Y Lianne Sander1,3
1National Institute for Public Health & the Environment (RIVM), Bilthoven, The Netherlands.
Abstract:
Our daily and continuous exposure to airborne micro- and nanoplastics (MNPs) together with the limited information on their potential hazards, warrants the need for more information on MNP-toxicity. In this study, we investigated the effects of diverse size ranges of amorphous MNPs from environmentally relevant polymers, on Air-Liquid-Interface (ALI)-cultured Normal Human Bronchial Epithelial cells (NHBEs) by analyzing immunological response parameters 24 h after exposure. In addition, we have used this setup to compare the responses of NHBEs to MNPs using nebulization or quasi-ALI (small droplet) exposure. NHBEs responded differently to exposures of polyamide (PA) or polyvinyl chloride (PVC) particles at nominal doses between 0.003 and 0.100 µg/cm2. PA particles < 1 μm (but not those > 1 μm) induced dose-dependent cell death, increased IL-8 secretion and decreased MCP-1 secretion. PVC particles (< 1 μm and 1-5 μm) induced cell death at lower concentrations than PA particles. Also, an increased IL-8 secretion and decreased MCP-1 secretion was observed for PVC particles in all size fractions (< 1 μm, 1-5 μm and 5-10 μm). Comparison of nebulization versus quasi-ALI exposure indicated differences related to the exposure method, but further experimental assessment is needed for definite conclusions and to ensure that the obtained data is relevant for toxicological effects occurring in humans. Our results indicate that PA and PVC particles increase IL-8 secretion and, PA only, decreases MCP-1 secretion. It needs to be established whether these effects on cytokines also indicate an activation of immune cells.
Supplementary Information:
The online version contains supplementary material available at 10.1186/s43591-026-00200-w.
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