Effect of Air Pollutants on Allergic Inflammation in Structural Cells of the Nasal Mucosa
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Objectives. Air pollution is an increasing global concern, and its effect on allergic inflammation has attracted the attentionof many researchers. Particulate matter (PM) is a major component of ambient air pollution, and heavy metals arethe primary toxic constituents of PM. As previous studies on the impact of air pollutants on allergic inflammation didnot adequately mimic real-world atmospheric exposure, we developed an experimental model to investigate the ef-fects of aerosolized air pollutants on nasal epithelial cells and fibroblasts. Methods. We collected particulate matter 2.5 (PM2.5) samples from ambient 24-hour air samples obtained in Seoul from Au-gust 2020 to August 2022, and then conducted component analysis for metallic constituents. Primary nasal epithelialcells and nasal fibroblasts, obtained and cultured from the turbinate tissues of human participants, were treated withPM2.5. The associations of heavy metals identified from the component analysis with cytokine expression were inves-tigated. A three-dimensional (3D)-hybrid culture model, consisting of co-culture of an air-liquid interface and nasal fi-broblast spheroids, was constructed to observe the impact of aerosolized air pollutants. Results. Among the heavy metals, Si was the predominant component of PM2.5, and Zn showed the highest correlation withthe concentration of PM2.5 in Seoul. PM2.5, Zn, and Si increased the production of epithelial cell-derived cytokines,and PM2.5 and Zn exhibited similar trends with one another. Exposure of the 3D-hybrid model to aerosolized PM2.5and Zn resulted in elevated periostin, alpha-smooth muscle actin, and fibronectin expression in fibroblast spheroids,and those without an epithelial barrier exhibited a similar increase in periostin expression. Conclusion. Ambient air pollutants in the form of aerosols increase the expression of allergic inflammatory cytokines inboth nasal epithelial cells and fibroblasts. Regulations on air pollution will help reduce the global burden of allergicdiseases in the future.
Abstract
Objectives. Air pollution is an increasing global concern, and its effect on allergic inflammation has attracted the attentionof many researchers. Particulate matter (PM) is a major component of ambient air pollution, and heavy metals arethe primary toxic constituents of PM. As previous studies on the impact of air pollutants on allergic inflammation didnot adequately mimic real-world atmospheric exposure, we developed an experimental model to investigate the ef-fects of aerosolized air pollutants on nasal epithelial cells and fibroblasts. Methods. We collected particulate matter 2.5 (PM2.5) samples from ambient 24-hour air samples obtained in Seoul from Au-gust 2020 to August 2022, and then conducted component analysis for metallic constituents. Primary nasal epithelialcells and nasal fibroblasts, obtained and cultured from the turbinate tissues of human participants, were treated withPM2.5. The associations of heavy metals identified from the component analysis with cytokine expression were inves-tigated. A three-dimensional (3D)-hybrid culture model, consisting of co-culture of an air-liquid interface and nasal fi-broblast spheroids, was constructed to observe the impact of aerosolized air pollutants. Results. Among the heavy metals, Si was the predominant component of PM2.5, and Zn showed the highest correlation withthe concentration of PM2.5 in Seoul. PM2.5, Zn, and Si increased the production of epithelial cell-derived cytokines,and PM2.5 and Zn exhibited similar trends with one another. Exposure of the 3D-hybrid model to aerosolized PM2.5and Zn resulted in elevated periostin, alpha-smooth muscle actin, and fibronectin expression in fibroblast spheroids,and those without an epithelial barrier exhibited a similar increase in periostin expression. Conclusion. Ambient air pollutants in the form of aerosols increase the expression of allergic inflammatory cytokines inboth nasal epithelial cells and fibroblasts. Regulations on air pollution will help reduce the global burden of allergicdiseases in the future.
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