A comparative study on the model of PM2.5 direct or indirect interaction with bronchial epithelial cells

炎症 细胞生物学 细胞毒性T细胞 氧化应激 活力测定 刺激 免疫学 细胞培养 体外 化学 生物 生物化学 内分泌学 遗传学
作者
Yan Wang,Xi‐Nian Zuo,Fuyang Jiang,Lin Hou,Qiyue Jiang,Zhonghui Zhu,Tian Lin
出处
期刊:Environmental Science and Pollution Research [Springer Science+Business Media]
卷期号:29 (27): 41567-41576 被引量:3
标识
DOI:10.1007/s11356-021-18324-2
摘要

The impact of PM2.5 on epithelial cells is a pivotal process leading to many lung pathological changes and pulmonary diseases. In addition to PM2.5 direct interaction with epithelia, macrophages that engulf PM2.5 may also influence the function of epithelial cells. However, among the toxic researches of PM2.5, there is a lack of evaluation of direct or indirect exposure model on human bronchial epithelial cell against PM2.5. In this present research, PM2.5-exposed human bronchial epithelial cell line (BEAS-2B) serves as the direct interaction model. By contrast, a PM2.5-stimulated co-culture model of macrophages and epithelial cells based on the transwell system was adopted as indirect stimulation model. By comparing these two models of interaction, we examined the viability of BEAS-2B and mRNA/protein expression profile of oxidative stress and inflammatory response-related transcription factors Nrf2, NF-kB, and according inflammatory indicators such as IL-1, IL-6, and IL-8, with a view to evaluating the effects of different interaction models of PM2.5 on epithelial cell damage in vitro. Our results indicated that under the same doses, the direct stimulation model of PM2.5 could inhibit the viability of BEAS-2B. Furthermore, the indirect stimulation model strengthen inflammation response of epithelia under the higher concentration of PM2.5 and induce epithelia to undergo EMT under the lower concentration of PM2.5. Overall, we have found that macrophage involvement may protect epithelia from PM2.5 cytotoxic effect, while it strengthens the inflammation response and induce epithelia to undergo EMT.

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