Abstract
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.
Highlights
PM2.5 is a sort of airborne particles and droplets with small particle size, long sustained in many developing countries
PM2.5-exposed human bronchial epithelial cell line (BEAS-2B) serves as the direct interaction model, while the contrast is to indirect stimulation model, which takes advantage of transwell co-culture system to carry out that PM2.5 is promptly contacted with macrophages rather than BEAS-2B
We have found that macrophage involvement may protect epithelia from PM2.5 cytotoxic effect, while strengthen the inflammation response
Summary
PM2.5 is a sort of airborne particles and droplets with small particle size, long sustained in many developing countries. It absorbs hazardous substances in the environment, entering into the respiratory tract and even across blood-gas barrier, prompting complex and harmful biological effects. When PM2.5 is inhaled into the lung tissue through the respiratory tract and reaches the end of the bronchi and alveoli, it can directly act on the surface of the tissue cells to undermine physical functions. PM2.5 may have an alternative mode of interaction with bronchial epithelia cells after entering the lung tissue comparing with the directly touch. The difference between the direct and indirect effects of PM2.5 on human bronchial epithelia cells in vitro is not well known
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