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Updated: Jul 12, 2026
Impact Assessment of Repeated Exposure of Organotypic 3D Bronchial and Nasal Tissue Culture Models to Whole Cigarette Smoke
Published on: February 12, 2015
A comparative study on the model of PM2.5 direct or indirect interaction with bronchial epithelial cells
Yan Wang1,2, Xin Zuo3, Fuyang Jiang1,2
1Department of Occupational and Environmental Health, School of Public Health, Capital Medical University, No. 10, Xitoutiao Youanmen Street, Beijing, 100069, China.
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.
Insights
Exposure to fine particulate matter (PM2.5) impacts lung epithelial cells. Macrophages can protect cells from PM2.5 toxicity but also enhance inflammation and epithelial-mesenchymal transition (EMT).
Area of Science:
- Environmental Health
- Cell Biology
- Toxicology
Background:
- Particulate matter (PM2.5) significantly impacts lung epithelial cells, contributing to various pulmonary diseases.
- The role of macrophages in mediating PM2.5 effects on epithelial cells remains incompletely understood.
- Existing research often lacks comparative models for direct vs. indirect PM2.5 exposure on human bronchial epithelial cells.
Purpose of the Study:
- To compare the effects of direct and indirect PM2.5 exposure on human bronchial epithelial cells (BEAS-2B).
- To evaluate the influence of macrophage-epithelial cell interactions in response to PM2.5.
- To assess PM2.5-induced changes in cell viability, oxidative stress, and inflammatory markers.
Main Methods:
- Utilized a direct exposure model using PM2.5-treated BEAS-2B cells.
- Employed an indirect exposure model involving a transwell co-culture of macrophages and BEAS-2B cells stimulated by PM2.5.
- Analyzed BEAS-2B cell viability, and mRNA/protein expression of Nrf2, NF-kB, IL-1, IL-6, and IL-8.
Main Results:
- Direct PM2.5 exposure inhibited BEAS-2B cell viability.
- Indirect exposure amplified epithelial inflammation at higher PM2.5 concentrations.
- Indirect exposure induced epithelial-mesenchymal transition (EMT) at lower PM2.5 concentrations.
Conclusions:
- Macrophage involvement may offer protection against PM2.5 cytotoxicity.
- Macrophage interaction with epithelial cells exacerbates inflammation and promotes EMT under PM2.5 exposure.
- Understanding these distinct interaction models is crucial for evaluating PM2.5 health risks.
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