Journal
MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS
Volume 839, Issue -, Pages 40-48Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.mrgentox.2018.12.005
Keywords
PM2.5; Human bronchial epithelial cells; CYP1A1/1B1; Oxidative stress; Pro-inflammatory response
Funding
- Collaborative research project of Southeast University-Nanjing Medical University [2242017K3DN16]
- National Key Research and Development Program of China [2017YFC0211600, 2017YFC0211605]
- Undergraduates Training Programs of Innovation and Entrepreneurship of Jiangsu Province [201510312001Z]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (Public Health and Preventive Medicine)
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We investigated the mechanism responsible for the oxidative stress and pro-inflammatory response triggered by PM2.5 collected from Nanjing of China. Two human bronchial epithelia cell lines (HBE and BEAS-2B) were used. Human gene expression profile microarray was performed to investigate the alteration of gene expression in PM2.5-treated HBE cells. The results of ROS assay and ELISA indicated that PM2.5 (150 mu g/ml) increased the level of cellular reactive oxygen species (ROS) and promoted the release of interleukin-6 (IL-6) in HBE cells. CYP1A1 and CYP1B1 were the top two up-regulated genes by PM2.5 (150 mu g/ml, 48 h of exposure) in HBE cells. Co-knockdown of CYP1A1/1B1 by siRNA substantially inhibited PM2.5-induced ROS generation, IL-6/IL-8 secretion and STAT3/P-STAT3 expression. Similarly, the knockdown of STAT3 also effectively inhibited PM2.5-induced rise in ROS level and IL-6/IL-8 secretion. In summary, PM2.5 mediated oxidative stress and pro-inflammatory response via up-regulating the expression of CYP1A1/1B1 in two human bronchial epithelial cell lines.
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