Ambient fine particulate matter (PM2.5) induces oxidative stress and pro-inflammatory response via up-regulating the expression of CYP1A1/1B1 in human bronchial epithelial cells in vitro

Publication date: Available online 12 December 2018Source: Mutation Research/Genetic Toxicology and Environmental MutagenesisAuthor(s): Qi Yuan, Yaoyao Chen, Xiaobo Li, Haiyan Chu, Zhengdong ZhangAbstractWe 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 µg/ml) increased the level of cellular reactive oxygen species (ROS) levels and promoted the release of interleukin-6 (IL-6) in HBE cells. CYP1 A1 and CYP1B1 were the top two up-regulated genes by PM2.5 (150 µg/ml, 48 h of exposure) in HBE cells. Co-knockdown of CYP1 A1/1B1 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 CYP1 A1/1B1 in two human bronchial epithelial cell lines.
Source: Mutation Research Genetic Toxicology and Environmental Mutagenesis - Category: Genetics & Stem Cells Source Type: research