Effects of different components of pm2.5on the expression levels of nf-κb family gene mrna and inflammatory molecules in human macrophage

Abstract

Background: Studies have found that exposure to fine particulate matter with sizes below 2.5 µm (PM2.5) might cause inflammation response via the NF-κB pathway. To date, only a few studies have focused on the toxicity of different components of PM2.5. We aimed to explore the effects of PM2.5 with different components on the expression levels of NF-κB family gene mRNA and inflammatory molecules in human macrophages. Methods: Human monocytic cell line THP-1-derived macrophages were exposed to water-soluble (W-PM2.5), fat-soluble (F-PM2.5), and insoluble (I-PM2.5) PM2.5. The cell survival rate was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The levels of inflammatory molecules were determined by enzyme-linked immunosorbent assay (ELISA), and the relative mRNA levels of the NF-κB family gene were determined by real time PCR. Results: PM2.5 could decrease the cell viability. After exposure to W-PM2.5, the levels of interleukins (IL)-1β and IL-12 p70 significantly increased. After exposure to F-PM2.5, the levels of IL-12 p70 significantly increased. The levels of IL-12 p70 and TNF-α after exposure to I-PM2.5 were significantly higher than that in W- and F-PM2.5 treatment groups. The levels of IL-8, C reactive protein (CRP), and cyclooxygenase (COX)-2 increased only after exposure to I-PM2.5. F-PM2.5 increased the mRNA levels of NF-κB genes, especially NF-κB1 and RelA. Conclusions: PM2.5 can decrease the cell survival rate and up-regulate the expression of NF-κB family gene mRNA and inflammatory molecules. The main toxic components of PM2.5 related to inflammatory response in macrophages were the I-PM2.5.