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.
Highlights
Epidemiological and experimental studies have proven that exposure to atmospheric particulate matter (PM), especially exposure to fine particulate matter with sizes below 2.5 μm (PM2.5 ), is closely associated with population mortality [1,2,3]
After treatment with 100 ng/mL PMA for 72 h, mature macrophages differentiated from THP-1 cells adhered to the bottom of the flask and presented an irregular shape with pseudopod (Figure 1B)
We found that the overexpression of nuclear factor-κB (NF-κB) mRNA levels was associated with inflammation and played a role in the development of chronic obstructive pulmonary disease (COPD) in a population experiment [58]
Summary
Epidemiological and experimental studies have proven that exposure to atmospheric particulate matter (PM), especially exposure to fine particulate matter with sizes below 2.5 μm (PM2.5 ), is closely associated with population mortality [1,2,3]. 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. 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. 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. 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
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