Effect of Atmospheric PM2.5 on Expression Levels of NF-κB Genes and Inflammatory Cytokines Regulated by NF-κB in Human Macrophage

• Published in: Inflammation Vol. 41; no. 3; pp. 784 - 794
• Main Authors: Zhang, Yuezhu, Wang, Shuyue, Zhu, Jian, Li, Chunyan, Zhang, Tianrong, Liu, Hongbo, Xu, Qi, Ye, Xiaofang, Zhou, Liting, Ye, Lin
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.06.2018; Springer Nature B.V
• Subjects: 12-O-Tetradecanoylphorbol-13-acetate; Acetic acid; Air Pollutants - pharmacology; Biomedical and Life Sciences; Biomedicine; Cell culture; Cell Line; Cell Survival - drug effects; Cytokines; Cytokines - metabolism; Dose-Response Relationship, Drug; Enzyme-linked immunosorbent assay; Genes; Humans; Immunology; Inflammation; Inflammation - etiology; Inflammation - metabolism; Internal Medicine; Macrophages; Macrophages - cytology; Macrophages - metabolism; Monocytes; NF-kappa B - genetics; NF-kappa B - metabolism; NF-κB protein; Original Article; Particulate Matter - pharmacology; Pathology; Pharmacology/Toxicology; Polymerase chain reaction; RelA protein; RelB protein; Rheumatology; RNA-directed DNA polymerase; Signal transduction; Tumor necrosis factor-α; NF-κB; inflammatory cytokines; cytotoxicity; PM2.5
• ISSN: 0360-3997; 1573-2576
• DOI: 10.1007/s10753-018-0732-8

Exposure to PM2.5 induces systemic inflammation, and the NF-κB signaling pathway plays an important role in the inflammation process. We aim to clarify whether the expression of NF-κB gene family affects inflammation caused by PM2.5. Human monocytic cells (THP-1) were induced to differentiate into macrophages using phorbol myristate acetate. The macrophages were then treated with 100, 200, and 400 μg/ml of PM2.5 for 12, 24, and 48 h, respectively. Then, we determined the survival rate of macrophages through the MTT assay. The TNF-α and CRP levels in the cell culture medium were measured through enzyme-linked immunosorbent assay. The NF-κB1 , NF-κB2 , RelA , RelB , and Rel mRNA levels in macrophages were measured with reverse transcriptase-polymerase chain reaction. As a consequence, the survival rate of macrophages decreased with increasing PM2.5 exposure time and dose. The TNF-α levels in PM2.5-treated groups were lower as compared with the control group and in contrast to the NF-κB mRNA levels at all exposure times. The TNF-α level in the 400-μg/ml group and the NF-κB1 , NF-κB2 , RelB , and Rel mRNA levels in all PM2.5-treated groups were found to be higher at 24 h than at 12 h. Furthermore, the TNF-α, CRP, and NF-κB2 mRNA levels in the group treated with 400 μg/ml PM2.5 were higher at 48 h that at 12 and 24 h. On the other hand, the NF-κB1 , RelA , RelB , and Rel mRNA levels in all PM2.5-treated groups were lower as compared to levels of TNF-α, CRP, and NF-κB2 mRNA. The levels of NF-κB genes and inflammatory cytokines demonstrated different correlations at different exposure times. Therefore, we conclude that PM2.5 reduces the survival rate of macrophages. As macrophages are exposed to PM2.5, the NF-κB gene family expression is increased, which subsequently affects inflammatory factor levels.