PM_2.5 induces inflammation in human bronchial epithelial cells through ROS-Nrf2 signaling pathway

  Objective  to investigate the effect of particulate matter less than 2.5 μm in aerodynamic diameter (PM_2.5) on inflammatory response of human bronchial epithelial cells (16-HBE).

  Methods  PM_2.5 samples in ambient air was collected in Shenyang city of Liaoning province in December 2018. The 16-HBE cells were treated with sampled PM_2.5 at concentrations of 12.5, 25, 50 and 100 g/mL for 0, 6, 12, and 24 hours, respectively. Cell counting kit-8 (CCK-8) assay was used to detect the activity of the 16-HBE cells. The contents of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and matrix metalloproteinase-9 (MMP-9) in cell culture supernatant were detected with enzyme-linked immunosorbent assay (ELISA). The relative levels of cell reactive oxygen species (ROS) were detected with fluorescence probe and the levels of I kappa B kinase (IKK) and P65 in the cell protein nuclear factor erythroid-2 related factor 2 (Nrf2) and nuclear factor-kappa B (NF-κB) pathway were detected with Western blot.

  Results  PM_2.5 can induce a decrease in proliferation and occurrence of inflammatory reaction of 16-HBE cells in time- and dose-dependent manner.

  Conclusion  PM_2.5 exposure can inhibit the proliferation and induce inflammatory reaction of human respiratory epithelial cells through ROS-Nrf2/Nf-kb signaling pathway.