ALTERED PROINFLAMMATORY CYTOKINES AND M1 POLARIZATION INDUCED BY PM2.5 IN ALVEOLAR MACROPHAGES

D MOON, S J PARK, S KIM, J KIM, M KIM, K KIM, Y S KIM, J KIM
2018 Applied Ecology and Environmental Research  
Moon et al.: Altered proinflammatory cytokines and M1 polarization induced by PM2.5 in alveolar macrophages -7699 -APPLIED ECOLOGY AND ENVIRONMENTAL RESEARCH 16(6):7699-7712. Abstract. Exposure to atmospheric particulate matter with aerodynamic diameter less than 2.5 μm (PM2.5) is epidemiologically implicated in pulmonary mortality and diseases. While it is known that PM2.5-exposed macrophages produce and secrete inflammatory cytokines, it is not clear how PM2.5 contributes to the upregulation
more » ... o the upregulation of proinflammatory cytokines in alveolar macrophages. Therefore, the present study aims to investigate the molecular mechanism of macrophage inflammatory responses to PM2.5. In a MH-S mouse alveolar macrophage cell line, exposure to PM2.5 significantly increased the intracellular levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in dose-and time-dependent manners, while it did not alter those of transforming growth factor-β1 (TGF-β1) and interleukin-10 (IL-10). PM2.5 also increased the expressional level of CD80 mRNA, but did not alter that of CD163 mRNA in alveolar macrophages, suggesting PM2.5-induced M1 phenotypic polarization. Treatment with nuclear factor-κB (NF-κB) inhibitors immediately after PM2.5 administration reduced the production of TNF-α, IL-1β, and IL-6 upregulated by PM2.5, and attenuated the CD80 mRNA expression induced by the PM2.5 exposure. In conclusion, these data suggest that PM2.5 exposure in alveolar macrophages induces the upregulation of proinflammatory cytokines as well as polarization to the M1 phenotype through the NF-κB activation.
doi:10.15666/aeer/1606_76997712 fatcat:oblkyutwnjanppkfshopqwadri