PM2.5 stimulated the release of cytokines from BEAS-2B cells through activation of IKK/NF-κB pathway. (March 2019)

• Record Type: Journal Article
• Authors: Wang, J; Zhang, WJ; Xiong, W; Lu, WH; Zheng, HY; Zhou, X; Yuan, J
• Is Part Of: Human & experimental toxicology. Volume 38:Number 3(2019)
• Page Start: 311
• Page End: 320
• Publication Date: 2019-03
• Subjects: Cytokine -- inflammatory response -- IKK -- NF-κB -- PM2.5; Toxicology -- Periodicals; 615.9
• DOI: 10.1177/0960327118802628
• Languages: English
• ISSNs: 0960-3271

Abstract

Previous studies indicated that exposure to fine particulate matter (PM2.5 ) was related to pulmonary inflammatory diseases through activation of nuclear factor kappa B (NF-κB) signaling pathway to trigger cytokine secretions in human lung carcinoma cells. To investigate the potential mechanisms underlying expression of cytokines via activated NF-κB by PM2.5, human bronchial epithelial cells (BEAS-2B cells) were treated with PM2.5 extracts at different concentrations (6, 13, 25, 50, 100, 200, and 400 µg mL −1 ) for 6 and 24 h. We found that 100 µg mL −1 PM2.5 increased interleukin 6 (IL-6) and IL-8 expression at 24 h ( p < 0.05 or p < 0.01). Moreover, 100 µg mL −1 PM2.5 upregulated phosphorylated IκB kinase (IKK), p65, and IκBα at 6 h, which could be reversed by the IKK inhibitor Bay11-7082 ( p < 0.05 or p < 0.01). The p65 subunit of NF-κB was translocated into the nucleus of the cells treated with 100 µg mL −1 PM2.5 at 6 and 24 h. Bay11-7082 partly inhibited PM2.5 -induced increases of IL-6 and IL-8 secretion. The results indicated that PM2.5 extract increased IL-6 and IL-8 levels in BEAS-2B cells through activation of IKK/NF-κB pathway. Our study will contribute to better understanding of the mechanism of PM2.5 -induced pulmonary inflammatory diseases.