Journal
ENVIRONMENTAL POLLUTION
Volume 273, Issue -, Pages -Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.envpol.2021.116452
Keywords
IL-33; Black carbon; 1, 4-naphthoquinone; Inflammation
Categories
Funding
- Major Program of National Natural Science Foundation of China [21190051]
- Project of Shandong Province Higher Educational Science and Technology [J16LC59]
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Black carbon (BC) reacts with different substances to form aged black carbon, which causes inflammation and lung damage. Both BC and aged BC can enhance the expression of IL-33, but epithelial cells are unlikely to be the source of lung inflammation caused by elevated IL-33 in BC and aged BC. MAPKs and PI3K/AKT pathways are involved in the elevation of IL-33.
Black carbon (BC) reacts with different substances to form secondary pollutants called aged black carbon, which causes inflammation and lung damage. BC and aged BC may enhance IL-33 in vivo, which may be derived from macrophages. The pro-inflammatory effect of IL-33 makes it essential to determine the source of IL-33, so it guides us to explore how to alleviate lung injury. In this study, a human bronchial epithelial cell line of 16HBE cells was selected, and aged BC (1,4-NQ coated BC and ozone oxidized BC) was used. We found that both BC and aged BC were able to up-regulate the mRNA expression of IL-1 beta, IL-6, and IL-8 except IL-33. However, the Mitogen-activated protein kinases (MAPKs) and Phosphatidylinositol 3-kinase (PI3K)/Protein kinase B (AKTs) pathways remained inactive. After pretreatment with Lipopolysaccharide (LPS), IL-33 mRNA expression was significantly increased in 16HBE cells and MAPKs and PI3K/AKT were activated. These results suggested that MAPKs and PI3K/AKT pathways were involved in the elevation of IL-33. Furthermore, epithelial cells are unlikely to be the source of lung inflammation caused by elevated IL-33 in BC and aged BC. (C) 2021 Elsevier Ltd. All rights reserved.
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