Ge Jianhong, Chu Hongqian, Xiao Qianqian, Hao Weidong, Shang Jing, Zhu Tong, Sun Zhaogang, Wei Xuetao
Department of Toxicology, School of Public Health, Peking University, Beijing, 100191, PR China; Beijing Key Laboratory of Toxicological Research and Risk Assessment for Food Safety, Beijing, 100191, PR China.
Translational Medicine Center, Beijing Chest Hospital, Capital Medical University, Beijing, 101149, PR China; Beijing Key Laboratory in Drug Resistant Tuberculosis Research, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, 101149, PR China.
Environ Pollut. 2021 Jan 14;273:116452. doi: 10.1016/j.envpol.2021.116452.
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-1β, 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.
黑碳（BC）与不同物质发生反应，形成名为老化黑碳的二次污染物，会引发炎症和肺部损伤。BC和老化BC可能会在体内增强白细胞介素-33（IL-33）的水平，IL-33可能源自巨噬细胞。IL-33的促炎作用使得确定其来源至关重要，这引导我们探索如何减轻肺部损伤。在本研究中，选用了人支气管上皮细胞系16HBE细胞，并使用了老化BC（1,4-萘醌包覆的BC和经臭氧氧化的BC）。我们发现，除IL-33外，BC和老化BC均能上调白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）和白细胞介素-8（IL-8）的mRNA表达。然而，丝裂原活化蛋白激酶（MAPKs）和磷脂酰肌醇3激酶（PI3K）/蛋白激酶B（AKT）信号通路仍未激活。在用脂多糖（LPS）预处理后，16HBE细胞中IL-33的mRNA表达显著增加，且MAPKs和PI3K/AKT被激活。这些结果表明，MAPKs和PI3K/AKT信号通路参与了IL-33的升高过程。此外，上皮细胞不太可能是BC和老化BC中IL-33升高所导致的肺部炎症的来源。
