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首页> 外文期刊>Toxicology and Applied Pharmacology >Interleukin-24 as a target cytokine of environmental aryl hydrocarbon receptor agonist exposure in the lung
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Interleukin-24 as a target cytokine of environmental aryl hydrocarbon receptor agonist exposure in the lung

机译：白细胞介素-24作为肺中环保芳基烃受体激动剂暴露的靶细胞因子

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摘要

Exposure to environmental aryl hydrocarbon receptor (AhR) agonists, such as halogenated aromatic hydrocarbons and polycyclic aromatic hydrocarbons (PAHs), has great impacts on the development of various lung diseases. As emerging molecular targets for AhR agonists, cytokines may contribute to the inflammatory or immunotoxic effects of environmental AhR agonists. However, general cytokine expression may not specifically indicate environmental AhR agonist exposure. By comparing cytokine and chemokine expression profiles in human lung adenocarcinoma cell line CL5 treated with AhR agonists and the non-AhR agonist polychlorinated biphenyl (PCB) 39, we identified a target cytokine of environmental AhR agonist exposure of in the lungs. Thirteen cytokine and chemokine genes were altered in the AhR agonists-treated cells, but none were altered in the PCB39-treated cells. Interleukin (IL)-24 was the most highly induced gene among AhR-modulated cytokines. Cotreatment with AhR antagonist completely prevented IL-24 induction by AhR agonists in the CL5 cells. Knock-down AhR expression with short-hairpin RNA (shRNA) significantly reduced benzo[a]pyrene (BaP)-induced IL-24 mRNA levels. We further confirmed that gene transcription, but not mRNA stability, was involved in IL-24 up-regulation by BaP. Particulate matter (PM) in the ambient air contains some PAHs and is reported to activate AhR. Oropharyngeal aspiration of PM significantly increased IL-24 levels in lung epithelia and in bronchoalveolar lavage fluid of mice 4 weeks after treatment. Thus, our data suggests that IL-24 is a pulmonary exposure target cytokine of environmental AhR agonists. (C) 2017 Elsevier Inc. All rights reserved.
机译：暴露于环境芳烃受体（AhR）激动剂，如卤化芳烃和多环芳烃（PAHs），对各种肺部疾病的发展有很大影响。作为AhR激动剂的新兴分子靶点，细胞因子可能参与环境AhR激动剂的炎症或免疫毒性作用。然而，一般的细胞因子表达可能并不特别表明环境AhR激动剂暴露。通过比较经AhR激动剂和非AhR激动剂多氯联苯（PCB）39处理的人肺腺癌细胞系CL5中的细胞因子和趋化因子表达谱，我们确定了环境AhR激动剂暴露于肺部的靶细胞因子。在AhR激动剂处理的细胞中有13个细胞因子和趋化因子基因发生了改变，但在PCB39处理的细胞中没有任何改变。白细胞介素（IL）-24是AhR调节的细胞因子中诱导率最高的基因。在CL5细胞中，与AhR拮抗剂联合治疗完全阻止AhR激动剂诱导IL-24。用短发夹RNA（shRNA）下调AhR表达显著降低苯并[a]芘（BaP）诱导的IL-24mRNA水平。我们进一步证实，BaP上调IL-24与基因转录有关，但与mRNA稳定性无关。环境空气中的颗粒物（PM）含有一些多环芳烃，据报道会激活AhR。治疗4周后，口咽吸入PM可显著增加小鼠肺上皮和支气管肺泡灌洗液中的IL-24水平。因此，我们的数据表明，IL-24是环境AhR激动剂的肺部暴露靶细胞因子。（C） 2017爱思唯尔公司版权所有。

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