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Chlorinated Flame-Retardant Dechlorane 602 Potentiates Type 2 Innate Lymphoid Cells and Exacerbates Airway Inflammation
Environmental Science & Technology ( IF 10.8 ) Pub Date : 2020-12-30 , DOI: 10.1021/acs.est.0c03758
Pengcheng Zhou 1, 2, 3 , Ting Zheng 1 , Yunping Li 4, 5, 6 , Xin Zhang 7 , Jinhong Feng 1 , Yunbo Wei 1 , Hao Wang 2 , Yin Yao 3, 8 , Fang Gong 9 , Wenjing Tian 1 , Lingyun Sun 7 , Zheng Liu 8 , Bin Zhao 4, 5, 6 , Di Yu 1, 2, 3
Affiliation  

Chlorinated flame-retardant dechloranes are emerging substitutes for restricted flame retardants. Recent studies have demonstrated that they are accumulated in wildlife and detectable in humans; however, their effects on human health are poorly understood. Here, for the first time, we revealed that widely used chlorinated flame-retardant dechlorane 602 (Dec 602) exacerbated airway inflammation in two mouse models induced by house dust mite (HDM) or IL-33, respectively. Deteriorated airway inflammation by Dec 602 was associated with a higher production of type 2 cytokines including IL-4, IL-5, and IL-13, and IgE, accompanied by enhanced mRNA expression of proinflammatory cytokines such as TNF-α and IL-6. Mechanistically, we found that Dec 602 directly potentiated mouse and human group 2 innate lymphoid cells and, as such, promoted airway inflammation even in the absence of conventional T cells in Rag–/– mice. These findings provide novel immunological insights necessary for further studies of the health impact of emerging flame-retardant dechloranes including Dec 602.

中文翻译:

氯化阻燃二氯乙烷602增强2型先天淋巴样细胞并加剧气道炎症

氯化阻燃剂十氯烷是限制性阻燃剂的新兴替代品。最近的研究表明,它们是在野生生物中积累并在人类中可检测到的。但是,它们对人类健康的影响知之甚少。在这里,我们首次揭示了广泛使用的氯化阻燃性十氯烷602(Dec 602)在分别由室内尘螨(HDM)或IL-33诱导的两种小鼠模型中加剧了气道炎症。到602年12月,气道炎症恶化与2型细胞因子(包括IL-4,IL-5和IL-13和IgE)的更高产生有关,同时促炎性细胞因子(如TNF-α和IL-6)的mRNA表达增强。从机理上讲,我们发现Dec 602可直接​​增强小鼠和人类第2组先天淋巴样细胞的增殖,因此,抹布– / –老鼠。这些发现提供了新的免疫学见解,对于进一步研究新兴的阻燃性十氯烷(包括Dec 602)的健康影响是必要的。
更新日期:2021-01-19
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