Chlorinated Flame-Retardant Dechlorane 602 Potentiates Type 2 Innate Lymphoid Cells and Exacerbates Airway Inflammation.
Pengcheng ZhouTing ZhengYunping LiXin ZhangJinhong FengYunbo WeiHao WangYin YaoFang GongWenjing TianLingyun SunZheng LiuBin ZhaoDi YuPublished in: Environmental science & technology (2020)
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.
Keyphrases
- gas chromatography
- human health
- induced apoptosis
- risk assessment
- mass spectrometry
- public health
- polycyclic aromatic hydrocarbons
- healthcare
- endothelial cells
- rheumatoid arthritis
- mental health
- mouse model
- signaling pathway
- oxidative stress
- metabolic syndrome
- case control
- adipose tissue
- social media
- pluripotent stem cells