Wang Yunxiu, Cao Zhiwei, Zhao He, Gu Zhaowei
Department of Otolaryngology Head and Neck Surgery, Shengjing Hospital of China Medical University, Shenyang City 110004, Liaoning Province, PR China.
Department of Otolaryngology Head and Neck Surgery, Shengjing Hospital of China Medical University, Shenyang City 110004, Liaoning Province, PR China.
Ecotoxicol Environ Saf. 2022 Sep 15;243:114005. doi: 10.1016/j.ecoenv.2022.114005. Epub 2022 Aug 24.
Nonylphenol (NP) can be widely used as a plasticizer, surfactant, antioxidant, textile printing, dyeing additive, and pesticide emulsifier. Animal studies have shown that NP aggravates ovalbumin (OVA)-induced allergic rhinitis (AR); however, the exact mechanism underlying its action has not yet been detailed. This study aimed to explore the aggravation of the AR inflammatory response following NP exposure and its possible mechanism. The AR mouse model was constructed using OVA. Under NP exposure, allergic nasal symptoms were observed, eosinophil infiltration was assessed by Sirius red staining, and the levels of IL-4, IL-5, and IL-13 in nasal mucosa samples were detected using cytometric bead array. The mRNA levels of OX40/OX40L and GATA3 in nasal mucosa were detected by qPCR, and the expression levels of the TSLP and JAK1/2-STAT3 signaling pathway components were also identified. Our results suggest that NP exposure exacerbated allergic nasal symptoms and that eosinophils accumulated in nasal mucosa after OVA challenge. The levels of the typical T helper 2 cytokines, as well as the mRNA levels of OX40/OX40L and GATA3, were elevated in the nasal mucosa of OVA-challenged mice exposed to NP. In addition, NP exposure elevated the TSLP, TSLPR, IL-7R, p-JAK1, p-JAK2, and p-STAT3 levels in the nasal mucosa after OVA stimulation. Overall, the present study suggests NP can exacerbate OVA-induced AR inflammatory responses; furthermore, this aggravating effect of NP may be related to the TSLP-TSLPR/IL-7R and JAK1/2-STAT3 signaling pathways.
壬基酚（NP）可广泛用作增塑剂、表面活性剂、抗氧化剂、纺织印染添加剂和农药乳化剂。动物研究表明，NP会加重卵清蛋白（OVA）诱导的过敏性鼻炎（AR）；然而，其确切作用机制尚未详细阐明。本研究旨在探讨NP暴露后AR炎症反应的加重情况及其可能机制。使用OVA构建AR小鼠模型。在NP暴露下，观察过敏性鼻症状，通过天狼星红染色评估嗜酸性粒细胞浸润，并使用细胞计数珠阵列检测鼻黏膜样本中IL-4、IL-5和IL-13的水平。通过qPCR检测鼻黏膜中OX40/OX40L和GATA3的mRNA水平，并鉴定TSLP和JAK1/2-STAT3信号通路成分的表达水平。我们的结果表明，NP暴露加剧了过敏性鼻症状，且OVA激发后嗜酸性粒细胞在鼻黏膜中积聚。在暴露于NP的OVA激发小鼠的鼻黏膜中，典型的辅助性T细胞2细胞因子水平以及OX40/OX40L和GATA3的mRNA水平升高。此外，NP暴露在OVA刺激后提高了鼻黏膜中TSLP、TSLPR、IL-7R、p-JAK1、p-JAK2和p-STAT3的水平。总体而言，本研究表明NP可加剧OVA诱导的AR炎症反应；此外，NP的这种加重作用可能与TSLP-TSLPR/IL-7R和JAK1/2-STAT3信号通路有关。
