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双酚 A 加剧卵清蛋白诱导的变应性鼻炎小鼠模型中的过敏炎症。

Bisphenol A Exacerbates Allergic Inflammation in an Ovalbumin-Induced Mouse Model of Allergic Rhinitis.

机构信息

Department of Otolaryngology Head and Neck Surgery, Shengjing Hospital of China Medical University, Shenyang City, 110004 Liaoning Province, China.

Department of Pharmaceutical Toxicology, School of Pharmacy, China Medical University, Shenyang City, 110122 Liaoning Province, China.

出版信息

J Immunol Res. 2020 Sep 8;2020:7573103. doi: 10.1155/2020/7573103. eCollection 2020.

DOI:10.1155/2020/7573103
PMID:32964057
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7495229/
Abstract

PURPOSE

Bisphenol A (BPA) is found in many plastic products and is thus a common environmental endocrine disruptor. Plastic-related health problems, including allergic diseases, are attracting increasing attention. However, few experimental studies have explored the effect of BPA on allergic rhinitis (AR). We explore whether BPA was directly related to the allergic inflammation induced by ovalbumin (OVA) in AR mice.

METHODS

We first constructed OVA-induced mouse model, and after BPA administration, we evaluated nasal symptoms and measured the serum OVA-specific IgE levels by ELISA. Th2 and Treg-related cytokines of nasal mucosa were measured by cytometric bead array. Th2 and Treg-specific transcription factor levels were assayed by PCR. The proportions of CD3CD4IL-4Th2 and CD4HeliosFoxp3 T cells (Tregs) in spleen tissue were determined by flow cytometry.

RESULTS

Compared to OVA-only-induced mice, BPA addition increased nasal symptoms and serum OVA-specific IgE levels. OVA and BPA coexposure significantly increased IL-4 and IL-13 protein levels compared to those after OVA exposure alone. BPA plus OVA tended to decrease the IL-10 protein levels compared to those after OVA alone. Coexposure to OVA and BPA significantly increased the GATA-3-encoding mRNA level, and decreased the levels of mRNAs encoding Foxp3 and Helios, compared to those after OVA exposure alone. BPA increased the Th2 cell proportion, and decreased that of Tregs, compared to the levels with OVA alone.

CONCLUSION

BPA exerted negative effects by exacerbating AR allergic symptoms, increasing serum OVA-specific IgE levels, and compromising Th2 and Treg responses.

摘要

目的

双酚 A(BPA)存在于许多塑料制品中,因此是一种常见的环境内分泌干扰物。与塑料相关的健康问题,包括过敏疾病,正受到越来越多的关注。然而,很少有实验研究探讨 BPA 对变应性鼻炎(AR)的影响。我们探讨了 BPA 是否与 AR 小鼠中由卵清蛋白(OVA)引起的过敏炎症直接相关。

方法

我们首先构建了 OVA 诱导的小鼠模型,在给予 BPA 后,通过 ELISA 评估鼻症状并测量血清 OVA 特异性 IgE 水平。通过流式细胞术检测脾组织中 CD3CD4IL-4Th2 和 CD4HeliosFoxp3 T 细胞(Tregs)的比例。通过细胞因子检测试剂盒检测鼻黏膜中 Th2 和 Treg 相关细胞因子。

结果

与仅 OVA 诱导的小鼠相比,BPA 加用增加了鼻症状和血清 OVA 特异性 IgE 水平。OVA 和 BPA 共暴露与仅 OVA 暴露相比,显著增加了 IL-4 和 IL-13 蛋白水平。与仅 OVA 暴露相比,BPA 加用 OVA 倾向于降低 IL-10 蛋白水平。与仅 OVA 暴露相比,OVA 和 BPA 共暴露显著增加了编码 GATA-3 的 mRNA 水平,降低了编码 Foxp3 和 Helios 的 mRNA 水平。与仅 OVA 暴露相比,BPA 增加了 Th2 细胞比例,降低了 Tregs 比例。

结论

BPA 通过加重 AR 过敏症状、增加血清 OVA 特异性 IgE 水平以及损害 Th2 和 Treg 反应,产生了负面影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/19f522089527/JIR2020-7573103.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/63bc10951c2b/JIR2020-7573103.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/c1d5c57d987d/JIR2020-7573103.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/5891371a65cd/JIR2020-7573103.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/0a7c72cbbbbe/JIR2020-7573103.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/bebdb29e4e1b/JIR2020-7573103.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/a995ac4e8f76/JIR2020-7573103.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/19f522089527/JIR2020-7573103.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/63bc10951c2b/JIR2020-7573103.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/c1d5c57d987d/JIR2020-7573103.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/5891371a65cd/JIR2020-7573103.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/0a7c72cbbbbe/JIR2020-7573103.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/bebdb29e4e1b/JIR2020-7573103.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/a995ac4e8f76/JIR2020-7573103.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd50/7495229/19f522089527/JIR2020-7573103.007.jpg

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