In vitro impact of bisphenol A on maturation and function of monocyte-derived dendritic cells in patients with primary Sjögren’s syndrome

FOXP3型 树突状细胞 流式细胞术 免疫系统 RAR相关孤儿受体γ 免疫学 单核细胞 混合淋巴细胞反应 化学 雌激素受体 内分泌学 医学 T细胞 生物 内科学 癌症 乳腺癌
作者
Jing Wang,Chunhui She,Zhiyuan Li,Ning Tang,Lishan Xu,Zhaoyang Liu,Bin Liu
出处
期刊:Immunopharmacology and Immunotoxicology [Taylor & Francis]
卷期号:42 (1): 28-36 被引量:14
标识
DOI:10.1080/08923973.2019.1706554
摘要

Background: Epidemiological studies have shown that environmental factors accelerate the progress of primary Sjögren's syndrome (pSS). Bisphenol A (BPA), a classic endocrine disrupting chemical, affects the immune system. However, the impact of BPA on pSS has not yet been reported. The present study aimed to evaluate the potential relationship between BPA, estrogen receptor (ER), and pSS.Methods: We studied the impact of BPA on monocyte-derived dendritic cells (moDCs) from pSS patients and age-matched healthy controls (HCs). Morphological effects were observed under inverted microscope. Surface markers were analyzed by flow cytometry. ER and cytokine profiles were assessed using real-time polymerase chain reaction. The ability of moDCs to stimulate CD4+ T cells activation was assessed by mixed lymphocyte reaction (MLR).Results: moDCs from both pSS patients and HCs expressed ERα as well as ERβ. After BPA-exposure, expression of ERα increased significantly in pSS patients, while that of ERβ remained unchanged. moDCs from BPA-exposed pSS patients showed irregular morphology and reduction in cell aggregation. BPA increased HLA-DR on moDCs of pSS patients via ERα, and promoted the secretion of IL6 and IL12. When co-cultured with BPA-treated moDCs, cytokines (IFN-γ, IL4, IL17, IL10) and transcription factors (T-bet, Gata3, RoR-γt, Foxp3) of CD4+ T cells showed imbalance of Th1/Th2/Th17/Treg polarization, with Th1 and Th17 dominating.Conclusions: BPA altered the function of moDCs through ERα, including antigen capture, secretion of inflammatory factors, and ability to stimulate T cells, as well as accelerated the progression and further deterioration of pSS.
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