Estrogen Receptor Alpha Gene (ESR1) Facilitates Th2-immune Response and Enhances Th2 Cytokines in Experimental Atopic Dermatitis Mice.

IF 1.1 4区医学 Q4 IMMUNOLOGY Iranian Journal of Immunology Pub Date : 2023-05-31 DOI:10.22034/iji.2023.97283.2494

Jianrong Niu, Hui Zhou, Rong Tian, Xudong Wang

{"title":"Estrogen Receptor Alpha Gene (ESR1) Facilitates Th2-immune Response and Enhances Th2 Cytokines in Experimental Atopic Dermatitis Mice.","authors":"Jianrong Niu, Hui Zhou, Rong Tian, Xudong Wang","doi":"10.22034/iji.2023.97283.2494","DOIUrl":null,"url":null,"abstract":"Background: Molecular markers are involved in atopic dermatitis (AD) pathogenesis. The estrogen receptor (ESR)-1 gene, encoding ERα, is reported to express aberrantly in AD patients.Objective: To detect the biological functions of ESR1 in 2,4 dinitrochlorobenzene (DNCB)-treated mice.Methods: The DNCB-treated mice received a topical application of emulsion containing the 1,3-bis(4 hydroxyphenyl)-4-methyl-5-[4-(2-piperidinyl ethoxy) phenol]-1H-pyrazole dihydrochloride (MPP; an ESR1-selective antagonist) to dorsal skins and ears. Then the dermatitis scores, histopathological changes, and cytokine levels were evaluated.Results: MPP specifically downregulated ESR1 expression in DNCB-applied mice. Functionally, application of MPP abolished the DNCB-induced promotion in dermatitis score. Additionally, MPP administration protected against DNCB-induced dermatitis severity, suppressed mast cell infiltration and reduced production of immunoglobulin E (IgE) and thymus and activation-regulated chemokine (TARC). Moreover, MPP treatment inhibited DNCB-induced production of Th2 cytokines and infiltration of CD4+ T cells.Conclusion: ESR1 facilitates Th2-immune response and enhances Th2 cytokines in AD mice.","PeriodicalId":54921,"journal":{"name":"Iranian Journal of Immunology","volume":"20 2","pages":"167-176"},"PeriodicalIF":1.1000,"publicationDate":"2023-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Iranian Journal of Immunology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.22034/iji.2023.97283.2494","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"IMMUNOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Background: Molecular markers are involved in atopic dermatitis (AD) pathogenesis. The estrogen receptor (ESR)-1 gene, encoding ERα, is reported to express aberrantly in AD patients.

Objective: To detect the biological functions of ESR1 in 2,4 dinitrochlorobenzene (DNCB)-treated mice.

Methods: The DNCB-treated mice received a topical application of emulsion containing the 1,3-bis(4 hydroxyphenyl)-4-methyl-5-[4-(2-piperidinyl ethoxy) phenol]-1H-pyrazole dihydrochloride (MPP; an ESR1-selective antagonist) to dorsal skins and ears. Then the dermatitis scores, histopathological changes, and cytokine levels were evaluated.

Results: MPP specifically downregulated ESR1 expression in DNCB-applied mice. Functionally, application of MPP abolished the DNCB-induced promotion in dermatitis score. Additionally, MPP administration protected against DNCB-induced dermatitis severity, suppressed mast cell infiltration and reduced production of immunoglobulin E (IgE) and thymus and activation-regulated chemokine (TARC). Moreover, MPP treatment inhibited DNCB-induced production of Th2 cytokines and infiltration of CD4+ T cells.

Conclusion: ESR1 facilitates Th2-immune response and enhances Th2 cytokines in AD mice.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

雌激素受体α基因(ESR1)促进实验性特应性皮炎小鼠Th2免疫反应并增强Th2细胞因子

背景:分子标志物参与了特应性皮炎(AD)的发病过程。据报道，雌激素受体(ESR)-1基因编码ERα，在AD患者中表达异常。目的:检测2,4二硝基氯苯(DNCB)处理小鼠ESR1的生物学功能。方法:给dncb处理的小鼠外用含有1,3-双(4 -羟基苯基)-4-甲基-5-[4-(2-哌啶基乙氧基)苯酚]- 1h -吡唑二盐酸盐(MPP;一种esr1选择性拮抗剂)作用于背侧皮肤和耳朵。然后评估皮炎评分、组织病理学变化和细胞因子水平。结果:MPP特异性下调dncb小鼠ESR1表达。功能上，MPP的应用消除了dncb对皮炎评分的促进作用。此外，MPP对dncb诱导的皮炎的严重程度有保护作用，抑制肥大细胞浸润，降低免疫球蛋白E (IgE)和胸腺及活化调节趋化因子(TARC)的产生。此外，MPP处理抑制dncb诱导的Th2细胞因子的产生和CD4+ T细胞的浸润。结论:ESR1促进AD小鼠Th2免疫反应，增强Th2细胞因子。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

Iranian Journal of Immunology Medicine-Immunology and Allergy

CiteScore

1.60

自引率

0.00%

发文量

审稿时长

12 weeks

期刊介绍： The Iranian Journal of Immunology (I.J.I) is an internationally disseminated peer-reviewed publication and publishes a broad range of experimental and theoretical studies concerned with all aspects of immunology.