过敏刺激和糖皮质激素对CD4+T细胞中miR-155的影响。

IF 1.4 Q4 IMMUNOLOGY American journal of clinical and experimental immunology Pub Date : 2018-08-20 eCollection Date: 2018-01-01
Elizabeth Daniel, Alanna Roff, Man-Hsun Hsu, Ronaldo Panganiban, Kristin Lambert, Faoud Ishmael
{"title":"过敏刺激和糖皮质激素对CD4+T细胞中miR-155的影响。","authors":"Elizabeth Daniel, Alanna Roff, Man-Hsun Hsu, Ronaldo Panganiban, Kristin Lambert, Faoud Ishmael","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Rationale: </strong>MicroRNAs (miRNAs) are emerging as important regulators of allergic inflammation and potential therapeutic targets. We sought to identify which miRNAs are expressed in CD4<sup>+</sup> T-cells and determine whether allergic stimuli or glucocorticoids alter their expression.</p><p><strong>Methods: </strong>After IRB approval, blood was collected from dust mite (DM) allergic rhinitis subjects (n=20), non-allergic controls (n=8), and asthmatics (n=16). Peripheral blood mononuclear cells were incubated with dust mite extract (DME), diluent control, or DME + dexamethasone (0.1 µM). CD4<sup>+</sup> T-cells were collected by magnetic bead column, and RNA was isolated by guanidinium/phenol-chloroform extraction. MicroRNA expression was measured using Nanostring microarray and quantitative real time PCR (qPCR).</p><p><strong>Results: </strong>We identified 196 miRNAs that were stably expressed in circulating CD4<sup>+</sup> T-cells. Allergen stimulation of CD4<sup>+</sup> T-cells with DME differentially induced miR-155 expression in cells of DM-allergic subjects as compared to non-allergic subjects. Induction of miR-155 expression was also observed with anti-CD3/anti-CD28 simulation and phorbol-12-Myristate-13-Acetate (PMA) treatment, and further augmented by calcium inophore and bromocyclic AMP in the latter treatment. The level of miR-155 expression was positively associated with expression of the T<sub>H</sub>2 cytokines IL-5 and IL-13. Inhibition of miR-155 in Jurkat T-cells inhibited the production of these cytokines. Glucocorticoids attenuated the effects of dust mite allergen, raising the possibility that inhibition of this miRNA could be a mechanism through which glucocorticoids exhibit their anti-inflammatory effects. The CD4<sup>+</sup> T-cells had a higher level of miR-155 expression in asthma compared to in allergic rhinitis and non-asthmatics. The inhibitory effects of glucocorticoids on CD4<sup>+</sup> T-cell miR-155 expression were lost in severe asthmatics.</p><p><strong>Conclusion: </strong>Mir-155 is differentially expressed in allergic T-cells exposed to DM extract compared to in non-allergic cells and it is inhibited by glucocorticoids. MiR-155 may play a role in mediating allergic inflammation in T-cells and could be an anti-inflammatory target of steroids. This pathway may be de-regulated in severe asthma.</p>","PeriodicalId":72163,"journal":{"name":"American journal of clinical and experimental immunology","volume":"7 4","pages":"57-66"},"PeriodicalIF":1.4000,"publicationDate":"2018-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6146153/pdf/ajcei0007-0057.pdf","citationCount":"0","resultStr":"{\"title\":\"Effects of allergic stimulation and glucocorticoids on miR-155 in CD4<sup>+</sup> T-cells.\",\"authors\":\"Elizabeth Daniel, Alanna Roff, Man-Hsun Hsu, Ronaldo Panganiban, Kristin Lambert, Faoud Ishmael\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Rationale: </strong>MicroRNAs (miRNAs) are emerging as important regulators of allergic inflammation and potential therapeutic targets. We sought to identify which miRNAs are expressed in CD4<sup>+</sup> T-cells and determine whether allergic stimuli or glucocorticoids alter their expression.</p><p><strong>Methods: </strong>After IRB approval, blood was collected from dust mite (DM) allergic rhinitis subjects (n=20), non-allergic controls (n=8), and asthmatics (n=16). Peripheral blood mononuclear cells were incubated with dust mite extract (DME), diluent control, or DME + dexamethasone (0.1 µM). CD4<sup>+</sup> T-cells were collected by magnetic bead column, and RNA was isolated by guanidinium/phenol-chloroform extraction. MicroRNA expression was measured using Nanostring microarray and quantitative real time PCR (qPCR).</p><p><strong>Results: </strong>We identified 196 miRNAs that were stably expressed in circulating CD4<sup>+</sup> T-cells. Allergen stimulation of CD4<sup>+</sup> T-cells with DME differentially induced miR-155 expression in cells of DM-allergic subjects as compared to non-allergic subjects. Induction of miR-155 expression was also observed with anti-CD3/anti-CD28 simulation and phorbol-12-Myristate-13-Acetate (PMA) treatment, and further augmented by calcium inophore and bromocyclic AMP in the latter treatment. The level of miR-155 expression was positively associated with expression of the T<sub>H</sub>2 cytokines IL-5 and IL-13. Inhibition of miR-155 in Jurkat T-cells inhibited the production of these cytokines. Glucocorticoids attenuated the effects of dust mite allergen, raising the possibility that inhibition of this miRNA could be a mechanism through which glucocorticoids exhibit their anti-inflammatory effects. The CD4<sup>+</sup> T-cells had a higher level of miR-155 expression in asthma compared to in allergic rhinitis and non-asthmatics. The inhibitory effects of glucocorticoids on CD4<sup>+</sup> T-cell miR-155 expression were lost in severe asthmatics.</p><p><strong>Conclusion: </strong>Mir-155 is differentially expressed in allergic T-cells exposed to DM extract compared to in non-allergic cells and it is inhibited by glucocorticoids. MiR-155 may play a role in mediating allergic inflammation in T-cells and could be an anti-inflammatory target of steroids. This pathway may be de-regulated in severe asthma.</p>\",\"PeriodicalId\":72163,\"journal\":{\"name\":\"American journal of clinical and experimental immunology\",\"volume\":\"7 4\",\"pages\":\"57-66\"},\"PeriodicalIF\":1.4000,\"publicationDate\":\"2018-08-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6146153/pdf/ajcei0007-0057.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American journal of clinical and experimental immunology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2018/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q4\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American journal of clinical and experimental immunology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2018/1/1 0:00:00","PubModel":"eCollection","JCR":"Q4","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

理由:微小RNA(miRNA)正在成为过敏性炎症的重要调节因子和潜在的治疗靶点。我们试图确定哪些miRNA在CD4+T细胞中表达,并确定过敏刺激或糖皮质激素是否改变了它们的表达。方法:在IRB批准后,从尘螨(DM)过敏性鼻炎受试者(n=20)、非过敏性对照者(n=8)和哮喘患者(n=16)中采集血液。外周血单核细胞与尘螨提取物(DME)、稀释剂对照或DME+地塞米松(0.1µM)一起孵育。通过磁珠柱收集CD4+T细胞,并通过胍/苯酚-氯仿提取分离RNA。结果:我们鉴定出196个miRNA在循环CD4+T细胞中稳定表达。与非过敏性受试者相比,用DME刺激CD4+T细胞的过敏原在DM过敏受试者的细胞中差异诱导miR-155表达。用抗CD3/抗CD28模拟和佛波醇-12-嘧啶酸盐13-乙酸酯(PMA)处理也观察到miR-155表达的诱导,并在后一种处理中通过无孔钙和溴环AMP进一步增强。miR-155的表达水平与TH2细胞因子IL-5和IL-13的表达呈正相关。Jurkat T细胞中miR-155的抑制抑制了这些细胞因子的产生。糖皮质激素减弱了尘螨过敏原的作用,增加了抑制这种miRNA可能是糖皮质激素发挥抗炎作用的机制的可能性。CD4+T细胞在哮喘中的miR-155表达水平高于过敏性鼻炎和非哮喘患者。糖皮质激素对CD4+T细胞miR-155表达的抑制作用在严重哮喘患者中消失。结论:Mir-155在暴露于DM提取物的过敏性T细胞中与非过敏性细胞相比有差异表达,并且受到糖皮质激素的抑制。MiR-155可能在介导T细胞的过敏性炎症中发挥作用,并且可能是类固醇的抗炎靶点。这种途径可能在严重哮喘中被解除调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

摘要图片

分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Effects of allergic stimulation and glucocorticoids on miR-155 in CD4+ T-cells.

Rationale: MicroRNAs (miRNAs) are emerging as important regulators of allergic inflammation and potential therapeutic targets. We sought to identify which miRNAs are expressed in CD4+ T-cells and determine whether allergic stimuli or glucocorticoids alter their expression.

Methods: After IRB approval, blood was collected from dust mite (DM) allergic rhinitis subjects (n=20), non-allergic controls (n=8), and asthmatics (n=16). Peripheral blood mononuclear cells were incubated with dust mite extract (DME), diluent control, or DME + dexamethasone (0.1 µM). CD4+ T-cells were collected by magnetic bead column, and RNA was isolated by guanidinium/phenol-chloroform extraction. MicroRNA expression was measured using Nanostring microarray and quantitative real time PCR (qPCR).

Results: We identified 196 miRNAs that were stably expressed in circulating CD4+ T-cells. Allergen stimulation of CD4+ T-cells with DME differentially induced miR-155 expression in cells of DM-allergic subjects as compared to non-allergic subjects. Induction of miR-155 expression was also observed with anti-CD3/anti-CD28 simulation and phorbol-12-Myristate-13-Acetate (PMA) treatment, and further augmented by calcium inophore and bromocyclic AMP in the latter treatment. The level of miR-155 expression was positively associated with expression of the TH2 cytokines IL-5 and IL-13. Inhibition of miR-155 in Jurkat T-cells inhibited the production of these cytokines. Glucocorticoids attenuated the effects of dust mite allergen, raising the possibility that inhibition of this miRNA could be a mechanism through which glucocorticoids exhibit their anti-inflammatory effects. The CD4+ T-cells had a higher level of miR-155 expression in asthma compared to in allergic rhinitis and non-asthmatics. The inhibitory effects of glucocorticoids on CD4+ T-cell miR-155 expression were lost in severe asthmatics.

Conclusion: Mir-155 is differentially expressed in allergic T-cells exposed to DM extract compared to in non-allergic cells and it is inhibited by glucocorticoids. MiR-155 may play a role in mediating allergic inflammation in T-cells and could be an anti-inflammatory target of steroids. This pathway may be de-regulated in severe asthma.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Application research of core stability training based on biofeedback in postpartum rectus abdominis muscle separation. Characterization of immortalized human podocytes infected with lentivirus as an in vitro model of viral infection-associated podocytopathy. Interaction between intratumoral microbiota and neutrophils influences tumor progression. Preliminary findings on the absence of PEPITEM release in B cells isolated from Saudi donors: implications for expanded population studies. Advance in the mechanism and clinical research of myalgia in long COVID.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1