Probiotic nucleotides increase IL-10 expression in airway macrophages to mitigate airway allergy.

IF 4.8 3区 医学 Q2 CELL BIOLOGY Inflammation Research Pub Date : 2024-11-01 Epub Date: 2024-09-05 DOI:10.1007/s00011-024-01940-2
Jinmei Xue, Zhizhen Liu, Bailing Xie, Rui Dong, Juan Wu, Yisha Wu, Zhihan Xu, Yuhe Tian, Yao Wei, Zhigang Geng, Lei Lu, Yu Liu, Jun Xie, Pingchang Yang
{"title":"Probiotic nucleotides increase IL-10 expression in airway macrophages to mitigate airway allergy.","authors":"Jinmei Xue, Zhizhen Liu, Bailing Xie, Rui Dong, Juan Wu, Yisha Wu, Zhihan Xu, Yuhe Tian, Yao Wei, Zhigang Geng, Lei Lu, Yu Liu, Jun Xie, Pingchang Yang","doi":"10.1007/s00011-024-01940-2","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Dysfunctional immune regulation plays a crucial role in the pathogenesis of airway allergies. Macrophages are one of the components of the immune regulation cells. The aim of this study is to elucidate the role of lysine demethylase 5 A (KDM5A) in maintaining macrophages' immune regulatory ability.</p><p><strong>Methods: </strong>DNA was extracted from Lactobacillus rhamnosus GG to be designated as LgDNA. LgDNA was administered to the mice through nasal instillations. M2 macrophages (M2 cells) were isolated from the airway tissues using flow cytometry.</p><p><strong>Results: </strong>We found that airway M2 cells of mice with airway Th2 polarization had reduced amounts of IL-10 and KDM5A. Mice with Kdm5a deficiency in M2 cells showed the airway Th2 polarization. The expression of Kdm5a in airway M2 cells was enhanced by nasal instillations containing LgDNA. KDM5A mediated the effects of LgDNA on inducing the Il10 expression in airway M2 cells. Administration of LgDNA mitigated experimental airway allergy.</p><p><strong>Conclusions: </strong>M2 macrophages in the airway tissues of mice with airway allergy show low levels of KDM5A. By upregulating KDM5A expression, LgDNA can increase Il10 expression and reconcile airway Th2 polarization.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":" ","pages":"1919-1930"},"PeriodicalIF":4.8000,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Inflammation Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s00011-024-01940-2","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/9/5 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Dysfunctional immune regulation plays a crucial role in the pathogenesis of airway allergies. Macrophages are one of the components of the immune regulation cells. The aim of this study is to elucidate the role of lysine demethylase 5 A (KDM5A) in maintaining macrophages' immune regulatory ability.

Methods: DNA was extracted from Lactobacillus rhamnosus GG to be designated as LgDNA. LgDNA was administered to the mice through nasal instillations. M2 macrophages (M2 cells) were isolated from the airway tissues using flow cytometry.

Results: We found that airway M2 cells of mice with airway Th2 polarization had reduced amounts of IL-10 and KDM5A. Mice with Kdm5a deficiency in M2 cells showed the airway Th2 polarization. The expression of Kdm5a in airway M2 cells was enhanced by nasal instillations containing LgDNA. KDM5A mediated the effects of LgDNA on inducing the Il10 expression in airway M2 cells. Administration of LgDNA mitigated experimental airway allergy.

Conclusions: M2 macrophages in the airway tissues of mice with airway allergy show low levels of KDM5A. By upregulating KDM5A expression, LgDNA can increase Il10 expression and reconcile airway Th2 polarization.

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
益生菌核苷酸能增加气道巨噬细胞中 IL-10 的表达,从而缓解气道过敏。
背景:免疫调节功能失调在气道过敏的发病机制中起着至关重要的作用。巨噬细胞是免疫调节细胞的组成部分之一。本研究旨在阐明赖氨酸去甲基化酶 5 A(KDM5A)在维持巨噬细胞免疫调节能力中的作用:方法:从鼠李糖乳杆菌 GG 中提取 DNA,命名为 LgDNA。小鼠通过鼻腔注射 LgDNA。使用流式细胞术从气道组织中分离出 M2 巨噬细胞(M2 细胞):结果:我们发现气道 Th2 极化的小鼠气道 M2 细胞的 IL-10 和 KDM5A 含量降低。M2细胞缺乏Kdm5a的小鼠表现出气道Th2极化。含有 LgDNA 的鼻腔灌注增强了气道 M2 细胞中 Kdm5a 的表达。KDM5A介导了LgDNA诱导气道M2细胞表达Il10的作用。结论:结论:气道过敏小鼠气道组织中的 M2 巨噬细胞显示出较低水平的 KDM5A。通过上调 KDM5A 的表达,LgDNA 可以增加 Il10 的表达,并调和气道 Th2 极化。
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
Inflammation Research
Inflammation Research 医学-免疫学
CiteScore
9.90
自引率
1.50%
发文量
134
审稿时长
3-8 weeks
期刊介绍: Inflammation Research (IR) publishes peer-reviewed papers on all aspects of inflammation and related fields including histopathology, immunological mechanisms, gene expression, mediators, experimental models, clinical investigations and the effect of drugs. Related fields are broadly defined and include for instance, allergy and asthma, shock, pain, joint damage, skin disease as well as clinical trials of relevant drugs.
期刊最新文献
Gastrin-releasing peptide receptor antagonist RC-3095 inhibits Porphyromonas gingivalis lipopolysaccharide-accelerated atherosclerosis by suppressing inflammatory responses in endothelial cells and macrophages. Inhibition of glycolytic reprogramming suppresses innate immune-mediated inflammation in experimental amyotrophic lateral sclerosis. Calprotectin is regulated by IL-17A and induces steroid hyporesponsiveness in asthma. Treatment with lipoxin A4 improves influenza A infection outcome, induces macrophage reprogramming, anti-inflammatory and pro-resolutive responses. A novel molecular classification based on efferocytosis-related genes for predicting clinical outcome and treatment response in acute myeloid leukemia.
×
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