The C/EBPβ-SESN2 Axis Promotes M2b Macrophage Polarization Induced by T.cp-MIF to Suppress Inflammation in Thelazia Callipaeda Infection.

IF 4.5 2区 医学 Q2 CELL BIOLOGY
Bo Luo, Yan-Ting Gou, Hong-Le Cui, Chang-Zhu Yin, Da Sun, Di Li, Ling-Jun Wang, Rong Yan, Hui Liu
{"title":"The C/EBPβ-SESN2 Axis Promotes M2b Macrophage Polarization Induced by T.cp-MIF to Suppress Inflammation in Thelazia Callipaeda Infection.","authors":"Bo Luo, Yan-Ting Gou, Hong-Le Cui, Chang-Zhu Yin, Da Sun, Di Li, Ling-Jun Wang, Rong Yan, Hui Liu","doi":"10.1007/s10753-024-02114-2","DOIUrl":null,"url":null,"abstract":"<p><p>Infection by the conjunctival sucking nematode Thelazia callipaeda results in ocular inflammation and immune impairment. T.cp-MIF, a macrophage migration inhibitor factor of T. callipaeda, can induce macrophage polarization and is involved in the host innate immune response, but little is known about the regulatory mechanisms and the actual immune effect. Understanding the immunoregulatory mechanisms carries significant clinical relevance for the development of novel preventative and therapeutic strategies. The macrophages were induced by T.cp-MIF in vitro, and the polarization direction at different times and the expression of inflammatory factors were detected by flow cytometry analysis, qPCR and western blotting. The key transcription factors and target genes were screened through transcriptome data, and the functions of transcription factors were verified by inhibition experiments in vitro. T.cp-MIF and T. callipaeda adult worms can cause inflammation of the ocular conjunctiva and macrophage infiltration. T.cp-MIF activated macrophages presenting M2b polarization after 48 h and played a role in inhibiting inflammation. Furthermore, based on the results of transcriptome data analysis and inhibition experiments, we demonstrate that this polarization is dependent on the involvement of the transcription factor C/EBPβ and its target gene SESN2. Our results demonstrated that the C/EBPβ-SESN2 axis plays an important regulatory role in T.cp-MIF-induced macrophage M2b polarization and it provides a new perspective for understanding the immune escape of ocular parasite infection.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":null,"pages":null},"PeriodicalIF":4.5000,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Inflammation","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s10753-024-02114-2","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Infection by the conjunctival sucking nematode Thelazia callipaeda results in ocular inflammation and immune impairment. T.cp-MIF, a macrophage migration inhibitor factor of T. callipaeda, can induce macrophage polarization and is involved in the host innate immune response, but little is known about the regulatory mechanisms and the actual immune effect. Understanding the immunoregulatory mechanisms carries significant clinical relevance for the development of novel preventative and therapeutic strategies. The macrophages were induced by T.cp-MIF in vitro, and the polarization direction at different times and the expression of inflammatory factors were detected by flow cytometry analysis, qPCR and western blotting. The key transcription factors and target genes were screened through transcriptome data, and the functions of transcription factors were verified by inhibition experiments in vitro. T.cp-MIF and T. callipaeda adult worms can cause inflammation of the ocular conjunctiva and macrophage infiltration. T.cp-MIF activated macrophages presenting M2b polarization after 48 h and played a role in inhibiting inflammation. Furthermore, based on the results of transcriptome data analysis and inhibition experiments, we demonstrate that this polarization is dependent on the involvement of the transcription factor C/EBPβ and its target gene SESN2. Our results demonstrated that the C/EBPβ-SESN2 axis plays an important regulatory role in T.cp-MIF-induced macrophage M2b polarization and it provides a new perspective for understanding the immune escape of ocular parasite infection.

Abstract Image

C/EBPβ-SESN2轴促进T.cp-MIF诱导的M2b巨噬细胞极化,从而抑制卡里巴蝇感染中的炎症。
结膜吸吮线虫(Thelazia callipaeda)感染会导致眼部炎症和免疫损伤。T.cp-MIF是T.callipaeda的一种巨噬细胞迁移抑制因子,可诱导巨噬细胞极化,参与宿主先天性免疫反应,但对其调节机制和实际免疫效果知之甚少。了解免疫调节机制对于开发新型预防和治疗策略具有重要的临床意义。研究人员在体外用 T.cp-MIF 诱导巨噬细胞,通过流式细胞仪分析、qPCR 和 Western 印迹法检测不同时期巨噬细胞的极化方向和炎症因子的表达。通过转录组数据筛选了关键转录因子和靶基因,并通过体外抑制实验验证了转录因子的功能。T.cp-MIF和T.callipaeda成虫可引起眼结膜炎症和巨噬细胞浸润。48 h后,T.cp-MIF能激活巨噬细胞,使其呈现M2b极化,并起到抑制炎症的作用。此外,根据转录组数据分析和抑制实验的结果,我们证明这种极化依赖于转录因子 C/EBPβ 及其靶基因 SESN2 的参与。我们的研究结果表明,C/EBPβ-SESN2轴在T.cp-MIF诱导的巨噬细胞M2b极化中起着重要的调控作用,它为理解眼寄生虫感染的免疫逃逸提供了一个新的视角。
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 求助全文
来源期刊
Inflammation
Inflammation 医学-免疫学
CiteScore
9.70
自引率
0.00%
发文量
168
审稿时长
3.0 months
期刊介绍: Inflammation publishes the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Contributions include full-length scientific reports, short definitive articles, and papers from meetings and symposia proceedings. The journal''s coverage includes acute and chronic inflammation; mediators of inflammation; mechanisms of tissue injury and cytotoxicity; pharmacology of inflammation; and clinical studies of inflammation and its modification.
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信