IL-1α is required for T cell-driven weight loss after respiratory viral infection

IF 7.9 2区 医学 Q1 IMMUNOLOGY Mucosal Immunology Pub Date : 2024-04-01 DOI:10.1016/j.mucimm.2024.02.005
Ziyin Wang , Leah F. Cuthbertson , Chubicka Thomas , Hadijatou J Sallah , Lucy G. Mosscrop , Haoyuan Li , Tiina Talts , Kartik Kumar , Miriam F. Moffatt , John S. Tregoning
{"title":"IL-1α is required for T cell-driven weight loss after respiratory viral infection","authors":"Ziyin Wang ,&nbsp;Leah F. Cuthbertson ,&nbsp;Chubicka Thomas ,&nbsp;Hadijatou J Sallah ,&nbsp;Lucy G. Mosscrop ,&nbsp;Haoyuan Li ,&nbsp;Tiina Talts ,&nbsp;Kartik Kumar ,&nbsp;Miriam F. Moffatt ,&nbsp;John S. Tregoning","doi":"10.1016/j.mucimm.2024.02.005","DOIUrl":null,"url":null,"abstract":"<div><p>Respiratory viral infections remain a major cause of hospitalization and death worldwide. Patients with respiratory infections often lose weight. While acute weight loss is speculated to be a tolerance mechanism to limit pathogen growth, severe weight loss following infection can cause quality of life deterioration. Despite the clinical relevance of respiratory infection-induced weight loss, its mechanism is not yet completely understood. We utilized a model of CD 8<sup>+</sup> T cell-driven weight loss during respiratory syncytial virus (RSV) infection to dissect the immune regulation of post-infection weight loss. Supporting previous data, bulk RNA sequencing indicated significant enrichment of the interleukin (IL)-1 signaling pathway after RSV infection. Despite increased viral load, infection-associated weight loss was significantly reduced after IL-1α (but not IL-1β) blockade. IL-1α depletion resulted in a reversal of the gut microbiota changes observed following RSV infection. Direct nasal instillation of IL-1α also caused weight loss. Of note, we detected IL-1α in the brain after either infection or nasal delivery. This was associated with changes in genes controlling appetite after RSV infection and corresponding changes in signaling molecules such as leptin and growth/differentiation factor 15. Together, these findings indicate a lung-brain-gut signaling axis for IL-1α in regulating weight loss after RSV infection.</p></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":null,"pages":null},"PeriodicalIF":7.9000,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1933021924000096/pdfft?md5=1e592548d066f32a36434581cfb5c3f6&pid=1-s2.0-S1933021924000096-main.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mucosal Immunology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1933021924000096","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Respiratory viral infections remain a major cause of hospitalization and death worldwide. Patients with respiratory infections often lose weight. While acute weight loss is speculated to be a tolerance mechanism to limit pathogen growth, severe weight loss following infection can cause quality of life deterioration. Despite the clinical relevance of respiratory infection-induced weight loss, its mechanism is not yet completely understood. We utilized a model of CD 8+ T cell-driven weight loss during respiratory syncytial virus (RSV) infection to dissect the immune regulation of post-infection weight loss. Supporting previous data, bulk RNA sequencing indicated significant enrichment of the interleukin (IL)-1 signaling pathway after RSV infection. Despite increased viral load, infection-associated weight loss was significantly reduced after IL-1α (but not IL-1β) blockade. IL-1α depletion resulted in a reversal of the gut microbiota changes observed following RSV infection. Direct nasal instillation of IL-1α also caused weight loss. Of note, we detected IL-1α in the brain after either infection or nasal delivery. This was associated with changes in genes controlling appetite after RSV infection and corresponding changes in signaling molecules such as leptin and growth/differentiation factor 15. Together, these findings indicate a lung-brain-gut signaling axis for IL-1α in regulating weight loss after RSV infection.

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
呼吸道病毒感染后,T 细胞驱动的体重减轻需要 IL-1α。
呼吸道病毒感染仍然是全球住院和死亡的主要原因。呼吸道感染患者通常会体重减轻。据推测,急性体重减轻是一种限制病原体生长的耐受机制,而感染后严重的体重减轻会导致生活质量下降。尽管呼吸道感染引起的体重减轻与临床相关,但其机制尚未完全明了。我们利用呼吸道合胞病毒(RSV)感染期间 CD8+ T 细胞驱动的体重减轻模型来剖析感染后体重减轻的免疫调节。大量 RNASeq 研究表明,RSV 感染后 IL-1 信号通路显著富集,这与之前的数据相吻合。尽管病毒载量增加,但阻断IL-1α(而非IL-1β)后,感染相关的体重下降明显减少。抑制IL-1α可逆转RSV感染后观察到的肠道微生物群变化。直接从鼻腔灌入IL-1α也会导致体重下降。值得注意的是,无论是感染还是鼻腔灌注,我们都在大脑中检测到了IL-1α。这与 RSV 感染后控制食欲基因的变化以及瘦素和 GDF15 等信号分子的相应变化有关。这些发现共同表明,IL-1α在调节RSV感染后体重减轻的过程中起着肺-脑-肠信号轴的作用。
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
Mucosal Immunology
Mucosal Immunology 医学-免疫学
CiteScore
16.60
自引率
3.80%
发文量
100
审稿时长
12 days
期刊介绍: Mucosal Immunology, the official publication of the Society of Mucosal Immunology (SMI), serves as a forum for both basic and clinical scientists to discuss immunity and inflammation involving mucosal tissues. It covers gastrointestinal, pulmonary, nasopharyngeal, oral, ocular, and genitourinary immunology through original research articles, scholarly reviews, commentaries, editorials, and letters. The journal gives equal consideration to basic, translational, and clinical studies and also serves as a primary communication channel for the SMI governing board and its members, featuring society news, meeting announcements, policy discussions, and job/training opportunities advertisements.
期刊最新文献
Airway macrophage glycolysis controls lung homeostasis and responses to aeroallergen. RelB and C/EBPα critically regulate the development of Peyer's patch mononuclear phagocytes. TRIM29 controls enteric RNA virus-induced intestinal inflammation by targeting NLRP6 and NLRP9b signaling pathways. A reappraisal of IL-9 in inflammation and cancer. Sensory neuroimmune interactions at the barrier.
×
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