屋尘螨过敏小鼠模型中肺醋酸盐水平下降与2型过敏标志物升高相关

IF 4 2区 医学 Q2 ALLERGY
Roos E. M. Verstegen, Rolf W. Sparidans, Atanaska I. Kostadinova, Johan Garssen, Gert Folkerts, Rudi W. Hendriks, Linette E. M. Willemsen
{"title":"屋尘螨过敏小鼠模型中肺醋酸盐水平下降与2型过敏标志物升高相关","authors":"Roos E. M. Verstegen,&nbsp;Rolf W. Sparidans,&nbsp;Atanaska I. Kostadinova,&nbsp;Johan Garssen,&nbsp;Gert Folkerts,&nbsp;Rudi W. Hendriks,&nbsp;Linette E. M. Willemsen","doi":"10.1002/clt2.70082","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Aims</h3>\n \n <p>Microbial dysbiosis is an important feature in allergic asthma. Short-chain fatty acids (SCFA) produced by the intestinal microbiome play a role in the gut-lung axis. Little is known about how the gut SCFA levels reflect SCFA levels in other tissues and how these link to the allergic asthma inflammatory status.</p>\n </section>\n \n <section>\n \n <h3> Materials and Methods</h3>\n \n <p>Male BALB/c mice were intranasally exposed to house dust mite (HDM) to induce allergic airway inflammation. Acetate, propionate, and butyrate levels were determined in caecum content, serum and lungs of control and HDM-allergic mice using liquid chromatography-mass spectrometry. Faecal microbiome composition was determined by DNA sequencing.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>Mean acetate:propionate:butyrate ratios were 75:15:10 in caecum content, 98:1.5:0.5 in serum, and 38:61:1 in the lung. SCFA levels did not correlate across compartments and propionate was relatively high in the lungs. The faecal microbiome of allergic mice differed from control, with increased Desulfovibrionaceae abundance. The lung acetate proportion was lower in allergic mice compared to control. In allergic mice, declining lung acetate levels correlated with increased HDM-specific IgE in serum and IL-13 release by ex vivo HDM-restimulated lung cells. Ex vivo acetate supplementation did not inhibit HDM-restimulated lung cell IL-13 production, while butyrate and propionate did.</p>\n </section>\n \n <section>\n \n <h3> Conclusions</h3>\n \n <p>Overall, HDM-driven murine allergic airway inflammation induced changes in the faecal microbiome and reduced acetate in serum and lung tissue. Hereby, lung acetate levels correlated negatively with sensitisation and type-2 inflammation, but acetate itself did not suppress ex vivo HDM-induced cytokine release. Our findings provide new insights on the systemic effects of HDM-allergic inflammation along the gut-lung axis.</p>\n </section>\n </div>","PeriodicalId":10334,"journal":{"name":"Clinical and Translational Allergy","volume":"15 8","pages":""},"PeriodicalIF":4.0000,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/clt2.70082","citationCount":"0","resultStr":"{\"title\":\"Lung Acetate Levels Decline in Correlation With Increased Type 2 Allergic Markers in a House Dust Mite Allergic Mouse Model\",\"authors\":\"Roos E. M. Verstegen,&nbsp;Rolf W. Sparidans,&nbsp;Atanaska I. Kostadinova,&nbsp;Johan Garssen,&nbsp;Gert Folkerts,&nbsp;Rudi W. Hendriks,&nbsp;Linette E. M. Willemsen\",\"doi\":\"10.1002/clt2.70082\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Aims</h3>\\n \\n <p>Microbial dysbiosis is an important feature in allergic asthma. Short-chain fatty acids (SCFA) produced by the intestinal microbiome play a role in the gut-lung axis. Little is known about how the gut SCFA levels reflect SCFA levels in other tissues and how these link to the allergic asthma inflammatory status.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Materials and Methods</h3>\\n \\n <p>Male BALB/c mice were intranasally exposed to house dust mite (HDM) to induce allergic airway inflammation. Acetate, propionate, and butyrate levels were determined in caecum content, serum and lungs of control and HDM-allergic mice using liquid chromatography-mass spectrometry. Faecal microbiome composition was determined by DNA sequencing.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>Mean acetate:propionate:butyrate ratios were 75:15:10 in caecum content, 98:1.5:0.5 in serum, and 38:61:1 in the lung. SCFA levels did not correlate across compartments and propionate was relatively high in the lungs. The faecal microbiome of allergic mice differed from control, with increased Desulfovibrionaceae abundance. The lung acetate proportion was lower in allergic mice compared to control. In allergic mice, declining lung acetate levels correlated with increased HDM-specific IgE in serum and IL-13 release by ex vivo HDM-restimulated lung cells. Ex vivo acetate supplementation did not inhibit HDM-restimulated lung cell IL-13 production, while butyrate and propionate did.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Conclusions</h3>\\n \\n <p>Overall, HDM-driven murine allergic airway inflammation induced changes in the faecal microbiome and reduced acetate in serum and lung tissue. Hereby, lung acetate levels correlated negatively with sensitisation and type-2 inflammation, but acetate itself did not suppress ex vivo HDM-induced cytokine release. Our findings provide new insights on the systemic effects of HDM-allergic inflammation along the gut-lung axis.</p>\\n </section>\\n </div>\",\"PeriodicalId\":10334,\"journal\":{\"name\":\"Clinical and Translational Allergy\",\"volume\":\"15 8\",\"pages\":\"\"},\"PeriodicalIF\":4.0000,\"publicationDate\":\"2025-08-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1002/clt2.70082\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical and Translational Allergy\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1002/clt2.70082\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ALLERGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical and Translational Allergy","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/clt2.70082","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ALLERGY","Score":null,"Total":0}
引用次数: 0

摘要

目的微生物生态失调是过敏性哮喘的重要特征。肠道微生物组产生的短链脂肪酸(SCFA)在肠-肺轴中发挥作用。关于肠道SCFA水平如何反映其他组织中的SCFA水平以及这些与过敏性哮喘炎症状态的关系,我们知之甚少。材料与方法将雄性BALB/c小鼠经鼻暴露于屋尘螨(HDM)诱导变应性气道炎症。采用液相色谱-质谱法测定对照组和hdm过敏小鼠的盲肠内容物、血清和肺中的乙酸、丙酸和丁酸水平。通过DNA测序测定粪便微生物组组成。结果盲肠中乙酸:丙酸:丁酸的平均比值为75:15:10,血清中为98:1.5:0.5,肺中为38:61:1。SCFA水平在肺间室之间没有相关性,丙酸在肺中相对较高。过敏小鼠的粪便微生物群与对照组不同,有增加的Desulfovibrionaceae丰度。与对照组相比,过敏小鼠肺中醋酸盐比例较低。在过敏小鼠中,肺醋酸盐水平的下降与血清中hdm特异性IgE和体外hdm再刺激肺细胞释放IL-13的增加相关。体外补充醋酸盐不会抑制hdm刺激的肺细胞IL-13的产生,而丁酸盐和丙酸盐则会。总体而言,hdm驱动的小鼠过敏性气道炎症诱导了粪便微生物组的变化以及血清和肺组织中醋酸盐的减少。因此,肺醋酸盐水平与致敏和2型炎症呈负相关,但醋酸盐本身并不抑制体外hdm诱导的细胞因子释放。我们的研究结果为hdm过敏性炎症沿肠-肺轴的全身影响提供了新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Lung Acetate Levels Decline in Correlation With Increased Type 2 Allergic Markers in a House Dust Mite Allergic Mouse Model

Lung Acetate Levels Decline in Correlation With Increased Type 2 Allergic Markers in a House Dust Mite Allergic Mouse Model

Aims

Microbial dysbiosis is an important feature in allergic asthma. Short-chain fatty acids (SCFA) produced by the intestinal microbiome play a role in the gut-lung axis. Little is known about how the gut SCFA levels reflect SCFA levels in other tissues and how these link to the allergic asthma inflammatory status.

Materials and Methods

Male BALB/c mice were intranasally exposed to house dust mite (HDM) to induce allergic airway inflammation. Acetate, propionate, and butyrate levels were determined in caecum content, serum and lungs of control and HDM-allergic mice using liquid chromatography-mass spectrometry. Faecal microbiome composition was determined by DNA sequencing.

Results

Mean acetate:propionate:butyrate ratios were 75:15:10 in caecum content, 98:1.5:0.5 in serum, and 38:61:1 in the lung. SCFA levels did not correlate across compartments and propionate was relatively high in the lungs. The faecal microbiome of allergic mice differed from control, with increased Desulfovibrionaceae abundance. The lung acetate proportion was lower in allergic mice compared to control. In allergic mice, declining lung acetate levels correlated with increased HDM-specific IgE in serum and IL-13 release by ex vivo HDM-restimulated lung cells. Ex vivo acetate supplementation did not inhibit HDM-restimulated lung cell IL-13 production, while butyrate and propionate did.

Conclusions

Overall, HDM-driven murine allergic airway inflammation induced changes in the faecal microbiome and reduced acetate in serum and lung tissue. Hereby, lung acetate levels correlated negatively with sensitisation and type-2 inflammation, but acetate itself did not suppress ex vivo HDM-induced cytokine release. Our findings provide new insights on the systemic effects of HDM-allergic inflammation along the gut-lung axis.

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
Clinical and Translational Allergy
Clinical and Translational Allergy Immunology and Microbiology-Immunology
CiteScore
7.50
自引率
4.50%
发文量
117
审稿时长
12 weeks
期刊介绍: Clinical and Translational Allergy, one of several journals in the portfolio of the European Academy of Allergy and Clinical Immunology, provides a platform for the dissemination of allergy research and reviews, as well as EAACI position papers, task force reports and guidelines, amongst an international scientific audience. Clinical and Translational Allergy accepts clinical and translational research in the following areas and other related topics: asthma, rhinitis, rhinosinusitis, drug hypersensitivity, allergic conjunctivitis, allergic skin diseases, atopic eczema, urticaria, angioedema, venom hypersensitivity, anaphylaxis, food allergy, immunotherapy, immune modulators and biologics, animal models of allergic disease, immune mechanisms, or any other topic related to allergic disease.
×
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:604180095
Book学术官方微信