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肠道微生物群移植后定植失败会加剧葡聚糖硫酸钠(DSS)诱导的结肠炎。

Failure of colonization following gut microbiota transfer exacerbates DSS-induced colitis.

作者信息

Gustafson Kevin L, Rodriguez Trevor R, McAdams Zachary L, Coghill Lyndon M, Ericsson Aaron C, Franklin Craig L

机构信息

Department of Veterinary Pathobiology, University of Missouri, Columbia, MO 65201, USA.

Comparative Medicine Program, University of Missouri, Columbia, MO 65201, USA.

出版信息

bioRxiv. 2024 Sep 25:2024.09.25.614792. doi: 10.1101/2024.09.25.614792.

DOI:10.1101/2024.09.25.614792
PMID:39386691
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11463381/
Abstract

To study the impact of differing specific pathogen-free gut microbiomes (GMs) on a murine model of inflammatory bowel disease, selected GMs were transferred using embryo transfer (ET), cross-fostering (CF), and co-housing (CH). Prior work showed that the GM transfer method and the microbial composition of donor and recipient GMs can influence microbial colonization and disease phenotypes in dextran sodium sulfate-induced colitis. When a low richness GM was transferred to a recipient with a high richness GM via CH, the donor GM failed to successfully colonize, and a more severe disease phenotype resulted when compared to ET or CF, where colonization was successful. By comparing CH and gastric gavage for fecal material transfer, we isolated the microbial component of this effect and determined that differences in disease severity and survival were associated with microbial factors rather than the transfer method itself. Mice receiving a low richness GM via CH and gastric gavage exhibited greater disease severity and higher expression of pro-inflammatory immune mediators compared to those receiving a high richness GM. This study provides valuable insights into the role of GM composition and colonization in disease modulation.

摘要

为了研究不同的无特定病原体肠道微生物群(GMs)对炎症性肠病小鼠模型的影响,采用胚胎移植(ET)、交叉寄养(CF)和同笼饲养(CH)的方法转移选定的GMs。先前的研究表明,GM转移方法以及供体和受体GMs的微生物组成会影响葡聚糖硫酸钠诱导的结肠炎中的微生物定植和疾病表型。当通过CH将低丰富度的GM转移到高丰富度GM的受体时,供体GM未能成功定植,与成功定植的ET或CF相比,疾病表型更严重。通过比较CH和胃灌胃进行粪便物质转移,我们分离出了这种效应的微生物成分,并确定疾病严重程度和存活率的差异与微生物因素有关,而不是转移方法本身。与接受高丰富度GM的小鼠相比,通过CH和胃灌胃接受低丰富度GM的小鼠表现出更严重的疾病和促炎免疫介质的更高表达。这项研究为GM组成和定植在疾病调节中的作用提供了有价值的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b121/11463381/01c949e969c9/nihpp-2024.09.25.614792v1-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b121/11463381/03728dbbfa87/nihpp-2024.09.25.614792v1-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b121/11463381/0f558d5de6f1/nihpp-2024.09.25.614792v1-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b121/11463381/3890675a46e6/nihpp-2024.09.25.614792v1-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b121/11463381/01c949e969c9/nihpp-2024.09.25.614792v1-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b121/11463381/03728dbbfa87/nihpp-2024.09.25.614792v1-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b121/11463381/0f558d5de6f1/nihpp-2024.09.25.614792v1-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b121/11463381/3890675a46e6/nihpp-2024.09.25.614792v1-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b121/11463381/01c949e969c9/nihpp-2024.09.25.614792v1-f0004.jpg

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本文引用的文献

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2
Human gut microbiota in health and disease: Unveiling the relationship.健康与疾病中的人类肠道微生物群:揭示其关系。
Front Microbiol. 2022 Sep 26;13:999001. doi: 10.3389/fmicb.2022.999001. eCollection 2022.
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Novel antigen-presenting cell imparts T-dependent tolerance to gut microbiota.新型抗原呈递细胞赋予肠道菌群 T 细胞依赖型耐受。
Nature. 2022 Oct;610(7933):752-760. doi: 10.1038/s41586-022-05309-5. Epub 2022 Sep 7.
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Role of Gut Microbiome in Autism Spectrum Disorder and Its Therapeutic Regulation.肠道微生物群在自闭症谱系障碍中的作用及其治疗调节。
Front Cell Infect Microbiol. 2022 Jul 22;12:915701. doi: 10.3389/fcimb.2022.915701. eCollection 2022.
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Imbalanced gut microbiota fuels hepatocellular carcinoma development by shaping the hepatic inflammatory microenvironment.肠道微生物菌群失衡通过塑造肝脏炎症微环境促进肝癌发展。
Nat Commun. 2022 Jul 8;13(1):3964. doi: 10.1038/s41467-022-31312-5.
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Microbiota in health and diseases.肠道菌群与健康和疾病。
Signal Transduct Target Ther. 2022 Apr 23;7(1):135. doi: 10.1038/s41392-022-00974-4.
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