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代谢独立性驱动肠道微生物定植和在健康与疾病中的恢复力。

Metabolic independence drives gut microbial colonization and resilience in health and disease.

机构信息

Department of Medicine, The University of Chicago, Chicago, IL, 60637, USA.

Committee On Microbiology, The University of Chicago, Chicago, IL, 60637, USA.

出版信息

Genome Biol. 2023 Apr 17;24(1):78. doi: 10.1186/s13059-023-02924-x.

DOI:10.1186/s13059-023-02924-x
PMID:37069665
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10108530/
Abstract

BACKGROUND

Changes in microbial community composition as a function of human health and disease states have sparked remarkable interest in the human gut microbiome. However, establishing reproducible insights into the determinants of microbial succession in disease has been a formidable challenge.

RESULTS

Here we use fecal microbiota transplantation (FMT) as an in natura experimental model to investigate the association between metabolic independence and resilience in stressed gut environments. Our genome-resolved metagenomics survey suggests that FMT serves as an environmental filter that favors populations with higher metabolic independence, the genomes of which encode complete metabolic modules to synthesize critical metabolites, including amino acids, nucleotides, and vitamins. Interestingly, we observe higher completion of the same biosynthetic pathways in microbes enriched in IBD patients.

CONCLUSIONS

These observations suggest a general mechanism that underlies changes in diversity in perturbed gut environments and reveal taxon-independent markers of "dysbiosis" that may explain why widespread yet typically low-abundance members of healthy gut microbiomes can dominate under inflammatory conditions without any causal association with disease.

摘要

背景

人类健康和疾病状态下微生物群落组成的变化引起了人们对人类肠道微生物组的极大兴趣。然而,要确定疾病中微生物演替的决定因素,仍然是一个巨大的挑战。

结果

在这里,我们使用粪便微生物群移植(FMT)作为一种自然实验模型,来研究在应激肠道环境中代谢独立性和弹性之间的关联。我们基于基因组的宏基因组调查表明,FMT 是一种环境筛选器,有利于具有更高代谢独立性的种群,其基因组编码完整的代谢模块,以合成关键代谢物,包括氨基酸、核苷酸和维生素。有趣的是,我们观察到在 IBD 患者中富集的微生物中,相同生物合成途径的完成度更高。

结论

这些观察结果表明了在扰动的肠道环境中多样性变化的一般机制,并揭示了与疾病无关的“菌群失调”的分类群独立标志物,这可能解释了为什么健康肠道微生物组中广泛存在但通常丰度较低的成员在炎症条件下可以占主导地位,而与疾病没有任何因果关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0192/10108530/84a4cb4c5f62/13059_2023_2924_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0192/10108530/a37a548c4fee/13059_2023_2924_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0192/10108530/3412b937841e/13059_2023_2924_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0192/10108530/84a4cb4c5f62/13059_2023_2924_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0192/10108530/a37a548c4fee/13059_2023_2924_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0192/10108530/3412b937841e/13059_2023_2924_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0192/10108530/84a4cb4c5f62/13059_2023_2924_Fig3_HTML.jpg

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