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肠道微生物衍生代谢物作为炎症性肠病的关键因素。

Gut microbiota-derived metabolites as key actors in inflammatory bowel disease.

机构信息

Sorbonne Université, Paris, France.

UMRS 938, Centre de Recherche Saint-Antoine (CRSA), Inserm, Paris, France.

出版信息

Nat Rev Gastroenterol Hepatol. 2020 Apr;17(4):223-237. doi: 10.1038/s41575-019-0258-z. Epub 2020 Feb 19.


DOI:10.1038/s41575-019-0258-z
PMID:32076145
Abstract

A key role of the gut microbiota in the establishment and maintenance of health, as well as in the pathogenesis of disease, has been identified over the past two decades. One of the primary modes by which the gut microbiota interacts with the host is by means of metabolites, which are small molecules that are produced as intermediate or end products of microbial metabolism. These metabolites can derive from bacterial metabolism of dietary substrates, modification of host molecules, such as bile acids, or directly from bacteria. Signals from microbial metabolites influence immune maturation, immune homeostasis, host energy metabolism and maintenance of mucosal integrity. Alterations in the composition and function of the microbiota have been described in many studies on IBD. Alterations have also been described in the metabolite profiles of patients with IBD. Furthermore, specific classes of metabolites, notably bile acids, short-chain fatty acids and tryptophan metabolites, have been implicated in the pathogenesis of IBD. This Review aims to define the key classes of microbial-derived metabolites that are altered in IBD, describe the pathophysiological basis of these associations and identify future targets for precision therapeutic modulation.

摘要

在过去的二十年中,人们已经确定了肠道微生物群在建立和维持健康以及疾病发病机制中的关键作用。肠道微生物群与宿主相互作用的主要方式之一是通过代谢物,这些小分子是微生物代谢的中间或终产物。这些代谢物可以来自细菌对膳食底物的代谢、宿主分子(如胆汁酸)的修饰,或直接来自细菌。微生物代谢物的信号影响免疫成熟、免疫稳态、宿主能量代谢和粘膜完整性的维持。在许多关于 IBD 的研究中都描述了微生物群组成和功能的改变。在 IBD 患者的代谢物谱中也描述了改变。此外,特定类别的代谢物,特别是胆汁酸、短链脂肪酸和色氨酸代谢物,与 IBD 的发病机制有关。这篇综述旨在定义在 IBD 中改变的关键类别的微生物衍生代谢物,描述这些关联的病理生理学基础,并确定用于精确治疗调节的未来靶点。

相似文献

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Gut microbiota-derived metabolites as key actors in inflammatory bowel disease.

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[2]
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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
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本文引用的文献

[1]
Microbial bile acid metabolites modulate gut RORγ regulatory T cell homeostasis.

Nature. 2019-12-25

[2]
Multi-omics of the gut microbial ecosystem in inflammatory bowel diseases.

Nature. 2019-5-29

[3]
A Forward Chemical Genetic Screen Reveals Gut Microbiota Metabolites That Modulate Host Physiology.

Cell. 2019-4-18

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A Weaning Reaction to Microbiota Is Required for Resistance to Immunopathologies in the Adult.

Immunity. 2019-3-19

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Nat Rev Immunol. 2019-5

[6]
Effect of Fecal Microbiota Transplantation on 8-Week Remission in Patients With Ulcerative Colitis: A Randomized Clinical Trial.

JAMA. 2019-1-15

[7]
Comparative analysis of Faecalibacterium prausnitzii genomes shows a high level of genome plasticity and warrants separation into new species-level taxa.

BMC Genomics. 2018-12-14

[8]
Gut microbiome structure and metabolic activity in inflammatory bowel disease.

Nat Microbiol. 2018-12-10

[9]
Transkingdom Networks: A Systems Biology Approach to Identify Causal Members of Host-Microbiota Interactions.

Methods Mol Biol. 2018

[10]
Dark matter in host-microbiome metabolomics: Tackling the unknowns-A review.

Anal Chim Acta. 2017-12-30

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