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肠道微生物组特征可区分健康人与肺结核患者。

The Gut Microbiome Signatures Discriminate Healthy From Pulmonary Tuberculosis Patients.

机构信息

State Key Laboratory of Animal Nutrition, College of Animal Science and Technology, China Agricultural University, Beijing, China.

CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.

出版信息

Front Cell Infect Microbiol. 2019 Apr 3;9:90. doi: 10.3389/fcimb.2019.00090. eCollection 2019.

DOI:10.3389/fcimb.2019.00090
PMID:31001490
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6456665/
Abstract

Cross talk occurs between the human gut and the lung through a gut-lung axis involving the gut microbiota. However, the signatures of the human gut microbiota after active infection have not been fully understood. Here, we investigated changes in the gut microbiota in tuberculosis (TB) patients by shotgun sequencing the gut microbiomes of 31 healthy controls and 46 patients. We observed a dramatic changes in gut microbiota in tuberculosis patients as reflected by significant decreases in species number and microbial diversity. The gut microbiota of TB patients were mostly featured by the striking decrease of short-chain fatty acids (SCFAs)-producingbacteria as well as associated metabolic pathways. A classification model based on the abundance of three species, , and , performed well for discriminating between healthy and diseased patients. Additionally, the healthy and diseased states can be distinguished by SNPs in the species of . We present a comprehensive profile of changes in the microbiota in clinical TB patients. Our findings will shed light on the design of future diagnoses and treatments for infections.

摘要

肠道与肺部通过涉及肠道微生物群的肠-肺轴进行交流。然而,人们对活动性感染后肠道微生物群的特征还没有完全了解。在这里,我们通过对 31 名健康对照者和 46 名患者的肠道微生物组进行鸟枪法测序,研究了结核病(TB)患者肠道微生物组的变化。我们观察到结核病患者的肠道微生物组发生了显著变化,反映在物种数量和微生物多样性显著减少。TB 患者的肠道微生物组主要以产生短链脂肪酸(SCFAs)的细菌以及相关代谢途径的显著减少为特征。基于三个物种丰度的分类模型 、 和 ,在区分健康和患病患者方面表现良好。此外,通过物种的 SNP 可以区分健康和患病状态。我们呈现了临床结核病患者肠道微生物组变化的综合特征。我们的发现将为未来感染的诊断和治疗设计提供启示。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd89/6456665/6574ac13607e/fcimb-09-00090-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd89/6456665/38f404d88f5e/fcimb-09-00090-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd89/6456665/ca297c2dc91a/fcimb-09-00090-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd89/6456665/7bd12c7decd6/fcimb-09-00090-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd89/6456665/6574ac13607e/fcimb-09-00090-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd89/6456665/38f404d88f5e/fcimb-09-00090-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd89/6456665/ca297c2dc91a/fcimb-09-00090-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd89/6456665/7bd12c7decd6/fcimb-09-00090-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd89/6456665/6574ac13607e/fcimb-09-00090-g0004.jpg

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Antibiotic treatment for Tuberculosis induces a profound dysbiosis of the microbiome that persists long after therapy is completed.抗结核治疗会导致微生物组发生深刻的失调,这种失调在治疗完成后会持续很长时间。
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Longitudinal profiling reveals a persistent intestinal dysbiosis triggered by conventional anti-tuberculosis therapy.
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