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腹主动脉瘤肠道微生物群的宏基因组分析

Metagenomic Analysis of Gut Microbiota for Abdominal Aortic Aneurysm.

作者信息

Ito Eisaku, Ohki Takao, Toya Naoki, Emoto Takuo, Yamashita Tomoya, Sugiyama Tomomi, Yamada Takuji, Mori Hiroshi, Toyoda Atsushi, Hirata Ken-Ichi

机构信息

Division of Vascular Surgery, The Jikei University Kashiwa Hospital, Kashiwa, Chiba, Japan.

Division of Vascular Surgery, Department of Surgery, The Jikei University School of Medicine, Tokyo, Japan.

出版信息

Ann Vasc Dis. 2025;18(1). doi: 10.3400/avd.oa.24-00105. Epub 2025 Jan 7.

Abstract

The pathophysiological mechanism of abdominal aortic aneurysm (AAA) remains unclear. We previously reported that levels were reduced in the feces of patients with AAA by 16S ribosomal ribonucleic acid (RNA) gene sequencing. In this study, we increased the number of cases and conducted metagenomic analyses to examine bacterial genes associated with the pathophysiology of AAA. For gut microbiota data, feces from 55 patients with AAA and 52 patients with no history of AAA, lower extremity artery disease, or coronary artery disease (control group) were collected. Metagenomic analysis was performed by collecting raw stool samples from patients. For intestinal microbiota analysis, metagenomic analysis of the fecal samples was performed. Oral bacteria, including ( <0.0001), ( <0.001), ( <0.001), and sp. ( <0.001), were increased in the feces of patients with AAA. In addition, bacterial genes related to alpha lipoic acid (ALA) biosynthesis (M00882, M00883, and M00884, <0.0001) were decreased in patients with AAA. In the feces of patients with AAA, there was an increase in oral bacteria, and the expression of bacterial genes related to ALA biosynthesis was reduced. The results suggest the possibility of developing gut microbial drug treatments for AAA.

摘要

腹主动脉瘤(AAA)的病理生理机制尚不清楚。我们之前通过16S核糖体核糖核酸(RNA)基因测序报告称,AAA患者粪便中的水平降低。在本研究中,我们增加了病例数量并进行了宏基因组分析,以检查与AAA病理生理学相关的细菌基因。对于肠道微生物群数据,收集了55例AAA患者和52例无AAA病史、下肢动脉疾病或冠状动脉疾病患者(对照组)的粪便。通过收集患者的原始粪便样本进行宏基因组分析。对于肠道微生物群分析,对粪便样本进行宏基因组分析。AAA患者粪便中的口腔细菌,包括(<0.0001)、(<0.001)、(<0.001)和sp.(<0.001)增加。此外,与α硫辛酸(ALA)生物合成相关的细菌基因(M00882、M00883和M00884,<0.0001)在AAA患者中减少。在AAA患者的粪便中,口腔细菌增加,与ALA生物合成相关的细菌基因表达降低。结果表明开发针对AAA的肠道微生物药物治疗方法具有可能性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87b5/11771153/2bde8b673373/avd-18-1-24-00105-figure01.jpg

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