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HIV 和代谢功能障碍相关脂肪性肝病的肠道微生物组特征。

A gut microbiome signature for HIV and metabolic dysfunction-associated steatotic liver disease.

机构信息

Department of Infectious Diseases, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Madrid, Spain.

CIBER de Enfermedades Infecciosas (CIBERINFEC), Instituto de Salud Carlos III, Madrid, Spain.

出版信息

Front Immunol. 2023 Dec 14;14:1297378. doi: 10.3389/fimmu.2023.1297378. eCollection 2023.

DOI:10.3389/fimmu.2023.1297378
PMID:38162648
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10755913/
Abstract

INTRODUCTION

Metabolic dysfunction-associated steatotic liver disease (MASLD), has emerged as an increasingly recognized problem among people living with HIV (PLWH). The gut-liver axis is considered to be strongly implicated in the pathogenesis of MASLD. We aimed to characterize the gut microbiota composition in PLWH and MASLD and compare it with that of two control groups: PLWH without MASLD and individuals with MASLD without HIV infection.

METHODS

We collected clinical data and stool samples from participants. Bacterial 16S rRNA genes were amplified, sequenced, and clustered into operational taxonomic unit. Alpha diversity was studied by Shannon and Simpson indexes. To study how different the gut microbiota composition is between the different groups, beta diversity estimation was evaluated by principal coordinate analysis (PCoA) using Bray-Curtis dissimilarity. To further analyze differences in microbiome composition we performed a linear discriminant analysis (LDA) effect size (LEfSe).

RESULTS

We included 30 HIVMASLD, 30 HIVMASLD and 20 HIVMASLD participants. Major butyrate producers, including , , and dominated the microbiota in all three groups. Shannon's and Simpson's diversity metrics were higher among MASLD individuals (Kruskal-Wallis p = 0.047). Beta diversity analysis showed distinct clustering in MASLD, with MASLD participants overlapping regardless of HIV status (ADONIS significance <0.001). MASLD was associated with increased homogeneity across individuals, in contrast to that observed in the HIV+NAFDL- group, in which the dispersion was higher (Permanova test, p value <0.001; ANOSIM, p value <0.001). MASLD but not HIV determined a different microbiota structure (HIV vs. HIVMASLD, q-value = 0.002; HIVMASLD vs. HIVMASLD, q-value = 0.930; and HIVMASLD vs. HIVMASLD, q-value < 0.001). The most abundant genera in MASLD- were , and . In contrast, the most enriched genera in MASLD+ were , and

CONCLUSIONS

We found a microbiome signature linked to MASLD, which had a greater influence on the overall structure of the gut microbiota than HIV status alone.

摘要

简介

代谢功能障碍相关脂肪性肝病(MASLD)已成为人类免疫缺陷病毒(HIV)感染者中日益受到关注的问题。肠-肝轴被认为与 MASLD 的发病机制密切相关。本研究旨在描述 HIV 感染者伴 MASLD 患者的肠道微生物组成,并与 MASLD 无 HIV 感染者和 MASLD 无 HIV 感染者的两组对照进行比较。

方法

我们收集了参与者的临床数据和粪便样本。扩增、测序并将细菌 16S rRNA 基因聚类为操作分类单元。使用 Shannon 和 Simpson 指数研究 alpha 多样性。为了研究不同组之间肠道微生物组成的差异,通过主坐标分析(PCoA)使用 Bray-Curtis 不相似性评估 beta 多样性估计。为了进一步分析微生物组组成的差异,我们进行了线性判别分析(LDA)效应大小(LEfSe)。

结果

我们纳入了 30 名 HIVMASLD、30 名 HIVMASLD 和 20 名 HIVMASLD 患者。主要的丁酸盐生产者,包括 、 、和 ,在所有三组中均占主导地位。Shannon 和 Simpson 的多样性指标在 MASLD 个体中更高(Kruskal-Wallis p = 0.047)。β多样性分析显示 MASLD 患者明显聚类,无论 HIV 状态如何,MASLD 患者都有重叠(ADONIS 显著性 <0.001)。MASLD 与个体之间的同质性增加有关,而与 HIV+NAFDL-组观察到的情况相反,后者的离散度更高(Permanova 检验,p 值 <0.001;ANOSIM,p 值 <0.001)。MASLD 而不是 HIV 决定了不同的微生物群结构(HIV 与 HIVMASLD,q 值 = 0.002;HIVMASLD 与 HIVMASLD,q 值 = 0.930;HIVMASLD 与 HIVMASLD,q 值 <0.001)。MASLD-中最丰富的属是 、和 。相比之下,MASLD+中最丰富的属是 、和 。

结论

我们发现了与 MASLD 相关的微生物组特征,其对肠道微生物组的整体结构的影响大于 HIV 状态本身。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e28e/10755913/9a46ca068642/fimmu-14-1297378-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e28e/10755913/c07c70e8e014/fimmu-14-1297378-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e28e/10755913/9b34d620e73e/fimmu-14-1297378-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e28e/10755913/441e6b043b88/fimmu-14-1297378-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e28e/10755913/01ad3df4aef1/fimmu-14-1297378-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e28e/10755913/9a46ca068642/fimmu-14-1297378-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e28e/10755913/c07c70e8e014/fimmu-14-1297378-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e28e/10755913/9b34d620e73e/fimmu-14-1297378-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e28e/10755913/441e6b043b88/fimmu-14-1297378-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e28e/10755913/01ad3df4aef1/fimmu-14-1297378-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e28e/10755913/9a46ca068642/fimmu-14-1297378-g005.jpg

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