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肺动脉高压大鼠肠道真菌微生物群的改变

Gut Fungal Microbiota Alterations in Pulmonary Arterial Hypertensive Rats.

作者信息

Chen Yihang, Meng Liukun, Yuan Wen, Gao Zehan, Zhang Xun, Xie Boqia, Song Jiawei, Li Jifeng, Zhong Jiuchang, Liu Xiaoyan

机构信息

Department of Cardiology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.

Heart Center and Beijing Key Laboratory of Hypertension, Beijing Institute of Respiratory Medicine, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.

出版信息

Biomedicines. 2024 Jan 27;12(2):298. doi: 10.3390/biomedicines12020298.

DOI:10.3390/biomedicines12020298
PMID:38397900
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10886911/
Abstract

The gut microbiome's imbalance has been implicated in the pathogenesis of pulmonary arterial hypertension (PAH), yet the contribution of the gut mycobiome remains largely unclear. This study delineates the gut mycobiome profile in PAH and examines its interplay with the bacterial microbiome alterations. Fecal samples from monocrotaline-induced PAH rats and matched controls were subjected to internal transcribed spacer 1 (ITS1) sequencing for fungal community assessment and 16S ribosomal RNA (rRNA) gene sequencing for bacterial community characterization. Comparative analysis revealed no significant disparities in the overall mycobiome diversity between the PAH and control groups. However, taxonomic profiling identified differential mycobiome compositions, with the PAH group exhibiting a significant enrichment of genera such as and Conversely, genera , and were more abundant in the controls. Correlations of and abundance with hemodynamic parameters were observed. Indications of bidirectional fungal-bacterial community interactions were also noted. This investigation reveals distinct gut mycobiome alterations in PAH, which are intricately associated with concurrent bacterial microbiome changes, suggesting a possible contributory role of gut fungi in PAH pathophysiology. These findings underscore the potential for novel gut mycobiome-targeted therapeutic interventions in PAH management.

摘要

肠道微生物群的失衡与肺动脉高压(PAH)的发病机制有关,但肠道真菌微生物群的作用仍不清楚。本研究描绘了PAH患者的肠道真菌微生物群特征,并研究了其与细菌微生物群变化的相互作用。对用野百合碱诱导的PAH大鼠和配对对照的粪便样本进行内转录间隔区1(ITS1)测序以评估真菌群落,并用16S核糖体RNA(rRNA)基因测序来表征细菌群落。比较分析显示,PAH组和对照组之间的总体真菌微生物群多样性没有显著差异。然而,分类学分析确定了不同的真菌微生物群组成,PAH组中 属和 属等显著富集。相反, 属、 属和 属在对照组中更为丰富。观察到 属和 属丰度与血流动力学参数之间的相关性。还注意到真菌-细菌群落双向相互作用的迹象。这项研究揭示了PAH患者肠道真菌微生物群的明显变化,这些变化与同时发生的细菌微生物群变化密切相关,表明肠道真菌在PAH病理生理学中可能起作用。这些发现强调了针对肠道真菌微生物群的新型治疗干预措施在PAH管理中的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ff/10886911/0d224ccec98c/biomedicines-12-00298-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ff/10886911/7a2f7a01a6b1/biomedicines-12-00298-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ff/10886911/acb53f1f3e4b/biomedicines-12-00298-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ff/10886911/1539a4802b7f/biomedicines-12-00298-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ff/10886911/b396bd2e8ae0/biomedicines-12-00298-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ff/10886911/abe7afd8fec9/biomedicines-12-00298-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ff/10886911/0d224ccec98c/biomedicines-12-00298-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ff/10886911/7a2f7a01a6b1/biomedicines-12-00298-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ff/10886911/acb53f1f3e4b/biomedicines-12-00298-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ff/10886911/1539a4802b7f/biomedicines-12-00298-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ff/10886911/b396bd2e8ae0/biomedicines-12-00298-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ff/10886911/abe7afd8fec9/biomedicines-12-00298-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ff/10886911/0d224ccec98c/biomedicines-12-00298-g006.jpg

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Connections between serum Trimethylamine N-Oxide (TMAO), a gut-derived metabolite, and vascular biomarkers evaluating arterial stiffness and subclinical atherosclerosis in children with obesity.血清三甲胺 N-氧化物(TMAO)与血管生物标志物之间的关系,TMAO 是一种肠道衍生代谢物,可评估肥胖儿童的动脉僵硬度和亚临床动脉粥样硬化。
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Enteric fungi protect against intestinal ischemia-reperfusion injury via inhibiting the SAA1-GSDMD pathway.
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