Cao Weitao, Wang Luyao, Mo Qiudi, Peng Fang, Hong Wei, Zhou Yumin, Sun Ruiting, Li Haiqing, Liang Chunxiao, Zhao Dongxing, Zheng Mengning, Li Bing, Peng Gongyong
State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Department of Respiratory, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Front Cell Dev Biol. 2024 Jul 12;12:1022181. doi: 10.3389/fcell.2024.1022181. eCollection 2024.
Pulmonary hypertension (PH) is a progressive disease affecting the lung vasculature that is characterized by sustained vasoconstriction and leads to vascular remodeling. The lung microbiome contributes to PH progression, but the function of the gut microbiome and the correlation between the gut microbiome and metabolome remain unclear. We have analyzed whether chronic hypoxia-induced PH alters the rat fecal microbiota.
We explored hypoxia-induced pulmonary hypertension model rats to find out the characteristic changes of intestinal microorganisms and metabolites of hypoxia-induced pulmonary hypertension, and provide a theoretical basis for clinical treatment.
In the current study, a chronic hypoxia-induced PH rat model was used to investigate the role of the gut microbiome and metabolome as a potential mechanism contributing to the occurrence and development of PH. 16S ribosomal ribonucleic acid (16S rRNA), short-chain fatty acid (SCFA) measurements, mass spectrometry (MS) metabolomics analysis and metatranscriptome were performed to analyze stool samples. The datasets were analyzed individually and integrated for combined analysis using bioinformatics approaches.
Our results suggest that the gut microbiome and metabolome of chronic hypoxia-induced PH rats are distinct from those of normoxic rats and may thus aid in the search for new therapeutic or diagnostic paradigms for PH.
The gut microbiome and metabolome are altered as a result of chronic hypoxia-induced PH. This imbalanced bacterial ecosystem might play a pathophysiological role in PH by altering homeostasis.
肺动脉高压（PH）是一种影响肺血管系统的进行性疾病，其特征是持续性血管收缩并导致血管重塑。肺部微生物群促成了PH的进展，但肠道微生物群的功能以及肠道微生物群与代谢组之间的相关性仍不清楚。我们分析了慢性缺氧诱导的PH是否会改变大鼠粪便微生物群。
探索缺氧诱导的肺动脉高压模型大鼠，以找出缺氧诱导的肺动脉高压肠道微生物和代谢产物的特征性变化，为临床治疗提供理论依据。
在本研究中，使用慢性缺氧诱导的PH大鼠模型来研究肠道微生物群和代谢组作为促成PH发生和发展的潜在机制的作用。对粪便样本进行16S核糖体核糖核酸（16S rRNA）、短链脂肪酸（SCFA）测量、质谱（MS）代谢组学分析和宏转录组分析。使用生物信息学方法对数据集进行单独分析并整合以进行综合分析。
我们的结果表明，慢性缺氧诱导的PH大鼠的肠道微生物群和代谢组与常氧大鼠不同，因此可能有助于寻找PH的新治疗或诊断模式。
慢性缺氧诱导的PH导致肠道微生物群和代谢组发生改变。这种失衡的细菌生态系统可能通过改变体内平衡在PH中发挥病理生理作用。
