Disease-associated gut microbiome and metabolome changes in rats with chronic hypoxia-induced pulmonary hypertension

代谢组 微生物群 缺氧(环境) 代谢组学 肺动脉高压 生物 肠道菌群 平衡 内科学 生物信息学 内分泌学 医学 免疫学 化学 氧气 有机化学
作者
Weitao Cao,Luyao Wang,Qiudi Mo,Fang Peng,Wei Hong,Yumin Zhou,Ruiting Sun,Haiqing Li,Chunxiao Liang,Dongxing Zhao,Mengning Zheng,Bing Li,Gongyong Peng
出处
期刊:Frontiers in Cell and Developmental Biology [Frontiers Media SA]
卷期号:12 被引量:1
标识
DOI:10.3389/fcell.2024.1022181
摘要

Background 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. Purpose 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. Methods 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. Results 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. Conclusion 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.
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