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ORIGINAL RESEARCH article

Front. Cell Dev. Biol.
Sec. Molecular and Cellular Pathology
Volume 12 - 2024 | doi: 10.3389/fcell.2024.1022181

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

Provisionally accepted
Weitao Cao Weitao Cao 1Luyao Wang Luyao Wang 1Qiudi Mo Qiudi Mo 1,2Fang Peng Fang Peng 1,3Wei Hong Wei Hong 1,4Yumin Zhou Yumin Zhou 1Ruiting Sun Ruiting Sun 1Haiqing Li Haiqing Li 1Chunxiao Liang Chunxiao Liang 1,5Dongxing Zhao Dongxing Zhao 1Mengning Zheng Mengning Zheng 6Bing Li Bing Li 4Gongyong Peng Gongyong Peng 1*
  • 1 State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China
  • 2 Department of Respiratory, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China
  • 3 Department of Critical Care Medicine, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China
  • 4 GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China
  • 5 Department of Thoracic Medicine, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Guangzhou, China
  • 6 Department of Respiratory and Critical Care Medicine, Guizhou Provincial People's Hospital, Guiyang, Guizhou Province, China

The final, formatted version of the article will be published soon.

    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.We explored hypoxia-induced pulmonary hypertension model rats to find out the characteristic changes of intestinal microorganisms and metabolites of hypoxiainduced 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.

    Keywords: chronic hypoxia, pH, gut microbiome, SCFAs, Gut metabolome

    Received: 18 Aug 2022; Accepted: 19 Jun 2024.

    Copyright: © 2024 Cao, Wang, Mo, Peng, Hong, Zhou, Sun, Li, Liang, Zhao, Zheng, Li and Peng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Gongyong Peng, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.