Predicting Hyperoxia-Induced Lung Injury from Associated Intestinal and Lung Dysbiosis in Neonatal Mice

被引:10
作者
Chen, Chung-Ming [1 ,2 ]
Chou, Hsiu-Chu [3 ]
Yang, Yu-Chen S. H. [4 ]
Su, Emily Chia-Yu [5 ,6 ]
Liu, Yun-Ru [4 ]
机构
[1] Taipei Med Univ Hosp, Dept Pediat, 252 Wu Hsing St, Taipei 11030, Taiwan
[2] Taipei Med Univ, Coll Med, Sch Med, Dept Pediat, Taipei, Taiwan
[3] Taipei Med Univ, Coll Med, Sch Med, Dept Anat & Cell Biol, Taipei, Taiwan
[4] Taipei Med Univ, Off Human Res, Joint Biobank, Taipei, Taiwan
[5] Taipei Med Univ, Coll Med Sci & Technol, Grad Inst Biomed Informat, Taipei, Taiwan
[6] Taipei Med Univ Hosp, Clin Big Data Res Ctr, Taipei, Taiwan
关键词
Hyperoxia; Microbiota; Mean linear intercept; Radial alveolar count; Vascular endothelial growth factor; von Willebrand factor; Occludin; Zonula occludens;
D O I
10.1159/000513553
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Background: Preclinical studies have demonstrated that hyperoxia disrupts the intestinal barrier, changes the intestinal bacterial composition, and injures the lungs of newborn animals. Objectives: The aim of the study was to investigate the effects of hyperoxia on the lung and intestinal microbiota and the communication between intestinal and lung microbiota and to develop a predictive model for the identification of hyperoxia-induced lung injury from intestinal and lung microbiota based on machine learning algorithms in neonatal mice. Methods: Neonatal C57BL/6N mice were reared in either room air or hyperoxia (85% O-2) from postnatal days 1-7. On postnatal day 7, lung and intestinal microbiota were sampled from the left lung and lower gastrointestinal tract for 16S ribosomal RNA gene sequencing. Tissue from the right lung and terminal ileum were harvested for Western blot and histology analysis. Results: Hyperoxia induced intestinal injury, decreased intestinal tight junction expression, and impaired lung alveolarization and angiogenesis in neonatal mice. Hyperoxia also altered intestinal and lung microbiota and promoted bacterial translocation from the intestine to the lung as evidenced by the presence of intestinal bacteria in the lungs of hyperoxia-exposed neonatal mice. The relative abundance of these bacterial taxa was significantly positively correlated with the increased lung cytokines. Conclusions: Neonatal hyperoxia induced intestinal and lung dysbiosis and promoted bacterial translocation from the intestine to the lung. Further studies are needed to clarify the pathophysiology of bacterial translocation to the lung.
引用
收藏
页码:163 / 173
页数:11
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