| Description |
This study subjected C57BL/6J mice to intermittent hypoxia (IH) treatment for 4 weeks. HE staining results showed that, compared to normoxic group mice, the lungs of mice in the intermittent hypoxia group exhibited significant inflammatory cell infiltration and alveolar wall thickening. ELISA results indicated that the levels of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α in the bronchoalveolar lavage fluid (BALF) of the intermittent hypoxia group mice were significantly increased, while the level of the anti-inflammatory cytokine IL-10 was decreased. To explore the effect of intermittent hypoxia on the pulmonary microbiome, we employed 16S rRNA gene sequencing technology. The results showed that in the pulmonary microbiome of the intermittent hypoxia group mice, the relative abundance of Firmicutes and Mycoplasma, which are associated with pro-inflammation, was significantly higher than that in the normoxic group. Meanwhile, the relative abundance of some species within the Proteobacteria phylum, which is associated with inflammation, and the anti-inflammatory Actinobacteriota phylum decreased. Furthermore, we used LC-MS metabolomics to analyze the metabolites in the bronchoalveolar lavage fluid. The results revealed that after intermittent hypoxia treatment, the pulmonary metabolic levels were significantly disrupted. The altered metabolites mainly included Prostaglandin E2, Stachydrine, Cohumulone, Nootkatone, and Embelin, which are related to various metabolic pathways. The involved metabolic pathways mainly include nicotinic acid and nicotinamide metabolism, regulation of inflammatory mediators by TRP channels, neuroactive ligand-receptor interaction, histidine metabolism, and nucleotide metabolism. |
