氧化应激
炎症
肺
免疫学
失调
生物标志物
蛋白质细菌
医学
生物
肠道菌群
内科学
细菌
生物化学
16S核糖体RNA
遗传学
作者
Simin Wang,Qixing Zhou,Yingze Tian,Xiangang Hu
标识
DOI:10.1021/acs.est.1c08888
摘要
Fine particulate matter (PM2.5) exposure causes respiratory diseases by inducing inflammation and oxidative stress. However, the correlation between the pulmonary microbiota and the progression of pulmonary inflammation and oxidative stress caused by PM2.5 is poorly understood. This study tested the hypothesis that the lung microbiota affects pulmonary inflammation and oxidative stress induced by PM2.5 exposure. Mice were exposed to PM2.5 intranasally for 12 days. Then, pulmonary microbiota transfer and antibiotic intervention were performed. Histological examinations, biomarker index detection, and transcriptome analyses were conducted. Characterization of the pulmonary microbiota using 16S rRNA gene sequencing showed that its diversity decreased by 75.2% in PM2.5-exposed mice, with increased abundance of Proteobacteria and decreased abundance of Bacteroidota. The altered composition of the microbiota was significantly correlated with pulmonary inflammation and oxidative stress-related indicators. Intranasal transfer of the pulmonary microbiota from PM2.5-exposed mice affected pulmonary inflammation and oxidative stress caused by PM2.5, as shown by increased proinflammatory cytokine levels and dysregulated oxidative damage-related biomarkers. Antibiotic intervention during PM2.5 exposure alleviated pulmonary inflammation and oxidative damage in mice. The pulmonary microbiota also showed substantial changes after antibiotic treatment, as reflected by the increased microbiota diversity, decreased abundance of Proteobacteria and increased abundance of Bacteroidota. These results suggest that pulmonary microbial dysbiosis can promote and affect pulmonary inflammation and oxidative stress during PM2.5 exposure.
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