Wang Simin, Zhou Qixing, Tian Yingze, Hu Xiangang
Key Laboratory of Pollution Processes and Environmental Criteria (Ministry of Education)/Tianjin Key Laboratory of Environmental Remediation and Pollution Control, College of Environmental Science and Engineering, Nankai University, Tianjin 300350, China.
State Environmental Protection Key Laboratory of Urban Ambient Air Particulate Matter Pollution Prevention and Control, College of Environmental Science and Engineering, Nankai University, Tianjin 300350, China.
Environ Sci Technol. 2022 Sep 6;56(17):12368-12379. doi: 10.1021/acs.est.1c08888. Epub 2022 Aug 19.
Fine particulate matter (PM) 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 PM is poorly understood. This study tested the hypothesis that the lung microbiota affects pulmonary inflammation and oxidative stress induced by PM exposure. Mice were exposed to PM 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 PM-exposed mice, with increased abundance of and decreased abundance of . The altered composition of the microbiota was significantly correlated with pulmonary inflammation and oxidative stress-related indicators. Intranasal transfer of the pulmonary microbiota from PM-exposed mice affected pulmonary inflammation and oxidative stress caused by PM, as shown by increased proinflammatory cytokine levels and dysregulated oxidative damage-related biomarkers. Antibiotic intervention during PM 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 and increased abundance of . These results suggest that pulmonary microbial dysbiosis can promote and affect pulmonary inflammation and oxidative stress during PM exposure.
暴露于细颗粒物（PM）会通过引发炎症和氧化应激导致呼吸系统疾病。然而，肺部微生物群与PM所致肺部炎症和氧化应激进展之间的相关性却知之甚少。本研究检验了以下假设：肺部微生物群会影响PM暴露所致的肺部炎症和氧化应激。将小鼠经鼻暴露于PM中12天。然后，进行肺部微生物群移植和抗生素干预。进行了组织学检查、生物标志物指标检测和转录组分析。使用16S rRNA基因测序对肺部微生物群进行表征，结果显示，暴露于PM的小鼠中其多样性降低了75.2%，[具体菌属1]丰度增加，[具体菌属2]丰度降低。微生物群组成的改变与肺部炎症和氧化应激相关指标显著相关。经鼻移植暴露于PM的小鼠的肺部微生物群会影响PM所致的肺部炎症和氧化应激，表现为促炎细胞因子水平升高以及氧化损伤相关生物标志物失调。在PM暴露期间进行抗生素干预可减轻小鼠的肺部炎症和氧化损伤。抗生素治疗后肺部微生物群也出现了显著变化，表现为微生物群多样性增加、[具体菌属1]丰度降低以及[具体菌属2]丰度增加。这些结果表明，肺部微生物群失调可在PM暴露期间促进并影响肺部炎症和氧化应激。
