慢性暴露于环境颗粒物会导致大鼠 COPD 模型中的肠道微生物失调。
Chronic exposure to ambient particulate matter induces gut microbial dysbiosis in a rat COPD model.
机构信息
Department of Allergy and Clinical Immunology, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510000, P.R. China.
Nanhai Hospital Southern Medical University, Foshan, 528000, P.R. China.
出版信息
Respir Res. 2020 Oct 19;21(1):271. doi: 10.1186/s12931-020-01529-3.
BACKGROUND
The role of the microbiota in the pathogenesis of chronic obstructive pulmonary disease (COPD) following exposure to ambient particulate matter (PM) is largely unknown.
METHODS
Fifty-four male Sprague-Dawley rats were exposed to clean air, biomass fuel (BMF), or motor vehicle exhaust (MVE) for 4, 12, and 24 weeks. We performed pulmonary inflammation evaluation, morphometric measurements, and lung function analysis in rat lung at three different times points during exposure. Lung and gut microbial composition was assessed by 16S rRNA pyrosequencing. Serum lipopolysaccharide levels were measured and short-chain fatty acids in colon contents were quantified.
RESULTS
After a 24-week PM exposure, rats exhibited pulmonary inflammation and pathological changes characteristic of COPD. The control and PM exposure (BMF and MVE) groups showed similar microbial diversity and composition in rat lung. However, the gut microbiota after 24 weeks PM exposure was characterized by decreased microbial richness and diversity, distinct overall microbial composition, lower levels of short-chain fatty acids, and higher serum lipopolysaccharide.
CONCLUSION
Chronic exposure to ambient particulate matter induces gut microbial dysbiosis and metabolite shifts in a rat model of chronic obstructive pulmonary disease.
背景
大气颗粒物（PM）暴露后慢性阻塞性肺疾病（COPD）发病机制中微生物群的作用在很大程度上尚不清楚。
方法
54 只雄性 Sprague-Dawley 大鼠分别暴露于清洁空气、生物质燃料（BMF）或机动车尾气（MVE）中 4、12 和 24 周。我们在暴露的三个不同时间点对大鼠肺部进行了肺部炎症评估、形态计量学测量和肺功能分析。通过 16S rRNA 焦磷酸测序评估肺和肠道微生物组成。测量血清脂多糖水平并定量结肠内容物中的短链脂肪酸。
结果
在 24 周的 PM 暴露后，大鼠表现出与 COPD 特征一致的肺部炎症和病理变化。对照和 PM 暴露（BMF 和 MVE）组大鼠肺部的微生物多样性和组成相似。然而，经过 24 周的 PM 暴露后，肠道微生物群的特征是微生物丰富度和多样性降低、整体微生物组成明显不同、短链脂肪酸水平较低和血清脂多糖水平较高。
结论
慢性暴露于大气颗粒物会导致慢性阻塞性肺疾病大鼠模型的肠道微生物失调和代谢物变化。
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