Air Pollution Exposure Laboratory, Vancouver Coastal Health Research Institute, Division of Respiratory Medicine, University of British Columbia, Vancouver, BC, Canada.
Centre for Heart and Lung Innovation, St. Paul's Hospital, University of British Columbia, Vancouver, BC, Canada.
Environ Res. 2023 Jan 1;216(Pt 4):114826. doi: 10.1016/j.envres.2022.114826. Epub 2022 Nov 17.
The lung microbiome plays a crucial role in airway homeostasis, yet we know little about the effects of exposures such as air pollution therein. We conducted a controlled human exposure study to assess the impact of diesel exhaust (DE) on the human airway microbiome. Twenty-four participants (former smokers with mild to moderate COPD (N = 9), healthy former smokers (N = 7), and control healthy never smokers (N = 8)) were exposed to DE (300 μg/m PM) and filtered air (FA) for 2 h in a randomized order, separated by a 4-week washout. Endobronchial brushing samples were collected 24 h post-exposure and sequenced for the 16S microbiome, which was analyzed using QIIME2 and PICRUSt2 to examine diversity and metabolic functions, respectively. DE exposure altered airway microbiome metabolic functions in spite of statistically stable microbiome diversity. Affected functions included increases in: superpathway of purine deoxyribonucleosides degradation (pathway differential abundance 743.9, CI 95% 201.2 to 1286.6), thiazole biosynthesis I (668.5, CI 95% 139.9 to 1197.06), and L-lysine biosynthesis II (666.5, CI 95% 73.3 to 1257.7). There was an exposure-by-age effect, such that menaquinone biosynthesis superpathways were the most enriched function in the microbiome of participants aged >60, irrespective of smoking or health status. Moreover, exposure-by-phenotype analysis showed metabolic alterations in former smokers after DE exposure. These observations suggest that DE exposure induced substantial changes in the metabolic functions of the airway microbiome despite the absence of diversity changes.
肺部微生物组在气道稳态中起着至关重要的作用，但我们对其中暴露于空气污染物等因素的影响知之甚少。我们进行了一项对照人体暴露研究，以评估柴油废气（DE）对人类气道微生物组的影响。24 名参与者（有轻度至中度 COPD 的前吸烟者（N=9）、健康的前吸烟者（N=7）和健康的从不吸烟者对照（N=8））以随机顺序暴露于 DE（300μg/m PM）和过滤空气（FA）2 小时，间隔 4 周冲洗期。暴露后 24 小时采集支气管刷检样本进行 16S 微生物组测序，并使用 QIIME2 和 PICRUSt2 分别分析多样性和代谢功能。尽管微生物多样性在统计学上保持稳定，但 DE 暴露改变了气道微生物组的代谢功能。受影响的功能包括：嘌呤脱氧核糖核苷降解超级途径（途径差异丰度 743.9，CI95%201.2 至 1286.6）、噻唑生物合成 I（668.5，CI95%139.9 至 1197.06）和 L-赖氨酸生物合成 II（666.5，CI95%73.3 至 1257.7）的增加。存在暴露与年龄的效应，即对于年龄>60 岁的参与者，无论吸烟或健康状况如何，甲萘醌生物合成超级途径都是微生物组中最丰富的功能。此外，暴露与表型分析表明，DE 暴露后前吸烟者的代谢发生改变。这些观察结果表明，尽管多样性没有变化，DE 暴露仍会引起气道微生物组代谢功能的实质性变化。
