A multi-omics investigation of the lung injury induced by PM2.5 at environmental levels via the lung-gut axis

文献类型： 外文期刊

第一作者： Dai, Shuiping

作者： Dai, Shuiping;Wang, Zhenglu;Wang, Zhenglu;Cai, Min;Guo, Tingting;Mao, Shengqiang;Yang, Ying

作者机构：

关键词： PM2.5; Lung inflammation; Lung-gut axis; Microbiomes; Metabolomes; Multi-omics analysis

期刊名称：SCIENCE OF THE TOTAL ENVIRONMENT （ 影响因子：9.8； 五年影响因子：9.6 ）

ISSN： 0048-9697

年卷期： 2024 年 926 卷

页码：

收录情况： SCI

摘要： Long-term exposure to fine particulate matter (PM 2.5 ) posed injury for gastrointestinal and respiratory systems, ascribing with the lung -gut axis. However, the cross -talk mechanisms remain unclear. Here, we attempted to establish the response networks of lung -gut axis in mice exposed to PM 2.5 at environmental levels. Male Balb/c mice were exposed to PM 2.5 (dose of 0.1, 0.5, and 1.0 mg/kg) collected from Chengdu, China for 10 weeks, through intratracheally instillation, and examined the effect of PM 2.5 on lung functions of mice. The changes of lung and gut microbiota and metabolic profiles of mice in different groups were determined. Furthermore, the results of multi-omics were conjointly analyzed to elucidate the primary microbes and the associated metabolites in lung and gut responsible for PM 2.5 exposure. Accordingly, the cross -talk network and key pathways between lung -gut axis were established. The results indicated that exposed to PM 2.5 0.1 mg/kg induced obvious inflammations in mice lung, while emphysema was observed at 1.0 mg/kg. The levels of metabolites guanosine, hypoxanthine, and hepoxilin B3 increased in the lung might contribute to lung inflammations in exposure groups. For microbiotas in lung, PM 2.5 exposure significantly declined the proportions of Halomonas and Lactobacillus . Meanwhile, the metabolites in gut including L-tryptophan, serotonin, and spermidine were upregulated in exposure groups, which were linked to the decreasing of Oscillospira and Helicobacter in gut. Via lung -gut axis, the activations of pathways including Tryptophan metabolism, ABC transporters, Serotonergic synapse, and Linoleic acid metabolism contributed to the cross -talk between lung and gut tissues of mice mediated by PM 2.5 . In summary, the microbes including Lactobacillus , Oscillospira , and Parabacteroides , and metabolites including hepoxilin B3, guanosine, hypoxanthine, L-tryptophan, and spermidine were the main drivers. In this lung -gut axis study, we elucidated some proand pre-biotics in lung and gut microenvironments contributed to the adverse effects on lung functions induced by PM 2.5 exposure.

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