A multi-omics investigation of the lung injury induced by PM 2.5 at environmental levels via the lung-gut axis.

Autor: Dai S; National Center for Geriatrics Clinical Medicine Research, Department of Geriatrics and Gerontology, West China Hospital, Sichuan University, Chengdu 610041, PR China., Wang Z; West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu 610041, PR China. Electronic address: m18018567955@163.com., Cai M; Eco-environmental Protection Institute, Shanghai Academy of Agricultural Science, Shanghai 201403, PR China., Guo T; Institute of Respiratory Health, West China Hospital, Sichuan University, Chengdu 610041, PR China., Mao S; Institute of Respiratory Health, West China Hospital, Sichuan University, Chengdu 610041, PR China., Yang Y; Institute of Respiratory Health, West China Hospital, Sichuan University, Chengdu 610041, PR China.
Jazyk: angličtina
Zdroj: The Science of the total environment [Sci Total Environ] 2024 May 20; Vol. 926, pp. 172027. Date of Electronic Publication: 2024 Mar 27.
DOI: 10.1016/j.scitotenv.2024.172027
Abstrakt: 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 up-regulated 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 pro- and pre-biotics in lung and gut microenvironments contributed to the adverse effects on lung functions induced by PM 2.5 exposure.
Competing Interests: Declaration of competing interest The authors have declared that no competing interests exist.
(Copyright © 2024 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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