Airway microbiota dysbiosis and metabolic disorder in ozone and PM2.5 co-exposure induced lung inflammatory injury in mice
Co-exposure to ground-level ozone (O3) and fine particles (PM2.5, ≤ 2.5 µm in diameter) has become a primary scenario for air pollution exposure of urbanites in China. Recent studies have suggested a synergistic effect of PM2.5 and O3 on induction of lung inflammatory injury. However, the underlying...
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Elsevier
2025-01-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651324017020 |
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| author | Lin Yang Fei Xu Shuaiqi Zhao Yuling Zeng Qiong Wu Ling Zhang Saige Shi Fengquan Zhang Juan Li Zhen An Huijun Li Hui Wu Jie Song Weidong Wu |
| author_facet | Lin Yang Fei Xu Shuaiqi Zhao Yuling Zeng Qiong Wu Ling Zhang Saige Shi Fengquan Zhang Juan Li Zhen An Huijun Li Hui Wu Jie Song Weidong Wu |
| author_sort | Lin Yang |
| collection | DOAJ |
| description | Co-exposure to ground-level ozone (O3) and fine particles (PM2.5, ≤ 2.5 µm in diameter) has become a primary scenario for air pollution exposure of urbanites in China. Recent studies have suggested a synergistic effect of PM2.5 and O3 on induction of lung inflammatory injury. However, the underlying mechanisms for respiratory toxicity induced by this co-exposure have not been adequately elucidated. In this study, a realistic exposure was based to set up the co-exposure condition of an animal model. Specifically, eighty male C57BL/6 mice (10 months old) were randomly divided into four groups: control, O3, PM2.5 and co-exposure (O3 + PM2.5). Mice in the co-exposure group breathed O3 and orally inhaled PM2.5 suspension. The scenario for O3 exposure was 0.6 ppm, 4 h/d, for 30 consecutive days while that for PM2.5 exposure was oral inhalation of PM2.5 suspension (5.6 mg/kg bw) once every other day and 4 h prior to O3 exposure. After last exposure, bronchoalveolar lavage fluids (BALF) were collected for inflammatory biomarker measurement, 16S rRNA sequencing and metabolite profiling. Lung tissues were processed for histological examination. The results demonstrated that co-exposure to O3 and PM2.5 exacerbated the pathological changes and inflammatory response induced by O3 or PM2.5. Further studies revealed that co-exposure to O3 and PM2.5 increased the abundance of Prevotella in the airways and caused more severe metabolic disorders compared to O3 or PM2.5 exposure. Spearman correlation analysis demonstrated correlations among airway microbiota dysbiosis, metabolic disorder, inflammation, and pathological alterations induced by co-exposure to O3 and PM2.5. In summary, co-exposure to O3 and PM2.5 worsens airway inflammatory injury, possibly through interrelated airway microbiota dysbiosis and metabolic disorder. |
| format | Article |
| id | doaj-art-6cea86089e0c4089a76eb5e1729852c5 |
| institution | Kabale University |
| issn | 0147-6513 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj-art-6cea86089e0c4089a76eb5e1729852c52025-02-12T05:30:02ZengElsevierEcotoxicology and Environmental Safety0147-65132025-01-01290117626Airway microbiota dysbiosis and metabolic disorder in ozone and PM2.5 co-exposure induced lung inflammatory injury in miceLin Yang0Fei Xu1Shuaiqi Zhao2Yuling Zeng3Qiong Wu4Ling Zhang5Saige Shi6Fengquan Zhang7Juan Li8Zhen An9Huijun Li10Hui Wu11Jie Song12Weidong Wu13School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, ChinaSchool of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, ChinaSchool of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, ChinaSchool of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, ChinaSchool of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, ChinaSchool of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, ChinaSchool of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, ChinaSchool of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, ChinaSchool of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, ChinaSchool of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, ChinaSchool of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, ChinaSchool of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, ChinaSchool of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, ChinaCorresponding author.; School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, ChinaCo-exposure to ground-level ozone (O3) and fine particles (PM2.5, ≤ 2.5 µm in diameter) has become a primary scenario for air pollution exposure of urbanites in China. Recent studies have suggested a synergistic effect of PM2.5 and O3 on induction of lung inflammatory injury. However, the underlying mechanisms for respiratory toxicity induced by this co-exposure have not been adequately elucidated. In this study, a realistic exposure was based to set up the co-exposure condition of an animal model. Specifically, eighty male C57BL/6 mice (10 months old) were randomly divided into four groups: control, O3, PM2.5 and co-exposure (O3 + PM2.5). Mice in the co-exposure group breathed O3 and orally inhaled PM2.5 suspension. The scenario for O3 exposure was 0.6 ppm, 4 h/d, for 30 consecutive days while that for PM2.5 exposure was oral inhalation of PM2.5 suspension (5.6 mg/kg bw) once every other day and 4 h prior to O3 exposure. After last exposure, bronchoalveolar lavage fluids (BALF) were collected for inflammatory biomarker measurement, 16S rRNA sequencing and metabolite profiling. Lung tissues were processed for histological examination. The results demonstrated that co-exposure to O3 and PM2.5 exacerbated the pathological changes and inflammatory response induced by O3 or PM2.5. Further studies revealed that co-exposure to O3 and PM2.5 increased the abundance of Prevotella in the airways and caused more severe metabolic disorders compared to O3 or PM2.5 exposure. Spearman correlation analysis demonstrated correlations among airway microbiota dysbiosis, metabolic disorder, inflammation, and pathological alterations induced by co-exposure to O3 and PM2.5. In summary, co-exposure to O3 and PM2.5 worsens airway inflammatory injury, possibly through interrelated airway microbiota dysbiosis and metabolic disorder.http://www.sciencedirect.com/science/article/pii/S0147651324017020OzonePM2.5Co-exposureAirway inflammationMicrobiomeMetabolism |
| spellingShingle | Lin Yang Fei Xu Shuaiqi Zhao Yuling Zeng Qiong Wu Ling Zhang Saige Shi Fengquan Zhang Juan Li Zhen An Huijun Li Hui Wu Jie Song Weidong Wu Airway microbiota dysbiosis and metabolic disorder in ozone and PM2.5 co-exposure induced lung inflammatory injury in mice Ecotoxicology and Environmental Safety Ozone PM2.5 Co-exposure Airway inflammation Microbiome Metabolism |
| title | Airway microbiota dysbiosis and metabolic disorder in ozone and PM2.5 co-exposure induced lung inflammatory injury in mice |
| title_full | Airway microbiota dysbiosis and metabolic disorder in ozone and PM2.5 co-exposure induced lung inflammatory injury in mice |
| title_fullStr | Airway microbiota dysbiosis and metabolic disorder in ozone and PM2.5 co-exposure induced lung inflammatory injury in mice |
| title_full_unstemmed | Airway microbiota dysbiosis and metabolic disorder in ozone and PM2.5 co-exposure induced lung inflammatory injury in mice |
| title_short | Airway microbiota dysbiosis and metabolic disorder in ozone and PM2.5 co-exposure induced lung inflammatory injury in mice |
| title_sort | airway microbiota dysbiosis and metabolic disorder in ozone and pm2 5 co exposure induced lung inflammatory injury in mice |
| topic | Ozone PM2.5 Co-exposure Airway inflammation Microbiome Metabolism |
| url | http://www.sciencedirect.com/science/article/pii/S0147651324017020 |
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