Airway microbiota dysbiosis and metabolic disorder in ozone and PM2.5 co-exposure induced lung inflammatory injury in mice

作者：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 · 发表于：Ecotoxicology and Environmental Safety · 年份：2024 · DOI：10.1016/j.ecoenv.2024.117626 · 被引用次数：6 · 研究领域：Medical and Biological Ozone Research、Air Quality and Health Impacts、Climate Change and Health Impacts

Co-exposure to ground-level ozone (O 3 ) and fine particles (PM 2.5 , ≤ 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 PM 2.5 and O 3 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, O 3 , PM 2.5 and co-exposure (O 3 + PM 2.5 ). Mice in the co-exposure group breathed O 3 and orally inhaled PM 2.5 suspension. The scenario for O 3 exposure was 0.6 ppm, 4 h/d, for 30 consecutive days while that for PM 2.5 exposure was oral inhalation of PM 2.5 suspension (5.6 mg/kg bw) once every other day and 4 h prior to O 3 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 O 3 and PM 2.5 exacerbated the pathological changes and inflammatory response induced by O 3 or PM 2.5 . Further studies revealed that co-exposure to O 3 and PM 2.5 increased the abundance of Prevotella in the airways and caused more severe metabolic disorders compared to O 3 or PM 2...