Zhou Xiaolei, Guo Yunnian, Jian Xiaotong, Miao Xinyi, Wang Pengpeng, Wang Xiaoke, Wang Ling, Chen Huaiyong, Feng Feifei
Department of Respiratory and Critical Care Medicine, Henan Provincial Chest Hospital, Chest Hospital of Zhengzhou University, Zhengzhou 450003, China.
Department of Toxicology, College of Public Health, Zhengzhou University, Zhengzhou 453001, China.
Toxics. 2025 Apr 2;13(4):271. doi: 10.3390/toxics13040271.
O (ozone) is an environmental pollutant that can exacerbate inflammatory damage and contribute to respiratory diseases. However, the molecular mechanisms and potential targets for intervention in ozone-induced lung inflammatory injury are not yet known. To address this, our study exposed mice to 0.6 ppm and 1.0 ppm of O (3 h/d, 14 d), evaluating lung inflammation through histopathological examinations, lung function assessments, and analyses of white blood cells and inflammatory factors in BALF. Furthermore, we employed transcriptomic and non-targeted metabolomic approaches to decipher differentially expressed genes (DEGs) and metabolites in mouse lung tissue from the 1.0 ppm O exposure group. A comprehensive integration analysis of these omics data was conducted using Pearson correlation analysis. Finally, our findings show that ozone exposure indeed elicits pulmonary inflammation. Transcriptomic analysis identified 311 differentially expressed genes, predominantly implicated in circadian rhythm, IL-17 signaling pathway, and PPAR signaling. Meanwhile, metabolomic profiling revealed 41 differentially regulated metabolites, mainly associated with riboflavin metabolism, glutathione metabolism, and ABC transporter pathways. Integrated multi-omics analysis through Pearson correlation identified three key components (Pla2g10, O-phosphoethanolamine, and phosphorylcholine) showing significant enrichment in glycerophospholipid metabolism. Collectively, our findings suggest that glycerophospholipid metabolism may serve as potential therapeutic targets and diagnostic biomarkers for ozone-induced pulmonary inflammatory injury.
臭氧（O）是一种环境污染物，可加剧炎症损伤并导致呼吸系统疾病。然而，臭氧诱导的肺部炎症损伤的分子机制和潜在干预靶点尚不清楚。为了解决这个问题，我们的研究将小鼠暴露于0.6 ppm和1.0 ppm的臭氧中（每天3小时，共14天），通过组织病理学检查、肺功能评估以及对支气管肺泡灌洗液中的白细胞和炎症因子进行分析来评估肺部炎症。此外，我们采用转录组学和非靶向代谢组学方法来解析1.0 ppm臭氧暴露组小鼠肺组织中差异表达的基因（DEGs）和代谢物。使用Pearson相关性分析对这些组学数据进行了全面的整合分析。最后，我们的研究结果表明，臭氧暴露确实会引发肺部炎症。转录组分析确定了311个差异表达基因，主要涉及昼夜节律、IL-17信号通路和PPAR信号通路。同时，代谢组学分析揭示了41种差异调节的代谢物，主要与核黄素代谢、谷胱甘肽代谢和ABC转运蛋白途径有关。通过Pearson相关性进行的综合多组学分析确定了三个关键成分（磷脂酶A2G10、O-磷酸乙醇胺和磷酸胆碱），它们在甘油磷脂代谢中显示出显著富集。总的来说，我们的研究结果表明，甘油磷脂代谢可能是臭氧诱导的肺部炎症损伤的潜在治疗靶点和诊断生物标志物。
