International Collaborative Laboratory for Air Pollution Health Effects and Intervention, School of Public Health, Xinxiang Medical University, Xinxiang, Henan 453003, China.
International Collaborative Laboratory for Air Pollution Health Effects and Intervention, School of Public Health, Xinxiang Medical University, Xinxiang, Henan 453003, China.
J Hazard Mater. 2024 Dec 5;480:135800. doi: 10.1016/j.jhazmat.2024.135800. Epub 2024 Sep 12.
The global ambient temperature has been rising in recent decades and high temperature is usually accompanied by ozone (O) pollution. Environmental change is an underlying factor for the increased prevalence of respiratory allergic disease. However, the potential mechanisms are complex and remain elusive. This study was performed to reveal toxic effects and molecular mechanisms of O or/and high temperature induced allergic rhinitis (AR) deterioration. The results indicated that O and high temperature co-exposure exacerbated rhinitis symptoms, destroyed ultrastructure of nasal mucosa and down-regulated the expression of nasal epithelial barrier structural proteins ZO-1 and occludin. Moreover, the levels of total protein and lactate dehydrogenase (LDH) in nasal lavage fluid and the levels of IL-1β and TNF-α in serum also exhibited a significant upward trend. Transcriptomic analysis revealed that immune and inflammatory signaling pathways such as IL-17 signaling pathway was involved in the combined toxicity of O and high temperature. Microbiome examination showed that Prevotella and Elizabethkingia were linked to nasal injury. What's more, spearman correlation analysis revealed correlations among nasal microbiota dysbiosis, inflammation and injury. To sum up, the present study assessed the combined toxicity of O and high temperature and found potential mechanisms, which provided important experimental evidence for making preventive intervention strategies and protecting vulnerable populations.
近几十年来,全球环境温度一直在上升,高温通常伴随着臭氧(O)污染。环境变化是导致呼吸道过敏性疾病发病率上升的一个潜在因素。然而,潜在的机制很复杂,仍然难以捉摸。本研究旨在揭示 O 和/或高温引起的过敏性鼻炎(AR)恶化的毒性作用和分子机制。结果表明,O 和高温共同暴露会加重鼻炎症状,破坏鼻黏膜超微结构,并下调鼻上皮屏障结构蛋白 ZO-1 和闭合蛋白的表达。此外,鼻灌洗液中的总蛋白和乳酸脱氢酶(LDH)水平以及血清中的 IL-1β 和 TNF-α 水平也呈显著上升趋势。转录组分析显示,IL-17 信号通路等免疫和炎症信号通路参与了 O 和高温的联合毒性作用。微生物组检查显示,普雷沃氏菌属和伊丽莎白菌属与鼻损伤有关。此外,Spearman 相关分析显示,鼻微生物群落失调、炎症和损伤之间存在相关性。总之,本研究评估了 O 和高温的联合毒性作用,并发现了潜在的机制,为制定预防干预策略和保护易感人群提供了重要的实验依据。