School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, China.
Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
Sci Total Environ. 2024 Dec 1;954:176604. doi: 10.1016/j.scitotenv.2024.176604. Epub 2024 Sep 29.
Ground-level ozone (O) has been shown to induce airway inflammation, the underlying mechanisms remain unclear. The aim of this study was to determine whether gut and airway microbiota dysbiosis, and airway metabolic alterations were associated with O-induced airway inflammation. Thirty-six 8-week-old male C57BL/6 N mice were divided into 2 groups: sterile water group and broad-spectrum antibiotics group (Abx). Each group was further divided into two subgroups, filtered air group (Air) and O group (O), with 9 mice in each subgroup. Mice in the Air and O groups were exposed to filtered air or 1 ppm O, 4 h/d for 5 consecutive days, respectively. Mice in Abx + Air and Abx + O groups were exposed to filtered air or O, respectively, after drinking broad-spectrum Abx. 24 h after the final O exposure, mouse feces and bronchoalveolar lavage fluids (BALF) were collected and subjected to measurements of airway oxidative stress and inflammation biomarkers, 16S rRNA sequencing and metabolite profiling. Hematoxylin-eosin staining of lung tissues was applied to examine the pathological changes of lung tissue. The results showed that O exposure resulted in airway oxidative stress and inflammation, as well as gut and airway microbiota dysbiosis, and airway metabolism alteration. Abx pre-treatment markedly changed gut and airway microbiota and promoted O-induced metabolic disorder and airway inflammation. Spearman correlation analyses indicated that inter-related gut and airway microbiota dysbiosis and airway metabolic disorder were associated with O-induced airway inflammation. Together, inhaled O causes airway inflammation, which may implicate gut and airway microbiota dysbiosis and airway metabolic alterations.
地面臭氧（O）已被证明会引起气道炎症，但其潜在机制尚不清楚。本研究旨在确定肠道和气道微生物群落失调以及气道代谢改变是否与 O 诱导的气道炎症有关。将 36 只 8 周龄雄性 C57BL/6N 小鼠分为两组：无菌水组和广谱抗生素组（Abx）。每组进一步分为两个亚组，空气过滤组（Air）和 O 组（O），每组 9 只小鼠。Air 和 O 组的小鼠分别暴露于过滤空气或 1ppm O，每天 4 小时，连续 5 天。Abx+Air 和 Abx+O 组的小鼠在饮用广谱 Abx 后分别暴露于过滤空气或 O。最后一次 O 暴露后 24 小时，收集小鼠粪便和支气管肺泡灌洗液（BALF），并进行气道氧化应激和炎症生物标志物、16S rRNA 测序和代谢物谱分析。应用苏木精-伊红染色观察肺组织的病理变化。结果表明，O 暴露导致气道氧化应激和炎症，以及肠道和气道微生物群落失调，气道代谢改变。Abx 预处理显著改变了肠道和气道微生物群，并促进了 O 诱导的代谢紊乱和气道炎症。Spearman 相关分析表明，相互关联的肠道和气道微生物群落失调和气道代谢紊乱与 O 诱导的气道炎症有关。总之，吸入 O 会引起气道炎症，这可能与肠道和气道微生物群落失调以及气道代谢改变有关。
