臭氧与PM2.5共暴露加重过敏性鼻炎并与PPAR/TRPV1相关屏障损伤有关：来自鼻转录组学和微生物组学的见解。
Ozone and PM2.5 co-exposure exacerbates allergic rhinitis and is associated with PPAR/TRPV1-related barrier damage: Insights from nasal transcriptomics and microbiomics.
文献信息
| PMID | 42767358 |
|---|---|
| 原文 | 在 PubMed 查看原文 ↗ |
| 发表日期 | 2026 |
| 作者 | Ning Wang |
| 作者单位 | School of Public Health, Henan Medical University, Xinxiang, Henan Province 453003, China. |
| 期刊 | Environmental pollution (Barking, Essex : 1987) |
| SCI 分区 | Q1 |
| IF | 8 |
| 研究类型 | 基础研究 · 基础／转化 |
| 所属专科 | 鼻科 |
中文摘要
臭氧（O3）和PM2.5是全球主要空气污染物，可分别加重过敏性呼吸道疾病，但它们对过敏性鼻炎（AR）的联合效应尚不清楚。因此，本研究旨在探讨O3和PM2.5共暴露对AR小鼠的加重效应，并研究其潜在机制。我们在C57BL/6J小鼠中建立AR模型，然后暴露于O3或/和PM2.5。小鼠随机分为五组：PBS对照组、AR组、AR_O3组、AR_PM2.5组和AR_PM2.5_O3组。研究鼻炎症状，并通过HE和IHC观察鼻黏膜屏障损伤。通过ELISA检测血清生物标志物（OVA-sIgE、IL-1β、TNF-α）。进行转录组测序和16S rRNA测序，以分析鼻黏膜中mRNA谱和微生物的变化。本研究采用急性高剂量暴露来阐明机制通路，并非旨在直接模拟环境暴露。O3和PM2.5共暴露显著加重打喷嚏，破坏黏膜完整性并降低ZO-1/occludin表达。多组学分析显示，联合毒性可能与PPAR/TRPV1信号通路的改变有关。进一步的相关性分析表明，微生物群失调、炎症反应和黏膜损伤之间存在串扰。总之，我们的研究结果表明，O3和PM2.5共暴露会加重小鼠AR，可能通过破坏PPAR/TRPV1信号传导和诱导鼻腔微生物群失调。
英文摘要
Ozone (O3) and PM2.5 are major global air pollutants that individually worsen allergic respiratory diseases, yet their combined effect on allergic rhinitis (AR) is unclear. Therefore, this study aimed to explore the aggravating effect of co-exposure to O3 and PM2.5 in AR mice and to investigate the underlying mechanisms. We established an AR model in C57BL/6J mice, which were then exposed to O3 or/and PM2.5. The mice were randomized into five groups: PBS control group, AR group, AR_O3 group, AR_PM2.5 group and AR_PM2.5_O3 group. The rhinitis symptoms were investigated and the nasal mucosal barrier injury was observed by HE and IHC. Serum biomarkers (OVA-sIgE, IL-1β, TNF-α) were examined by ELISA. Transcriptomic sequencing and 16S rRNA sequencing were conducted to analyze the changes of mRNA profiles and microbes in nasal mucosa. This study employed acute high-dose exposures to elucidate mechanistic pathways and was not designed to directly model environmental exposures. Co-exposure to O3 and PM2.5 markedly aggravated sneezing, disrupted mucosal integrity and decreased ZO-1/occludin expression. Multi-omics analysis revealed that the combined toxicity was associated with altered PPAR/TRPV1 signaling pathways. Further correlation analyses indicated crosstalk among microbiota dysbiosis, inflammatory responses and mucosal injury. In summary, our findings illustrated that co-exposure to O3 and PM2.5 exacerbates AR in mice, likely through disruption of PPAR/TRPV1 signaling and induction of nasal microbial dysbiosis.