Effects of PM2.5 on mucus secretion and tissue remodeling in a rabbit model of chronic rhinosinusitis

Background According to epidemiologic studies, fine particulate matter (particulate matter ≤2.5 μm, PM2.5) is closely associated with increases in the incidence and severity of chronic rhinosinusitis (CRS). However, the role of PM2.5 in the pathophysiology of CRS remains largely unknown. In this stu...

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Published inInternational forum of allergy & rhinology Vol. 8; no. 11; pp. 1349 - 1355
Main Authors Zhao, Renwu, Guo, Zhiqiang, Dong, Weiyang, Deng, Congrui, Han, Zhijin, Liu, Jian, Wang, Hanwei, Zhuang, Guoshun, Zhang, Ruxin
Format Journal Article
LanguageEnglish
Published United States Wiley Subscription Services, Inc 01.11.2018
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Summary:Background According to epidemiologic studies, fine particulate matter (particulate matter ≤2.5 μm, PM2.5) is closely associated with increases in the incidence and severity of chronic rhinosinusitis (CRS). However, the role of PM2.5 in the pathophysiology of CRS remains largely unknown. In this study, we investigated the effects of PM2.5 on nasal cilia, tissue remodeling, and mucus hypersecretion in a rabbit model of CRS. Methods CRS rabbits were exposed to ambient PM2.5 via a PM2.5 inhalation exposure system. The degree of ciliary damage was evaluated using scanning electron microscopy (SEM). Histopathologic changes were determined using periodic acid‐Schiff (PAS) staining of goblet cells and Masson trichrome (MT) staining for collagen in the nasal mucosa. MUC5AC expression was assessed by immunohistochemistry. Results PM2.5 exposure substantially aggravated ciliary disruption in rabbits with CRS. PM2.5 also significantly increased goblet cell hyperplasia and collagen deposition, as reflected by PAS and MT staining. The nasal mucosa of CRS rabbits displayed markedly elevated MUC5AC expression after PM2.5 exposure. Conclusion Increases in ciliary disruption, nasal remodeling, and mucus hypersecretion may be the pathophysiologic mechanisms underlying the PM2.5‐induced aggravation of CRS. 背景 流行病学研究表明, 细颗粒物 (颗粒物≤2.5 μm, PM2.5) 与慢性鼻窦炎 (CRS) 发病率升高和严重程度加剧密切相关。但是, PM2.5在CRS的病理生理学中的作用并不清楚。本研究中, 我们在CRS兔模型中, 探讨PM2.5对鼻黏膜纤毛、组织重塑和黏液高分泌的可能作用。 方法 通过PM2.5吸入暴露系统, 将CRS兔模型暴露于PM2.5中。采用扫描电镜技术 (SEM) 检测纤毛损坏程度。通过杯状细胞过碘酸希夫反应 (PAS) 染色、胶原Masson三重染色 (MT) 进行评估鼻黏膜组织病理学改变。应用免疫组织化学检测MUC5AC表达情况。 结果 PM2.5暴露明显加重兔CRS模型中的纤毛受损。PAS和MT染色结果表明, PM2.5显著增强了杯状细胞增生和胶原沉积。PM2.5暴露使兔CRS模型的鼻黏膜MUC5AC表达水平发生明显上调。 结论 PM2.5可能通过促进纤毛破坏、组织重塑和黏液高分泌等病理生理学机制, 从而加重CRS炎症。
Bibliography:Potential conflict of interest: None provided.
Funding sources for the study: National Natural Science Foundation of China (81670906).
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ISSN:2042-6976
2042-6984
DOI:10.1002/alr.22182