细胞自噬在PM2.5诱导变应性鼻炎发病及其病理机制中的作用

Allergic rhinitis(AR) is a common and frequently-occurring disease, serious impact on human health. The role of PM2.5 cannot be ignored, Autophagy plays an important role in the pathogenesis of environmental factors.This study proposed PM2.5 intervention cultivation of nasal mucosa epithelial cells, autophagy characteristic structure were observed. Specific knock out autophagy related genes, the effect of PM2.5 on inflammation and damage were evaluated. Using autophagy genetic knockout AR animal models in mice by inhaling different concentrations of PM2.5, the biological behavior、 immunology and pathology change were analyzed. We will explore autophagy gene knockout in animal model of overall performance whether can relieve airway allergic inflammation、nasal mucus secretion and alleviate the phenotype of AR. Through exploring autophagy in the role of airway inflammation and revealing the effect of autophagy in the PM2.5 on AR pathological mechanism,it may provide theoretical basis for the prevention and treatment of AR and important.

变应性鼻炎（allergic rhinitis，AR）是鼻科学领域常见病多发病，严重影响人类的健康。 PM2.5对AR发病发挥不可忽视的作用。 细胞自噬在环境因素致病中发挥重要作用，我们推测PM2.5可能通过细胞自噬参与AR疾病的发病过程。本研究拟通过PM2.5干预离体培养的鼻黏膜上皮细胞，观察PM2.5诱导细胞自噬过程及其自噬特征性结构的变化，并利用siRNA特异性敲除自噬相关基因下调细胞自噬水平，观察是否能够减轻PM2.5对鼻黏膜上皮细胞的炎症效应及损害。采用细胞自噬基因缺陷小鼠AR动物模型吸入PM2.5，观察其生物学行为、病理学及免疫学变化，探讨敲除自噬基因在动物模型中整体表现。观察小鼠自噬基因敲除是否可以缓解变应性鼻炎小鼠气道过敏性炎症、鼻腔黏液高分泌，从而缓解变应性鼻炎的症状。通过研究证实细胞自噬在PM2.5诱导变应性鼻炎发病及其病理机制，为AR的防治提供理论依据。

变应性鼻炎(allergic rhinitis, AR)是鼻科学领域常见病多发病，严重影响人类的健康。PM2.5对AR发病发挥不可忽视的作用。细胞自噬在环境因素致病中发挥重要作用，我们推测PM2.5可能通过细胞自噬参与AR疾病的发病过程。本研究拟通过PM2.5干预离体培养的鼻黏膜上皮细胞，观察PM2.5诱导细胞自噬过程及其自噬特征性结构的变化，并利用siRNA特异性敲除自噬相关基因下调细胞自噬水平，观察是否能够减轻PM2.5对鼻黏膜上皮细胞的炎症效应及损害。采用细胞自噬基因缺陷小鼠AR动物模型吸入PM2.5，观察其生物学行为、病理学及免疫学变化，探讨敲除自噬基因在动物模型中整体表现。观察小鼠自噬基因敲除是否可以缓解变应性鼻炎小鼠气道过敏性炎症、鼻腔黏液高分泌，从而缓解变应性鼻炎的症状。通过研究证实细胞自噬在PM2.5诱导变应性鼻炎发病及其病理机制，为AR的防治提供理论依据。