IL-33在PM2.5暴露加重变应性鼻炎黏膜炎症反应中的作用
发布时间：2019-05-18 20:58
【摘要】：目的:本文主要探讨1.PM2.5暴露下是否加重变应性鼻炎(Allergic Rhinitis,AR)小鼠粘膜炎症反应;2.白细胞介素-33(interleukin-33 IL-33)在其中所起的作用,及可能的途径。方法:1.采集PM2.5,行理化分析及制备染毒样品;2.建立变应性鼻炎小鼠模型,行行为学计分;3.造模成功后,PM2.5干预,建立PM2.5暴露后小鼠模型;4.抗IL-33抗体处理PM2.5暴露下变应性鼻炎小鼠模型;取三组小鼠外周血行血涂片计数嗜酸性粒细胞,ELISA检测IgE及IL-33水平;取鼻粘膜观察其形态学的改变;鼻粘膜另行western blot检测NF-κB表达水平。结果:1.PM2.5颗粒染毒样品制备成功;2.AR小鼠模型建模成功,典型症状明显;3.外周血涂片结果:AR模型组嗜酸性粒细胞计数低于PM2.5干预组,P0.05;抗IL-33治疗组嗜酸性粒细胞计数低于PM2.5干预组,P0.05;4.ELISA结果:AR模型组血清IgE、IL-33水平明显低于PM2.5干预组,P0.05;抗IL-33治疗组血清IgE、IL-33水平低于PM2.5干预组,P0.05;5.鼻粘膜HE染色结果:AR模型组:鼻粘膜上皮结构紊乱,纤毛脱落,粘膜下层可见EOS、中性粒细胞等炎细胞浸润。PM2.5干预组:鼻粘膜上皮细胞结构不完整,纤毛大量脱落,粘膜下层EOS、中性粒细胞等炎细胞浸润明显,可见组织水肿,腺体增生。抗IL-33治疗组:鼻粘膜可见基本完整的纤毛结构,且上皮细胞排列较为整齐,轻度炎细胞浸润。6.Western blot结果:AR模型组鼻粘膜NF-κB水平低于PM2.5干预组,P0.05;抗IL-33治疗组鼻粘膜NF-κB水平低于PM2.5干预组,P0.05。结论:1.PM2.5粒径小,面积大,活性强,成分复杂,易附带重金属、病原微生物、多环芳烃及其衍生物等有毒、有害物质。2.PM2.5可加重变应性鼻炎黏膜炎症反应。3.PM2.5暴露下的AR小鼠外周血IL-33水平增高。4.抗IL-33抗体可减轻PM2.5暴露下变应性鼻炎黏膜炎症反应。5.IL-33可能通过NF-κB途径发挥其作用。
[Abstract]:Objective: to investigate whether the inflammatory reaction of allergic rhinitis (Allergic Rhinitis,AR) mice is aggravated by 1.PM2.5 exposure. The role and possible pathways of IL-33 (interleukin-33 IL-33) in it. Method: 1. PM2.5, was collected for physical and chemical analysis and the samples were prepared. 2. The mouse model of allergic rhinitis was established, and the action score was 3. After successful modeling, PM2.5 intervened to establish the mouse model after PM2.5 exposure. 4. The mice model of allergic rhinitis exposed to PM2.5 was treated with anti-IL-33 antibody, the peripheral blood smears of the three groups were taken to count eosinophils, the levels of IgE and IL-33 were detected by ELISA, and the morphological changes of nasal mucosa were observed. The expression of NF- kappa B was detected by western blot in nasal mucosa. Results: the sample of 1.PM2.5 particles was successfully prepared, the model of 2.AR mice was established successfully, and the typical symptoms were obvious. The results of peripheral blood smear showed that the count of eosinophils in AR model group was lower than that in PM2.5 intervention group (P0.05), and that in anti-IL-33 treatment group was lower than that in PM2.5 intervention group (P0.05). 4.ELISA results: the level of serum IgE,IL-33 in AR model group was significantly lower than that in PM2.5 intervention group (P0.05), and that in anti-IL-33 treatment group was lower than that in PM2.5 intervention group (P0.05 鈮，
本文编号：2480331
[Abstract]:Objective: to investigate whether the inflammatory reaction of allergic rhinitis (Allergic Rhinitis,AR) mice is aggravated by 1.PM2.5 exposure. The role and possible pathways of IL-33 (interleukin-33 IL-33) in it. Method: 1. PM2.5, was collected for physical and chemical analysis and the samples were prepared. 2. The mouse model of allergic rhinitis was established, and the action score was 3. After successful modeling, PM2.5 intervened to establish the mouse model after PM2.5 exposure. 4. The mice model of allergic rhinitis exposed to PM2.5 was treated with anti-IL-33 antibody, the peripheral blood smears of the three groups were taken to count eosinophils, the levels of IgE and IL-33 were detected by ELISA, and the morphological changes of nasal mucosa were observed. The expression of NF- kappa B was detected by western blot in nasal mucosa. Results: the sample of 1.PM2.5 particles was successfully prepared, the model of 2.AR mice was established successfully, and the typical symptoms were obvious. The results of peripheral blood smear showed that the count of eosinophils in AR model group was lower than that in PM2.5 intervention group (P0.05), and that in anti-IL-33 treatment group was lower than that in PM2.5 intervention group (P0.05). 4.ELISA results: the level of serum IgE,IL-33 in AR model group was significantly lower than that in PM2.5 intervention group (P0.05), and that in anti-IL-33 treatment group was lower than that in PM2.5 intervention group (P0.05 鈮，
本文编号：2480331
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