虾原肌球蛋白联合脂多糖诱导的小鼠哮喘气道炎症模型的研究  

A model of airway inflammation in asthma mice induced by shrimp tropomyosin plus lipopolysaccharide

作　　者：高翔 莫艳 朱嘉豪 董耀 陈永鑫 徐良玉 侯瑞涛 方蕾[1] GAO Xiang;MO Yan;ZHU Jiahao;DONG Yao;CHEN Yongxin;XU Liangyu;HOU Ruitao;FANG Lei(College of Medicine,Yangzhou University,Yangzhou 225009,China;Guangxi Pediatric Disease Clinical Research Center,Guangxi Zhuang Autonomous Region Women and Children Care Hospital,Nanning 530000,China)

机构地区：[1]扬州大学医学院,江苏扬州225009 [2]广西壮族自治区妇幼保健医院广西儿科疾病临床医学研究中心,南宁530000

出　　处：《扬州大学学报（农业与生命科学版）》2024年第3期55-63,共9页Journal of Yangzhou University：Agricultural and Life Science Edition

基　　金：江苏省卫健委科研基金面上项目(M2022034);扬州大学大学生科创项目(XCX20230830)。

摘　　要：为明确脂多糖(lipopolysaccharide, LPS)联合致敏原诱导的哮喘模型类型,建立虾原肌球蛋白(shrimp tropomyosin, ST)联合LPS诱导的小鼠哮喘气道炎症模型,并与卵清蛋白(ovalbumin, OVA)联合弗氏完全佐剂(complete Freund’s adjuvant, CFA)诱导的中性粒细胞哮喘模型或ST联合铝佐剂诱导的T2型嗜酸性粒细胞哮喘模型比较。结果表明:与对照组相比,ST联合LPS组小鼠肺组织气道炎症、气道上皮黏液分泌、肺泡灌洗液细胞总数均增加,肺泡灌洗液中以嗜酸性粒细胞为主,肺组织IL-17A含量和肺组织IL-1β、IL-5、IL-17A、Eotaxin、Mu5ac mRNA表达水平升高,肺组织气道上皮E-CDH蛋白表达水平和肺组织Cdh1 mRNA表达水平降低,气道周围ARG-1蛋白表达水平和肺组织Arg-1 mRNA水平升高,地塞米松给药能部分改善ST联合LPS诱导的气道炎症、黏液高分泌和细胞因子IL-17A表达水平,但对肺组织Cdh1、IL-5、IL-1β表达没有显著作用。综上,虾原肌球蛋白联合脂多糖小鼠模型是处于嗜酸性粒细胞哮喘型向中性粒细胞哮喘型过渡阶段的一种模型。Aim to definite the type of asthma model induced by lipopolysaccharide(LPS)combined with allergens.We established a mouse model of asthmatic airway inflammation induced by shrimp tropomyosin(ST)plus LPS and compared this model with models induced by ovalbumin(OVA)plus complete Freund's adjuvant(CFA)for neutrophilic asthma or ST combined with aluminum adjuvant for eosinophilic asthma.Compared to the control group,ST plus LPS induced the increased airway inflammation,airway epithelial mucus secretion,and total cell count in BALF.Lung IL-17Aprotein level and IL-1β,IL-5,IL-17A,Eotaxin,and Mu5ac mRNA expression in lung tissue were elevated,while the protein expression of E-CDH in airway epithelium and the mRNA expression of Cdh1in the lung tissues were decreased.The protein expression of ARG-1around the airway and the mRNA level of Arg-1in the lung tissues were increased.DEX treatment partially improved airway inflammation,excessive mucus secretion,and cytokine levels induced by ST combined with LPS,but DEX had no significant effect on the expression of Cdh1,IL-5,and IL-1βin lung tissue.In conclusion,the model induced by ST plus LPS might be an animal model of the advanced stage from eosinophil asthma to neutrophilic asthma.

关 键 词：哮喘 气道炎症 虾原肌球蛋白 脂多糖 卵清蛋白 

分 类 号：S852.4[农业科学—基础兽医学] R562.25[农业科学—兽医学]