摘要
目的通过观察IL-31在OVA诱导小鼠哮喘模型中的动态表达及IL-31对肺泡上皮细胞表达趋化因子CCL11和CCL22的影响,探讨IL-31在哮喘气道炎症中的作用。方法常规OVA法建立小鼠哮喘模型,于末次激发后取肺组织HE染色及AB-PAS染色,收集支气管肺泡灌洗液(BALF)进行白细胞和嗜酸性粒细胞(EOS)计数,ELISA法检测血浆中IgE、IL-4、IFN-γ、IL-31水平,荧光定量PCR检测肺组织IL-31R mRNA表达水平,同时体外培养小鼠肺泡上皮细胞,用IL-31处理24 h后检测CCL11和CCL22 mRNA的表达水平。结果成功构建哮喘小鼠模型,哮喘小鼠BALF中白细胞总数、嗜酸性粒细胞百分比和血浆中IgE水平明显增多。哮喘小鼠肺组织病理切片见中性粒细胞、EOS浸润。哮喘小鼠血浆中Th2类细胞因子IL-4水平明显高于对照组,Th1类细胞因子IFN-γ明显低于对照组。哮喘小鼠血浆IL-31水平和肺组织IL-31R mRNA表达水平明显增高,第2周至第8周虽略有降低但仍明显高于对照组。IL-31作用小鼠肺泡上皮细胞24h后,趋化因子CCL11、CCL22mRNA表达增高。结论IL-31通过刺激趋化因子表达募集炎性细胞,促进气道炎症的发生发展。
It is reported that IL-31 plays an important role in bronchial asthma, but the mechanism is not clear. To investigate the role of IL-31 in airway inflammation of asthma, we observed the dynamic expression of IL-31 in OVA-induced mouse asthma model and investigate the effect of IL-31 on the expression of chemokines CCL11 and CCL22 in alveolar epithelial cells. An allergic asthma mouse model was constructed by ovalbumin(OVA), and the lung tissues were collected for HE staining and AB-PAS staining after final stimulation.Bronchoalveolar lavage fluid(BALF) was collected for counting white blood cells(WBC) and eosinophils(EOS). The levels of IGE, IL-4, IFN-γ and IL-31 in plasma were detected by ELISA. And the mRNA expression of the IL-31 R in lung tissues was detected by fluorescent real-time PCR. Mouse alveolar epithelial cells were cultured in vitro and treated with IL-31 for 24 hours, then the expression of CCL11 and CCL22 mRNA were detected by fluorescent realtime PCR. In this study, neutrophil and EOS infiltration were found in pathological sections of lung tissue from asthmatic mice. The level of Th2 cytokine IL-4 in the plasma of asthmatic mice was significantly higher than that of the control group, and the level of Th1 cytokine IFN-γ was significantly lower than that of the control group(P<0.05). The levels of plasma IL-31 and IL-31 R mRNA expression in lung tissue increased significantly in asthmatic mice(P<0.05), and decreased slightly from the 2 ndweek to the 8 thweek, but still significant higher than those of the control group(P<0.05). IL-31 increased the expression of chemokines CCL11 and CCL22 mRNA after 24 h of treatment on mouse alveolar epithelial cells(P<0.05). Therefore, we concluded that IL-31 promotes the development of airway inflammation by stimulating chemokines expression to recruit inflammatory cells.
作者
刘福慧
高婧
江涛
岳欢
黄俊琼
LIU Fuhui;GAO Jing;JIANG Tao;YUE Huan;HUANG Junqiong(Department of Blood Transfusion, Affiliated Hospital of Zurtyi Medical University, Zunyi 563099, China;Clinical Laboratory, Affiliated Hospital of Zunyi Medical University, Zunyi 563099, China)
出处
《免疫学杂志》
CAS
CSCD
北大核心
2019年第6期507-511,共5页
Immunological Journal
基金
国家自然科学基金(81260266)
贵州省科学技术基金(黔科合J字20142184)
