军事医学2017，Vol.41Issue(10)：796-799,4.DOI:10.7644/j.issn.1674-9960.2017.10.003
miR-155/SOCS1通路协同IL-17调控日本血吸虫早期感染的研究
The role of miR-155/SOCS1 pathway in collaboration with IL-17 in modulating the early progression of Schistosoma japonica
摘要
Abstract
Objective To explore the role of microRNA-155 ( miR-155 )/suppressor of cytokine signaling 1 ( SOCS1 ) pathway combined with IL-17 in modulating the early progression of Schistosoma japonicum.Methods BALB/c mice were infected subcutaneously with cercariae of S.japonicum before being sacrificed at 8 and 14 weeks after infection to collect liver samples for pathological observation by H&E staining .The spleens of mice were collected to calculate the spleen index.The level of IL-17 in serum was determined using ELISA.Furthermore, qRT-PCR was used to detect the expression of miR-155 and SOCS1 mRNA in the spleens of mice .Results Compared with normal group , the spleen index in the model group was increased significantly along with the loss of relative body mass .H&E staining revealed that the deposition of parasite eggs began to appear in the liver tissue at week 8 post-infection.Meanwhile, there were a large number of inflammatory cells infiltrating to form the eosinophilic granuloma.Over time, the formation of egg granulomas and the infiltration of inflammatory cells were alleviated on week 14 post-infection.The level of IL-17 in serum and the expression of miR-155 in the spleen were peaked on week 8 post-infection, and decreased sharply on week 14, but were still evidently higher than those in normal group .The expression of SOCS1 mRNA was progressively increased both on week 8 and 14. Conclusion The data indicates that miR-155 might cooperate with IL-17 to modulate SOCS1 in the development of S.japonicum infection.关键词
日本血吸虫/免疫应答/白细胞介素17/肉芽肿/微小核糖核酸/基因表达Key words
Schistosoma japonicum/immune response/interleukin-17/granuloma/microRNAs/gene expression分类
医药卫生引用本文复制引用
李覃,尤伟杰,葛新,马萍,邢杰..miR-155/SOCS1通路协同IL-17调控日本血吸虫早期感染的研究[J].军事医学,2017,41(10):796-799,4.基金项目
武警后勤学院基础研究项目(WHJ2016013) （WHJ2016013）
