The role of miR-155/SOCS1 pathway in collaboration with IL-17 in modulating the early progression of Schistosoma japonica
10.7644/j.issn.1674-9960.2017.10.003
- VernacularTitle:miR-155/SOCS1通路协同IL-17调控日本血吸虫早期感染的研究
- Author:
Tan LI
1
;
Wei-Jie YOU
;
Xin GE
;
Ping MA
;
Jie XING
Author Information
1. 武警后勤学院病原生物学教研室
- Keywords:
Schistosoma japonicum;
immune response;
interleukin-17;
granuloma;
microRNAs;
gene expression
- From:
Military Medical Sciences
2017;41(10):796-799
- CountryChina
- Language:Chinese
-
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.