Sja‐miR‐71a in Schistosome egg‐derived extracellular vesicles suppresses liver fibrosis caused by schistosomiasis via targeting semaphorin 4D

Journal of extracellular vesicles - Tập 9 Số 1 - 2020
Lifu Wang1,2,3,4, Yao Liao1,2,3,4, Ruibing Yang5,4, Zilong Yu6,4, Lichao Zhang1,2,3, Zifeng Zhu1,2,3, Xiaoying Wu7, Jia Shen1,2,3, Jiahua Liu1,2,3, Lian Xu8, Zhongdao Wu1,2,3, Xi Sun1,2,3
1Department of Parasitology of Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China
2Key Laboratory of Tropical Disease Control, Ministry of Education, Sun Yat-sen University, Guangzhou, China
3Provincial Engineering Technology Research Center for Biological Vector Control, Guangzhou, China
4these authors contributed equally to this work
5Medical Department of Xizang Minzu University, Xianyang, China
6Guangdong second provincial general Hospital, Guangzhou, China
7The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China
8Nantong University, Nantong, China

Tóm tắt

ABSTRACT

Schistosomiasis is characterized by liver fibrosis, and studies have indicated that Schistosoma japonicum (S. japonicum) eggs can limit the progression of liver fibrosis. However, the detailed molecular mechanisms are yet unclear. Extracellular vesicles (EVs) contain a selection of miRNAs for long‐distance exchange of information and act as an important pathway for host‐parasite communication. This study aimed to explore the potential role of S. japonicum egg‐derived EVs and its key miRNA in liver fibrosis. Herein, we found that S. japonicum egg‐derived EVs can inhibit the activation of hepatic stellate cells, which is mediated via the high expression of Sja‐miR‐71a. Sja‐miR‐71a in EVs attenuates the pathological progression and liver fibrosis in S. japonicum infection. Sja‐miR‐71a inhibiting TGF‐β1/SMAD and interleukin (IL)‐13/STAT6 pathways via directly targeting semaphorin 4D (Sema4D). In addition, Sja‐miR‐71a can also suppress liver fibrosis by regulating Th1/Th2/Th17 and Treg balance. This study contributes to further understanding of the molecular mechanisms underlying Schistosoma‐host interactions, and Sema4D may be a potential target for schistosomiasis liver fibrosis treatment.

Từ khóa


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