Original Research ARTICLE
miRNA-seq of Echinococcus multilocularis extracellular vesicles and immunomodulatory effects of miR-4989
- 1Xinjiang University, China
- 2Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, China
- 3Dali University, China
- 4National Research Centre (Egypt), Egypt
- 5Siberian Branch of the Russian Academy of Sciences (RAS), Russia
- 6Cholistan University of Veterinary and Animal Sciences, Pakistan
- 7State Key Laboratory of Veterinary Etiological Biology, Lanzhou Institute of Veterinary Research (CAAS), China
- 8Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, College of Veterinary Medicine, Yangzhou University, China
Alveolar echinococcosis caused by Echinococcus multilocularis is an important zoonotic disease. In the infected mice, emu-miR-4989-3p is present in sera, but its role remains unknown. Using high-throughput sequencing and qPCR, emu-miR-4989-3p was herein confirmed to be encapsulated into E. multilocularis extracellular vesicles. In the transfected macrophages, emu-miR-4989-3p was demonstrated to significantly inhibit NO production compared to the control (p < 0.05). Moreover, transfection of emu-miR-4989-3p also gave rise to the increased expression of TNF-α (p < 0.01). Furthermore, emu-miR-4989-3p induced the dysregulation of several key components in the LPS/TLR4 signaling pathway compared with the control, especially TLR4 and NF-κB that both were upregulated. Conversely, the NO production and the expression of TNF-α, TLR4 and NF-κB tended to be increased and decreased in the mimics-transfected cells upon emu-miR-4989-3p low expression, respectively. These results suggest that emu-miR-4989-3p is one of ‘virulence’ factors encapsulated into the extracellular vesicles, potentially playing a role in the pathogenesis of E. multilocularis.
Keywords: Echinococcus multilocularis, Emu-miR-4989-3p, extracellular vesicles, macrophage, miRNA
Received: 13 Jul 2019;
Accepted: 08 Nov 2019.
Copyright: © 2019 Ding, He, Wu, Yang, Guo, Yang, Kandil, Kutyrev, Ayaz and Zheng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: PhD. Yadong Zheng, State Key Laboratory of Veterinary Etiological Biology, Lanzhou Institute of Veterinary Research (CAAS), Lanzhou, China, email@example.com