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Published on: November 28, 2019
Effects of Echinococcus multilocularis miR-71 mimics on murine macrophage RAW264.7 cells
Yadong Zheng1, Xiaola Guo2, Wei He2
1National Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention; Key Laboratory of Parasite and Vector Biology, MOH, China; National Center for International Research on Tropical Diseases, China; WHO Collaborating Center for Tropical Diseases, Shanghai 200025, China; State Key Laboratory of Veterinary Etiological Biology, Key Laboratory of Veterinary Parasitology of Gansu Province, Lanzhou Veterinary Research Institute, CAAS, Lanzhou, Gansu, China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou 225009, China.
Abstract:
The microRNAs (miRNAs) are a class of small regulatory non-coding RNA that contributes to the activation of host-pathogen cross-talk during infection. In helminthes, miR-71 is highly conserved and it has recently been detected in nematode exosomes, as well as in the sera and/or fluids of infected humans and mice. However, the role of miR-71 during infection remains poorly characterized. Herein, we show that Ago1 and Ago4, which encode key components of the small RNA-induced silencing complex (RISC), were up-regulated in murine macrophage RAW264.7 cells transfected by Echinococcus multilocularis miR-71 (emu-miR-71) mimics. Using a miRNA PCR array, none of the 84 miRNAs involved in inflammation or autoimmunity were significantly up- or down-regulated in the transfected cells (p>0.05). Although it did not influence IL-10 production by the treated cells (p>0.05), the mimics significantly repressed the production of NO 12 h after treatment with LPS and IFN-γ (p<0.01), identifying another potential mechanism whereby parasites can carefully regulate host levels of NO. These findings indicate that the release of parasite-derived miR-71 into hosts can affect the functions of macrophages, and possibly represents an exciting direction for studies of the interplay between parasites and hosts.
Insights
Parasite-derived microRNA-71 (miR-71) affects macrophage function during infection. This study reveals that emu-miR-71 up-regulates Ago1/Ago4 and represses nitric oxide production in host cells.
Area of Science:
- Immunology
- Molecular Biology
- Parasitology
Background:
- MicroRNAs (miRNAs) are key regulators of host-pathogen interactions.
- miR-71 is conserved in helminths and found in host fluids during infection.
- The precise function of parasite-derived miR-71 in host immunity is largely unknown.
Purpose of the Study:
- To investigate the functional role of Echinococcus multilocularis miR-71 (emu-miR-71) in host macrophage responses.
- To determine the impact of emu-miR-71 on host immune gene expression and mediator production.
Main Methods:
- Murine macrophage RAW264.7 cells were transfected with emu-miR-71 mimics.
- miRNA PCR array was used to analyze changes in inflammatory and autoimmune miRNAs.
- Nitric oxide (NO) and Interleukin-10 (IL-10) production were measured after stimulation.
Main Results:
- Transfection with emu-miR-71 mimics led to the up-regulation of Ago1 and Ago4, components of the RNA-induced silencing complex (RISC).
- No significant changes were observed in the expression of 84 screened inflammation- or autoimmunity-related miRNAs.
- emu-miR-71 mimics significantly repressed nitric oxide (NO) production in response to LPS and IFN-γ stimulation.
- IL-10 production remained unaffected by emu-miR-71 mimic treatment.
Conclusions:
- Parasite-derived miR-71 can modulate host macrophage function by influencing RISC components.
- emu-miR-71 plays a role in suppressing host NO production, representing a potential parasite immune evasion strategy.
- These findings highlight a novel mechanism of host-pathogen interaction mediated by parasite miRNAs.
