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Cysticercus pisiformis-derived novel-miR1 targets TLR2 to inhibit the immune response in rabbits

Cysticercosis pisiformis, a highly prevalent parasitic disease worldwide, causes significant economic losses in the rabbit breeding industry. Previous investigations have identified a novel microRNA, designated as novel-miR1, within the serum of rabbit infected with Cysticercus pisiformis. In the pr...

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Autores principales: Chen, Guoliang, Pu, Guiting, Wang, Liqun, Li, Yanping, Liu, Tingli, Li, Hong, Zhang, Shaohua, Wang, Xuelin, Liu, Xiaolei, Luo, Xuenong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10408446/
https://www.ncbi.nlm.nih.gov/pubmed/37559722
http://dx.doi.org/10.3389/fimmu.2023.1201455
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author Chen, Guoliang
Pu, Guiting
Wang, Liqun
Li, Yanping
Liu, Tingli
Li, Hong
Zhang, Shaohua
Wang, Xuelin
Liu, Xiaolei
Luo, Xuenong
author_facet Chen, Guoliang
Pu, Guiting
Wang, Liqun
Li, Yanping
Liu, Tingli
Li, Hong
Zhang, Shaohua
Wang, Xuelin
Liu, Xiaolei
Luo, Xuenong
author_sort Chen, Guoliang
collection PubMed
description Cysticercosis pisiformis, a highly prevalent parasitic disease worldwide, causes significant economic losses in the rabbit breeding industry. Previous investigations have identified a novel microRNA, designated as novel-miR1, within the serum of rabbit infected with Cysticercus pisiformis. In the present study, we found that C. pisiformis-derived novel-miR1 was released into the rabbit serum via exosomes. Through computational analysis using TargetScan, miRanda, and PITA, a total of 634 target genes of novel-miR1 were predicted. To elucidate the functional role of novel-miR1, a dual-luciferase reporter assay was utilized and demonstrated that novel-miR1 targets rabbit Toll-like receptor 2 (TLR2). Rabbit peripheral blood lymphocytes (PBLCs) were transfected with novel-miR1 mimic and mimic NC, and the in vitro experiments confirmed that novel-miR1 suppressed the expression of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 through the nuclear factor kappa B (NF-κB) pathway. In vivo experiments demonstrated that novel-miR1 was significantly upregulated during the 1–3 months following infection with C. pisiformis in rabbits. Notably, this upregulation coincided with a downregulation of TLR2, P65, pP65, TNF-α, IL-1β, and IL-6 in PBLCs. Collectively, these results indicate that the novel-miR1 derived from C. pisiformis inhibited the rabbits’ immune response by suppressing the NF-κB-mediated immune response. This immune modulation facilitates parasite invasion, survival, and establishment of a persistent infection.
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spelling pubmed-104084462023-08-09 Cysticercus pisiformis-derived novel-miR1 targets TLR2 to inhibit the immune response in rabbits Chen, Guoliang Pu, Guiting Wang, Liqun Li, Yanping Liu, Tingli Li, Hong Zhang, Shaohua Wang, Xuelin Liu, Xiaolei Luo, Xuenong Front Immunol Immunology Cysticercosis pisiformis, a highly prevalent parasitic disease worldwide, causes significant economic losses in the rabbit breeding industry. Previous investigations have identified a novel microRNA, designated as novel-miR1, within the serum of rabbit infected with Cysticercus pisiformis. In the present study, we found that C. pisiformis-derived novel-miR1 was released into the rabbit serum via exosomes. Through computational analysis using TargetScan, miRanda, and PITA, a total of 634 target genes of novel-miR1 were predicted. To elucidate the functional role of novel-miR1, a dual-luciferase reporter assay was utilized and demonstrated that novel-miR1 targets rabbit Toll-like receptor 2 (TLR2). Rabbit peripheral blood lymphocytes (PBLCs) were transfected with novel-miR1 mimic and mimic NC, and the in vitro experiments confirmed that novel-miR1 suppressed the expression of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 through the nuclear factor kappa B (NF-κB) pathway. In vivo experiments demonstrated that novel-miR1 was significantly upregulated during the 1–3 months following infection with C. pisiformis in rabbits. Notably, this upregulation coincided with a downregulation of TLR2, P65, pP65, TNF-α, IL-1β, and IL-6 in PBLCs. Collectively, these results indicate that the novel-miR1 derived from C. pisiformis inhibited the rabbits’ immune response by suppressing the NF-κB-mediated immune response. This immune modulation facilitates parasite invasion, survival, and establishment of a persistent infection. Frontiers Media S.A. 2023-07-25 /pmc/articles/PMC10408446/ /pubmed/37559722 http://dx.doi.org/10.3389/fimmu.2023.1201455 Text en Copyright © 2023 Chen, Pu, Wang, Li, Liu, Li, Zhang, Wang, Liu and Luo https://creativecommons.org/licenses/by/4.0/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.
spellingShingle Immunology
Chen, Guoliang
Pu, Guiting
Wang, Liqun
Li, Yanping
Liu, Tingli
Li, Hong
Zhang, Shaohua
Wang, Xuelin
Liu, Xiaolei
Luo, Xuenong
Cysticercus pisiformis-derived novel-miR1 targets TLR2 to inhibit the immune response in rabbits
title Cysticercus pisiformis-derived novel-miR1 targets TLR2 to inhibit the immune response in rabbits
title_full Cysticercus pisiformis-derived novel-miR1 targets TLR2 to inhibit the immune response in rabbits
title_fullStr Cysticercus pisiformis-derived novel-miR1 targets TLR2 to inhibit the immune response in rabbits
title_full_unstemmed Cysticercus pisiformis-derived novel-miR1 targets TLR2 to inhibit the immune response in rabbits
title_short Cysticercus pisiformis-derived novel-miR1 targets TLR2 to inhibit the immune response in rabbits
title_sort cysticercus pisiformis-derived novel-mir1 targets tlr2 to inhibit the immune response in rabbits
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10408446/
https://www.ncbi.nlm.nih.gov/pubmed/37559722
http://dx.doi.org/10.3389/fimmu.2023.1201455
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