期刊
FRONTIERS IN IMMUNOLOGY
卷 14, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2023.1201455
关键词
rabbit; Cysticercosis pisiformis; novel-miR1; TLR2; NF kappa B
类别
C. pisiformis-derived novel-miR1 was released into rabbit serum via exosomes and suppressed the expression of TLR2, inhibiting the immune response and facilitating parasite infection.
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-alpha, IL-1 beta, and IL-6 through the nuclear factor kappa B (NF-kappa B) 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-alpha, IL-1 beta, 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-kappa B-mediated immune response. This immune modulation facilitates parasite invasion, survival, and establishment of a persistent infection.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据