Guo Xiaola, Zheng Yadong
State Key Laboratory of Veterinary Etiological Biology, Key Laboratory of Veterinary Parasitology of Gansu Province, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Gansu, China.
Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University College of Veterinary Medicine, Yangzhou, China.
Front Cell Infect Microbiol. 2020 Apr 3;10:132. doi: 10.3389/fcimb.2020.00132. eCollection 2020.
Alveolar echinococcosis (AE) is a zoonotic helminthic disease caused by infection with the larval of in human and animals. Here, we compared miRNA profiles of the peritoneal macrophages of -infected and un-infected female BALB/c mice using high-throughput sequencing. A total of 87 known miRNAs were differentially expressed (fold change ≥ 2, < 0.05) in peritoneal macrophages in mice 30- and 90-day post infection compared with ones in un-infected mice. An increase of mmu-miR-155-5p expression was observed in peritoneal macrophages in -infected mice. Compared with the control group, the production of nitric oxide (NO) was increased in peritoneal macrophages transfected with mmu-miR-155-5p mimics at 12 h after transfection ( < 0.001). Two key genes (CD14 and NF-κB) in the LPS/TLR4 signaling pathway were also markedly altered in mmu-miR-155-5p mimics transfected cells ( < 0.05). Moreover, mmu-miR-155-5p mimics suppressed mRNA expression and promoted and mRNA expression. Luciferase assays showed that mmu-miR-155-5p was able to bind to the 3' UTR of the gene and decreased luciferase activity. Finally, we found the expression of was significantly downregulated in both macrophages transfected with mmu-miR-155-5p and macrophages isolated from -infected mice. These results demonstrate an immunoregulatory effect of mmu-miR-155 on macrophages, suggesting a role in regulation of host immune responses against infection.
肺泡型包虫病（AE）是一种人畜共患的蠕虫病，由人体和动物感染幼虫引起。在此，我们使用高通量测序比较了感染和未感染细粒棘球绦虫的雌性BALB/c小鼠腹腔巨噬细胞的miRNA谱。与未感染小鼠相比，感染后30天和90天的小鼠腹腔巨噬细胞中共有87种已知miRNA差异表达（折叠变化≥2，P<0.05）。在感染细粒棘球绦虫的小鼠腹腔巨噬细胞中观察到mmu-miR-155-5p表达增加。与对照组相比，转染mmu-miR-155-5p模拟物的腹腔巨噬细胞在转染后12小时一氧化氮（NO）的产生增加（P<0.001）。LPS/TLR4信号通路中的两个关键基因（CD14和NF-κB）在转染mmu-miR-155-5p模拟物的细胞中也有明显改变（P<0.05）。此外，mmu-miR-155-5p模拟物抑制了某基因的mRNA表达，并促进了其他基因的mRNA表达。荧光素酶报告基因检测表明，mmu-miR-155-5p能够与该基因的3'UTR结合并降低荧光素酶活性。最后，我们发现转染mmu-miR-155-5p的巨噬细胞和从感染细粒棘球绦虫的小鼠分离的巨噬细胞中该基因的表达均显著下调。这些结果证明了mmu-miR-155对巨噬细胞的免疫调节作用，提示其在调节宿主针对细粒棘球绦虫感染的免疫反应中发挥作用。
