State Key Laboratory of Veterinary Etiological Biology, Key Laboratory of Veterinary Parasitology of Gansu Province, Lanzhou Veterinary Research Institute, CAAS, Lanzhou 730046, China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou 225009, China.
Int Immunopharmacol. 2018 Nov;64:252-255. doi: 10.1016/j.intimp.2018.09.004. Epub 2018 Sep 11.
During Echinococcus multilocularis infection, serum miR-222-3p is dramatically downregulated, but its role is yet to be established. Here the expression of miR-222-3p in the spleen of infected mice was shown to be significantly decreased in response to parasite infection (p < 0.05). Using RAW264.7 macrophages, it was further demonstrated that E. multilocularis crude antigens significantly inhibited miR-222-3p expression (p < 0.01). In macrophages transfected with a miR-222-3p inhibitor, NO secretion was moderately decreased compared with the control (p < 0.05). Although all the pro- and anti-inflammatory cytokine genes tested kept constant in expression, four key genes involved in the LPS/TLR4 signaling pathway were significantly down- or up-regulated in transfected cells (p < 0.05), including CD14, TLR4, TICAM2 and AP-1. These results suggest that downregulated miR-222-3p is capable of modulating macrophage immune functions, possibly contributing to the pathogenesis during E. multilocularis infection.
在泡状棘球蚴感染期间，血清 miR-222-3p 显著下调，但其作用尚未确定。本研究显示，感染寄生虫后，感染小鼠脾脏中 miR-222-3p 的表达显著降低（p<0.05）。用 RAW264.7 巨噬细胞进一步证明，泡状棘球蚴粗抗原显著抑制 miR-222-3p 的表达（p<0.01）。在转染 miR-222-3p 抑制剂的巨噬细胞中，与对照组相比，NO 分泌适度降低（p<0.05）。尽管所有测试的促炎和抗炎细胞因子基因的表达保持不变，但 LPS/TLR4 信号通路中涉及的四个关键基因在转染细胞中显著下调或上调（p<0.05），包括 CD14、TLR4、TICAM2 和 AP-1。这些结果表明，下调的 miR-222-3p 能够调节巨噬细胞免疫功能，可能有助于泡状棘球蚴感染的发病机制。
