|کد مقاله||کد نشریه||سال انتشار||مقاله انگلیسی||ترجمه فارسی||نسخه تمام متن|
|2540284||1559756||2016||4 صفحه PDF||سفارش دهید||دانلود رایگان|
• Emu-miR-71 mimics up-regulate Argonaute expression in transfected macrophages.
• Emu-miR-71 mimics repress NO secretion by stimulated macrophages.
• We identify an additional approach whereby parasites regulate host NO levels.
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.
Journal: International Immunopharmacology - Volume 34, May 2016, Pages 259–262