Department of Clinical Microbiology and Immunology, College of Medical Laboratory Science, Third Military Medical University, Chongqing, China.
FEBS Lett. 2010 Apr 16;584(8):1481-6. doi: 10.1016/j.febslet.2010.02.063. Epub 2010 Feb 26.
MicroRNA-155 (miR-155) has been implicated as a central regulator of the immune system. We have previously reported that miR-155 negatively regulates Helicobacter pylori (H. pylori)-induced inflammation, but the molecular mechanism of miR-155 regulating the inflammation is not fully clear. Here, we identified myeloid differentiation protein 88 (MyD88) as a target gene of miR-155, and found that miR-155 decreased MyD88 expression at the protein but not the mRNA message level, suggesting that the miR-155-mediated inhibition is a post-transcriptional event. Furthermore, the overexpression of miR-155 led to significantly reduced IL-8 production induced by H. pylori infection. Thus, we have demonstrated that miR-155 can negatively regulate inflammation by targeting a key adaptor molecule MyD88 in inflammatory pathways.
microRNA-155(miR-155)被认为是免疫系统的核心调节因子。我们之前曾报道过,miR-155 负调控幽门螺杆菌(H. pylori)诱导的炎症,但 miR-155 调节炎症的分子机制尚不完全清楚。在这里,我们鉴定出髓样分化蛋白 88(MyD88)是 miR-155 的靶基因,并发现 miR-155 在蛋白水平而非 mRNA 水平上降低了 MyD88 的表达,表明 miR-155 介导的抑制是一种转录后事件。此外,miR-155 的过表达导致由 H. pylori 感染诱导的 IL-8 产生显著减少。因此,我们证明了 miR-155 可以通过靶向炎症途径中的关键衔接分子 MyD88 负调控炎症。