Molecular, Cellular, and Developmental Biology Program, The Ohio State University Columbus, OH, USA.
Front Cell Infect Microbiol. 2012 Jun 1;2:73. doi: 10.3389/fcimb.2012.00073. eCollection 2012.
MiR-155 regulates numerous aspects of innate and adaptive immune function. This miR is induced in response to Toll-like receptor ligands, cytokines, and microbial infection. We have previously shown that miR-155 is induced in monocytes/macrophages infected with Francisella tularensis and suppresses expression of the inositol phosphatase SHIP to enhance activation of the PI3K/Akt pathway, which in turn promotes favorable responses for the host. Here we examined how miR-155 expression is regulated during infection. First, our data demonstrate that miR-155 can be induced through soluble factors of bacterial origin and not the host. Second, miR-155 induction is not a direct effect of infection and it requires NF-κB signaling to up-regulate fos/jun transcription factors. Finally, we demonstrate that the requirement for NF-κB-dependent de novo protein synthesis is globally shared by microbial ligands and live bacteria. This study provides new insight into the complex regulation of miR-155 during microbial infection.
miR-155 调节先天和适应性免疫功能的众多方面。这种 mir 是响应 Toll 样受体配体、细胞因子和微生物感染而诱导的。我们之前已经表明，miR-155 在感染弗朗西斯氏菌的单核细胞/巨噬细胞中被诱导，并抑制肌醇磷酸酶 SHIP 的表达，以增强 PI3K/Akt 途径的激活，这反过来又促进了宿主的有利反应。在这里，我们研究了 miR-155 在感染过程中的表达是如何被调节的。首先，我们的数据表明，miR-155 可以通过细菌来源的可溶性因子诱导，而不是由宿主诱导。其次，miR-155 的诱导不是感染的直接作用，它需要 NF-κB 信号转导来上调 fos/jun 转录因子。最后，我们证明，NF-κB 依赖性从头蛋白质合成的要求是微生物配体和活细菌共有的。这项研究为微生物感染过程中 miR-155 的复杂调节提供了新的见解。
