期刊
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
卷 2, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcimb.2012.00073
关键词
microRNA; microbial pathogenesis; miR-155
资金
- NIH/NIAID Regional Center of Excellence for Biodefense and Emerging Infectious Diseases Research (RCE) Program
- Region V Great Lakes RCE (NIH award) [1-U54-AI-057153]
- NIH/NIAID award [1-T32-AI-065411]
- NRSA training grant at The Ohio State University
- NIH [K12 CA133250]
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-kappa B signaling to up-regulate fos/jun transcription factors. Finally, we demonstrate that the requirement for NF-kappa B-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.
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