| Autor: |
Cremer, Thomas J., Fatehchand, Kavin, Shah, Prexy, Gillette, Devyn, Patel, Hemal, Marsh, Rachel L., Besecker, Beth Y., Rajaram, Murugesan V. S., Cormet-Boyaka, Estelle, Kanneganti, Thirumala-Devi, Schlesinger, Larry S., Butchar, Jonathan P., Tridandapani, Susheela |
| Předmět: |
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| Zdroj: |
Frontiers in Cellular & Infection Microbiology; Jun2012, Vol. 2, p1-12, 12p |
| Abstrakt: |
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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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