Journal
PLOS ONE
Volume 7, Issue 3, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0033299
Keywords
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Categories
Funding
- Institut Pasteur
- Inserm
- INRA
- ERC [233348]
- Fondation Pasteur-Weizmann
- Fondation le Roch Les Mousquetaires
- Science Foundation Ireland
- Irish Research Council for Science, Engineering and Technology [RS/2005/190]
- Austrian Research Foundation [SFB-28, P20522-B05]
- Austrian Science Fund (FWF) [P20522] Funding Source: Austrian Science Fund (FWF)
- Austrian Science Fund (FWF) [F 2803] Funding Source: researchfish
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Synthesis of interferon-beta (IFN-beta) is an innate response to cytoplasmic infection with bacterial pathogens. Our recent studies showed that Listeria monocytogenes limits immune detection and IFN-beta synthesis via deacetylation of its peptidoglycan, which renders the bacterium resistant to lysozyme degradation. Here, we examined signaling requirements for the massive IFN-beta production resulting from the infection of murine macrophages with a mutant strain of L. monocytogenes, Delta pgdA, which is unable to modify its peptidoglycan. We report the identification of unconventional signaling pathways to the IFN-beta gene, requiring TLR2 and bacterial internalization. Induction of IFN-beta was independent of the Mal/TIRAP adaptor protein but required TRIF and the transcription factors IRF3 and IRF7. These pathways were stimulated to a lesser degree by wild-type L. monocytogenes. They operated in both resident and inflammatory macrophages derived from the peritoneal cavity, but not in bone marrow-derived macrophages. The novelty of our findings thus lies in the first description of TLR2 and TRIF as two critical components leading to the induction of the IFN-beta gene and in uncovering that individual macrophage populations adopt different strategies to link pathogen recognition signals to IFN-beta gene expression.
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