Both TLR2 and TRIF contribute to interferon-? production during Listeria infection.
Citation:Aubry C, Corr SC, Wienerroither S, Goulard C, Jones R, Jamieson AM, Decker T, O'Neill LA, Dussurget O, Cossart P, Both TLR2 and TRIF contribute to interferon-? production during Listeria infection., PloS one, 7, 3, 2012, e33299
journal.pone.0033299.pdf (Published (publisher's copy) - Peer Reviewed) 754.1Kb
Synthesis of interferon-? (IFN-?) is an innate response to cytoplasmic infection with bacterial pathogens. Our recent studies showed that Listeria monocytogenes limits immune detection and IFN-? synthesis via deacetylation of its peptidoglycan, which renders the bacterium resistant to lysozyme degradation. Here, we examined signaling requirements for the massive IFN-? production resulting from the infection of murine macrophages with a mutant strain of L. monocytogenes, ?pgdA, which is unable to modify its peptidoglycan. We report the identification of unconventional signaling pathways to the IFN-? gene, requiring TLR2 and bacterial internalization. Induction of IFN-? 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-? gene and in uncovering that individual macrophage populations adopt different strategies to link pathogen recognition signals to IFN-? gene expression.
Type of material:Journal Article
Series/Report no:PloS one
Availability:Full text available
Subject (TCD):Immunology, Inflammation & Infection