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Both TLR2 and TRIF Contribute to Interferon-β Production during <em>Listeria</em> Infection

By Camille Aubry (177586), Sinéad C. Corr (177587), Sebastian Wienerroither (177591), Céline Goulard (177594), Ruth Jones (170929), Amanda M. Jamieson (177599), Thomas Decker (158226), Luke A. J. O'Neill (177603), Olivier Dussurget (141783) and Pascale Cossart (25004)

Abstract

<div><p>Synthesis of interferon-β (IFN-β) is an innate response to cytoplasmic infection with bacterial pathogens. Our recent studies showed that <em>Listeria monocytogenes</em> limits immune detection and IFN-β synthesis via deacetylation of its peptidoglycan, which renders the bacterium resistant to lysozyme degradation. Here, we examined signaling requirements for the massive IFN-β production resulting from the infection of murine macrophages with a mutant strain of <em>L. monocytogenes</em>, Δ<em>pgdA</em>, which is unable to modify its peptidoglycan. We report the identification of unconventional signaling pathways to the IFN-β gene, requiring TLR2 and bacterial internalization. Induction of IFN-β 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 <em>L. monocytogenes</em>. 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-β gene and in uncovering that individual macrophage populations adopt different strategies to link pathogen recognition signals to IFN-β gene expression.</p> </div

Topics: Microbiology, Cell Biology, Molecular Biology, Immunology, tlr2, trif
Year: 2012
DOI identifier: 10.1371/journal.pone.0033299
OAI identifier: oai:figshare.com:article/127589
Provided by: FigShare
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