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* Max F. Perutz Laboratories, University Departments at the Vienna Biocenter, Department of Microbiology and Genetics, University of Vienna,
Intercell AG, and
Institute of Animal Breeding and Genetics, Veterinary University of Vienna, Vienna, Austria;
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan;
¶
Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Tokyo, Japan; and
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Department of Infectious Diseases, St. Jude Children’s Research Hospital, Memphis, TN 38105
Like viruses, intracellular bacteria stimulate their host cells to produce type I IFNs (IFN-
and IFN-
). In our study, we investigated the signals and molecules relevant for the synthesis of and response to IFN by mouse macrophages infected with Listeria monocytogenes. We report that IFN- is the critical immediate-early IFN made during infection, because the synthesis of all other type I IFN, expression of a subset of infection-induced genes, and the biological response to type I IFN was lost upon IFN- deficiency. The induction of IFN- mRNA and the IFN--dependent sensitization of macrophages to bacteria-induced death, in turn, was absolutely dependent upon the presence of the transcription factor IFN regulatory factor 3 (IRF3). IFN- synthesis and signal transduction occurred in macrophages deficient for TLR or their adaptors MyD88, TRIF, or TRAM. Expression of Nod2, a candidate receptor for intracellular bacteria, increased during infection, but the protein was not required for Listeria-induced signal transduction to the Ifn- gene. Based on our data, we propose that IRF3 is a convergence point for signals derived from structurally unrelated intracellular pathogens, and that L. monocytogenes stimulates a novel TLR- and Nod2-independent pathway to target IRF3 and the type I IFN genes.
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