Definition: In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
Input: Introduction. Cytosolic pattern recognition receptors (PRR) have been shown to detect nucleic acids from RNA and DNA viruses in order to launch a type I interferon mediated antiviral state [1]. Here we show that RNA of the facultative intracellular bacterium Salmonella typhimurium is a ligand for RIG-I, triggers production of type-I interferons and contributes to pathogenicity in vivo. Methods. We use RIG-IÀ/À MEFs [2] or human epithelial cells depleted of RIG-I by lentiviral shRNA transduction for transfection and infection experiments. IFNbeta production was measured by 293T IFNbeta-reporter cells or qPCR. Intracellular bacterial titers were determined by gentamycin protection assay. In vivo infection experiments were performed as described [3] using SL1344 or SL1344 aroA deficient Salmonella strains in RIG-I+/+ and RIG-IÀ/À mice [4]. Results. Infection of fibroblasts and epithelial cells with S. typhimurium, but not with non-invasive E. coli, triggers IFNbeta transcription, suggesting that intracellular replication is required. RIG-I dependent recognition of bacterial RNA is dominant in non-phagocytic cells, as shown in RIG-I knockout and knockdown model cells. Despite presence of other pathogen-associated patterns (PAMP), like LPS or flagellin, no IFNbeta was produced in fibroblasts and epithelial cells lacking RIG-I upon S. typhimurium infection. In contrast, in macrophages TLR dependent recognition of bacterial PAMPs through TRIF/Myd88 overcomes RIG-I deficiency and leads to robust induction of type I interferon. We observed higher bacterial titers at early time points after infection in the cecum of S. typhimurium infected RIG-IÀ/À mice, when compared to wild type animals. However, at later stages of infection, S. typhimurium overcomes the innate response leading to similar weight loss and mortality in wildtype and RIG-IÀ/À mice. Conclusion. In summary, our data implicate a role of RIG-I mediated innate immune recognition of bacterial RNA in early control of bacterial replication, most likely mediated by non-phagocytic intestinal epithelial cells targeted by S. typhimurium. Disclosure of interest: None declared. Combined action of type I and type III IFN restricts initial replication of SARScoronavirus in the lung but fails to inhibit systemic virus spread

P133 RIG-I mediates recognition of Salmonella RNA in non-phagocytic cells and con- tributes to early bacterial replication in vivo P135 Defining the intracellular innate immune synapse