title: Type I interferon promotes cell-to-cell spread of Listeria monocytogenes.
abstract: Type I interferons (IFNs) play a critical role in antiviral immune responses, but can be deleterious to the host during some bacterial infections. Listeria monocytogenes (Lm) induces a type I IFN response by activating cytosolic antiviral surveillance pathways. This is beneficial to the bacteria as mice lacking the type I IFN receptor (IFNAR1-/-) are resistant to systemic infection by Lm. The mechanisms by which type I IFNs promote Lm infection are unclear. Here, we show that IFNAR1 is required for dissemination of Lm within infection foci in livers of infected mice and for efficient cell-to-cell spread in vitro in macrophages. IFNAR1 promotes ActA polarization and actin-based motility in the cytosol of host cells. Our studies suggest type I IFNs directly impact the intracellular life cycle of Lm and provide new insight into the mechanisms used by bacterial pathogens to exploit the type I IFN response.
authors: Cell Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada.
authors: Suzanne E
authors: SE
authors: Osborne
authors: Cell Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada.|Department of Immunology, University of Toronto, Toronto, Ontario, Canada.
authors: Brandon
authors: B
authors: Sit
authors: Cell Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada.|Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.
authors: Andrew
authors: A
authors: Shaker
authors: Cell Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada.|Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.
authors: Elissa
authors: E
authors: Currie
authors: Cell Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada.
authors: Joël M J
authors: JM
authors: Tan
authors: Cell Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada.
authors: Jorik
authors: J
authors: van Rijn
authors: Department of Microbiology and Immunology, Harvard Medical School, Boston, Massachusetts, USA.
authors: Darren E
authors: DE
authors: Higgins
authors: Cell Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada.|Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.|Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada.|SickKids IBD Centre, Hospital for Sick Children, Toronto, Ontario, Canada.
authors: John H
authors: JH
authors: Brumell
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D054884:Host-Pathogen Interactions; D007370:Interferon Type I / Q000378:metabolism*; D008089:Listeria monocytogenes / Q000254:growth & development*; D008088:Listeriosis / Q000382:microbiology / Q000473:pathology; D008099:Liver / Q000382:microbiology / Q000473:pathology; D008264:Macrophages / Q000382:microbiology; D051379:Mice; D053633:Receptor, Interferon alpha-beta / Q000378:metabolism
chemical_list: C508032:Ifnar1 protein, mouse; D007370:Interferon Type I; D053633:Receptor, Interferon alpha-beta