Type I interferon production enhances susceptibility to Listeria monocytogenes infection

J Exp Med. 2004 Aug 16;200(4):437-45. doi: 10.1084/jem.20040712. Epub 2004 Aug 9.


Numerous bacterial products such as lipopolysaccharide potently induce type I interferons (IFNs); however, the contribution of this innate response to host defense against bacterial infection remains unclear. Although mice deficient in either IFN regulatory factor (IRF)3 or the type I IFN receptor (IFNAR)1 are highly susceptible to viral infection, we show that these mice exhibit a profound resistance to infection caused by the Gram-positive intracellular bacterium Listeria monocytogenes compared with wild-type controls. Furthermore, this enhanced bacterial clearance is accompanied by a block in L. monocytogenes-induced splenic apoptosis in IRF3- and IFNAR1-deficient mice. Thus, our results highlight the disparate roles of type I IFNs during bacterial versus viral infections and stress the importance of proper IFN modulation in host defense.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis / immunology*
  • DNA Primers
  • DNA-Binding Proteins / deficiency*
  • Disease Susceptibility
  • Enzyme-Linked Immunosorbent Assay
  • Immunoblotting
  • In Situ Nick-End Labeling
  • Interferon Regulatory Factor-3
  • Interferon Type I / immunology*
  • Listeriosis / immunology*
  • Liver / pathology
  • Macrophages / immunology
  • Membrane Proteins
  • Mice
  • Mice, Inbred C57BL
  • Polymerase Chain Reaction / methods
  • Receptor, Interferon alpha-beta
  • Receptors, Interferon / deficiency*
  • Spleen / immunology
  • Transcription Factors / deficiency*


  • DNA Primers
  • DNA-Binding Proteins
  • Ifnar1 protein, mouse
  • Interferon Regulatory Factor-3
  • Interferon Type I
  • Irf3 protein, mouse
  • Membrane Proteins
  • Receptors, Interferon
  • Transcription Factors
  • Receptor, Interferon alpha-beta