Production of type I IFN sensitizes macrophages to cell death induced by Listeria monocytogenes

Silvia Stockinger, Tilo Materna, Dagmar Stoiber, Lourdes Bayr, Ralf Steinborn, Thomas Kolbe, Hermann Unger, Trinad Chakraborty, David E Levy, Mathias Müller, Thomas Decker

Research output: Journal article (peer-reviewed)Journal article

138 Citations (Scopus)


Type I IFNs (IFN-alpha/beta) modulate innate immune responses. Here we show activation of transcription factor IFN regulatory factor 3, the synthesis of large amounts of IFN-beta mRNA, and type I IFN signal transduction in macrophages infected with Listeria monocytogenes. Expression of the bacterial virulence protein listeriolysin O was necessary, but not sufficient, for efficient IFN-beta production. Signaling through a pathway involving the type I IFN receptor and Stat1 sensitized macrophages to L. monocytogenes-induced cell death in a manner not requiring inducible NO synthase (nitric oxide synthase 2) or protein kinase R, potential effectors of type I IFN action during microbial infections. The data stress the importance of type I IFN for the course of infections with intracellular bacteria and suggest that factors other than listeriolysin O contribute to macrophage death during Listeria infection.

Original languageEnglish
Pages (from-to)6522-9
Number of pages8
JournalJournal of Immunology
Issue number11
Publication statusPublished - 01 Dec 2002
Externally publishedYes


  • Animals
  • Bacterial Toxins
  • Base Sequence
  • Cell Death/drug effects
  • DNA-Binding Proteins/metabolism
  • Heat-Shock Proteins/toxicity
  • Hemolysin Proteins
  • Interferon Regulatory Factor-3
  • Interferon-alpha/biosynthesis
  • Interferon-beta/biosynthesis
  • Listeria monocytogenes/immunology
  • Macrophages/drug effects
  • Membrane Proteins
  • Mice
  • Mice, Knockout
  • RNA, Messenger/biosynthesis
  • Receptor, Interferon alpha-beta
  • Receptors, Interferon/deficiency
  • Signal Transduction
  • Transcription Factors/metabolism
  • Virulence


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