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* Vienna Biocenter and University of Vienna, Institute of Microbiology and Genetics, Vienna, Austria;
Institute of Animal Breeding and Genetics and
Institute of Virology, Veterinary University of Vienna, Vienna, Austria;
Department of Biotechnology in Animal Production, Institute of Agrobiotechnology, Tulln, Austria;
¶ Institute of Medical Microbiology, Justus-Liebig University, Giessen, Germany; and
|| Department of Pathology and Kaplan Comprehensive Cancer Center, New York University School of Medicine, New York, NY 10016
Type I IFNs (IFN-
/
) modulate innate immune responses. Here we
show activation of transcription factor IFN regulatory factor 3, the
synthesis of large amounts of IFN- 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- 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.
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