The Journal of Experimental Medicine
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Published online 9 August 2004 doi:10.1084/jem.20040712
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 200, Number 4, 437-445
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Type I Interferon Production Enhances Susceptibility to Listeria monocytogenes Infection

Ryan M. O'Connell1, Supriya K. Saha1,2, Sagar A. Vaidya1,2, Kevin W. Bruhn1, Gustavo A. Miranda4,5, Brian Zarnegar1, Andrea K. Perry1, Bidong O. Nguyen1, Timothy F. Lane4,5, Tadatsugu Taniguchi6, Jeff F. Miller1,3, and Genhong Cheng1,3,4

1 Department of Microbiology, Immunology and Molecular Genetics, 2 Medical Scientist Training Program, 3 Molecular Biology Institute, 4 Jonsson Comprehensive Cancer Center, and 5 Department of Obstetrics and Gynecology and Department of Biological Chemistry, University of California, Los Angeles, Los Angeles, CA 90095
6 Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Tokyo 113-0033, Japan

Address correspondence to Genhong Cheng, Dept. of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, 8-240 Factor Bldg., 10833 Le Conte Ave., Los Angeles, CA 90095. Phone: (310) 825-8896; Fax: (310) 206-5553; email: genhongc{at}microbio.ucla.edu

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.

Key Words: IRF3 • IFNAR • apoptosis • intracellular bacteria • IFN target gene

R.M. O'Connell, S.K. Saha, and S.A. Vaidya contributed equally to this work.

Abbreviations used in this paper: BHI, brain heart infusion; BMM, bone marrow–derived macrophage; IFNAR, type I IFN receptor; IRF, IFN regulatory factor; LLO, listeriolysin O; Q-PCR, quantitative real-time PCR; TUNEL, TdT-mediated dUTP nick-end labeling; USF, upstream stimulating factor.


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