The Journal of Experimental Medicine
Fluorescence In Vivo Endomicroscopy
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Published online 9 August 2004 doi:10.1084/jem.20040976
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 200, Number 4, 527-533
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Brief Definitive Report

 Mice Lacking the Type I Interferon Receptor Are Resistant to Listeria monocytogenes

Victoria Auerbuch1, Dirk G. Brockstedt3, Nicole Meyer-Morse1, Mary O'Riordan1, and Daniel A. Portnoy1,2

1 Department of Molecular and Cell Biology and 2 School of Public Health, University of California, Berkeley, Berkeley, CA 94720
3 Cerus Corporation, Concord, CA 94520

Address correspondence to Daniel A. Portnoy, Dept. of Molecular and Cell Biology, 508 Barker Hall, University of California, Berkeley, Berkeley, CA 94720. Phone: (510) 643-3925; Fax: (510) 643-6334; email: portnoy{at}berkeley.edu

Listeria monocytogenes is a facultative intracellular pathogen that induces a cytosolic signaling cascade resulting in expression of interferon (IFN)-ß. Although type I IFNs are critical in viral defense, their role in immunity to bacterial pathogens is much less clear. In this study, we addressed the role of type I IFNs by examining the infection of L. monocytogenes in BALB/c mice lacking the type I IFN receptor (IFN-{alpha}/ßR–/–). During the first 24 h of infection in vivo, IFN-{alpha}/ßR–/– and wild-type mice were similar in terms of L. monocytogenes survival. In addition, the intracellular fate of L. monocytogenes in macrophages cultured from IFN-{alpha}/ßR–/– and wild-type mice was indistinguishable. However, by 72 h after inoculation in vivo, IFN-{alpha}/ßR–/– mice were ~1,000-fold more resistant to a high dose L. monocytogenes infection. Resistance was correlated with elevated levels of interleukin 12p70 in the blood and increased numbers of CD11b+ macrophages producing tumor necrosis factor {alpha} in the spleen of IFN-{alpha}/ßR–/– mice. The results of this study suggest that L. monocytogenes might be exploiting an innate antiviral response to promote its pathogenesis.

Key Words: TNF-{alpha} • CD11b antigen • macrophages • IL-12 • pathogen

Mary O'Riordan's present address is Dept. of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109.


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