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

Author:

Auerbuch Victoria1,Brockstedt Dirk G.2,Meyer-Morse Nicole1,O'Riordan Mary1,Portnoy Daniel A.13

Affiliation:

1. Department of Molecular and Cell Biology

2. Cerus Corporation, Concord, CA 94520

3. School of Public Health, University of California, Berkeley, Berkeley, CA 94720

Abstract

Listeria monocytogenes is a facultative intracellular pathogen that induces a cytosolic signaling cascade resulting in expression of interferon (IFN)-β. 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-α/βR−/−). During the first 24 h of infection in vivo, IFN-α/βR−/− 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-α/βR−/− and wild-type mice was indistinguishable. However, by 72 h after inoculation in vivo, IFN-α/βR−/− 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 α in the spleen of IFN-α/βR−/− mice. The results of this study suggest that L. monocytogenes might be exploiting an innate antiviral response to promote its pathogenesis.

Publisher

Rockefeller University Press

Subject

Immunology,Immunology and Allergy

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