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Infection and Immunity, September 2008, p. 3881-3890, Vol. 76, No. 9
0019-9567/08/$08.00+0     doi:10.1128/IAI.01651-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Decreased Susceptibility of Mice to Infection with Listeria monocytogenes in the Absence of Interleukin-18{triangledown}

Matthias Lochner,1,{dagger} Kathrin Kastenmüller,1,3 Michael Neuenhahn,1 Heike Weighardt,4 Dirk H. Busch,1,3 Wolfgang Reindl,2 and Irmgard Förster1,4*

Institute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich, Munich, Germany,1 Department of Internal Medicine II, Technical University of Munich, Munich, Germany,2 Clinical Cooperation Group Antigen-Specific Immunotherapy, Helmholtz Zentrum München—German Research Center for Environmental Health and Technical University of Munich, Neuherberg, Germany,3 Institut für Umweltmedizinische Forschung, Heinrich-Heine Universität Düsseldorf, Düsseldorf, Germany4

Received 12 December 2007/ Returned for modification 28 January 2008/ Accepted 5 June 2008

The induction of proinflammatory cytokines such as gamma interferon (IFN-{gamma}) and tumor necrosis factor alpha is crucial for the early control of bacterial infections. Since interleukin-18 (IL-18) acts as a potent inducer of IFN-{gamma}, it might play an important role in the induction of a protective immune response in listeriosis. We used a murine model of systemic Listeria monocytogenes infection to study the immune response to these intracellular bacteria in the absence of IL-18. For this purpose, IL-18-deficient mice and mice treated with anti-IL-18 neutralizing antibody were infected with L. monocytogenes, and their innate and adaptive immune responses were compared to those of control mice. Unexpectedly, we found that mice deficient in IL-18 were partially resistant to primary infection with L. monocytogenes. At day 3 after infection, the numbers of listeriae in the livers and spleens of control mice were up to 500 times higher than those in IL-18-deficient or anti-IL-18 antibody-treated mice. In addition, the level of proinflammatory cytokines was markedly reduced in IL-18-deficient mice. Enhanced resistance to L. monocytogenes infection in IL-18-deficient mice was accompanied by increased numbers of leukocytes and reduced apoptosis in the spleen 48 to 72 h after infection. In contrast, control and IL-18-deficient mice showed no significant differences in their abilities to mount a protective L. monocytogenes-specific T-cell response.

* Corresponding author. Mailing address: Institut für Umweltmedizinische Forschung, Heinrich-Heine Universität Düsseldorf, Auf'm Hennekamp 50, D-40225 Düsseldorf, Germany. Phone: 49 211 3389210. Fax: 49 211 312976. E-mail: Irmgard.Foerster{at}uni-duesseldorf.de

{triangledown} Published ahead of print on 23 June 2008.

Editor: R. P. Morrison

{dagger} Present address: Laboratory of Lymphoid Tissue Development, Institut Pasteur, Paris, France.

Infection and Immunity, September 2008, p. 3881-3890, Vol. 76, No. 9
0019-9567/08/$08.00+0     doi:10.1128/IAI.01651-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Haring, J. S., Harty, J. T. (2009). Interleukin-18-Related Genes Are Induced during the Contraction Phase but Do Not Play Major Roles in Regulating the Dynamics or Function of the T-Cell Response to Listeria monocytogenes Infection. Infect. Immun. 77: 1894-1903 [Abstract] [Full Text]  


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