Macrophage migration inhibitory factor (MIF) plays a pivotal role in immunity against<i>Salmonella typhimurium</i>

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  • Heidrun Koebernick
    Max Planck Institute for Infection Biology, Department of Immunology, Schumannstrasse 20/21, 10117 Berlin, Germany; Harvard School of Public Health, Department of Immunology and Infectious Diseases, 665 Huntington Avenue, Boston, MA 02115; Institute of Experimental Endocrinology, Humboldt University Medical School (Charité), Schumannstrasse 20/21, 10117 Berlin, Germany; and Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, Sydney NSW 2010, Australia
  • Leander Grode
    Max Planck Institute for Infection Biology, Department of Immunology, Schumannstrasse 20/21, 10117 Berlin, Germany; Harvard School of Public Health, Department of Immunology and Infectious Diseases, 665 Huntington Avenue, Boston, MA 02115; Institute of Experimental Endocrinology, Humboldt University Medical School (Charité), Schumannstrasse 20/21, 10117 Berlin, Germany; and Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, Sydney NSW 2010, Australia
  • John R. David
    Max Planck Institute for Infection Biology, Department of Immunology, Schumannstrasse 20/21, 10117 Berlin, Germany; Harvard School of Public Health, Department of Immunology and Infectious Diseases, 665 Huntington Avenue, Boston, MA 02115; Institute of Experimental Endocrinology, Humboldt University Medical School (Charité), Schumannstrasse 20/21, 10117 Berlin, Germany; and Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, Sydney NSW 2010, Australia
  • Wolfgang Rohde
    Max Planck Institute for Infection Biology, Department of Immunology, Schumannstrasse 20/21, 10117 Berlin, Germany; Harvard School of Public Health, Department of Immunology and Infectious Diseases, 665 Huntington Avenue, Boston, MA 02115; Institute of Experimental Endocrinology, Humboldt University Medical School (Charité), Schumannstrasse 20/21, 10117 Berlin, Germany; and Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, Sydney NSW 2010, Australia
  • Michael S. Rolph
    Max Planck Institute for Infection Biology, Department of Immunology, Schumannstrasse 20/21, 10117 Berlin, Germany; Harvard School of Public Health, Department of Immunology and Infectious Diseases, 665 Huntington Avenue, Boston, MA 02115; Institute of Experimental Endocrinology, Humboldt University Medical School (Charité), Schumannstrasse 20/21, 10117 Berlin, Germany; and Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, Sydney NSW 2010, Australia
  • Hans-Willi Mittrücker
    Max Planck Institute for Infection Biology, Department of Immunology, Schumannstrasse 20/21, 10117 Berlin, Germany; Harvard School of Public Health, Department of Immunology and Infectious Diseases, 665 Huntington Avenue, Boston, MA 02115; Institute of Experimental Endocrinology, Humboldt University Medical School (Charité), Schumannstrasse 20/21, 10117 Berlin, Germany; and Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, Sydney NSW 2010, Australia
  • Stefan H. E. Kaufmann
    Max Planck Institute for Infection Biology, Department of Immunology, Schumannstrasse 20/21, 10117 Berlin, Germany; Harvard School of Public Health, Department of Immunology and Infectious Diseases, 665 Huntington Avenue, Boston, MA 02115; Institute of Experimental Endocrinology, Humboldt University Medical School (Charité), Schumannstrasse 20/21, 10117 Berlin, Germany; and Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, Sydney NSW 2010, Australia

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<jats:p>The cytokine macrophage migration inhibitory factor (MIF) exerts a multitude of biological functions. Notably, it induces inflammation at the interface between the immune system and the hypothalamus–pituitary–adrenal stress axis. The role of MIF in infectious diseases is not understood completely. Here, we show that MIF-deficient (MIF<jats:sup>−/−</jats:sup>) knockout mice fail to control an infection with wild-type<jats:italic>Salmonella</jats:italic><jats:italic>typhimurium</jats:italic>. Increased susceptibility was accompanied by a reduced Th1 response, demonstrated by decreased levels of IL-12, IFNγ, and tumor necrosis factor α. In<jats:italic>Salmonella</jats:italic>-infected MIF<jats:sup>−/−</jats:sup>mice, levels of IL-1β were markedly increased. Additionally, infected MIF<jats:sup>−/−</jats:sup>mice showed elevated serum levels of nitric oxide and corticosterone as compared with control mice. Our results point to MIF as a key mediator in the host response to<jats:italic>S. typhimurium</jats:italic>. MIF not only promotes development of a protective Th1 response but ameliorates disease by altering levels of reactive nitrogen intermediates and corticosteroid hormones, which both exert immunosuppressive functions.</jats:p>

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