Role of Mincle in Alveolar Macrophage-Dependent Innate Immunity against Mycobacterial Infections in Mice

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  • Friederike Behler
    Department of Experimental Pneumology, Hannover Medical School , Hannover 30625,
  • Kathrin Steinwede
    Department of Experimental Pneumology, Hannover Medical School , Hannover 30625,
  • Luciana Balboa
    Instituto de Medicina Experimental, Consejo Nacional de Investigaciones Científicas y Técnicas de Argentina, Academia Nacional de Medicina , 1425 Buenos Aires,
  • Bianca Ueberberg
    Department of Experimental Pneumology, Hannover Medical School , Hannover 30625,
  • Regina Maus
    Department of Experimental Pneumology, Hannover Medical School , Hannover 30625,
  • Gabriele Kirchhof
    Department of Experimental Pneumology, Hannover Medical School , Hannover 30625,
  • Sho Yamasaki
    Division of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University , Fukuoka 812-8582,
  • Tobias Welte
    Clinic for Pneumology, Hannover Medical School , Hannover 30625,
  • Ulrich A Maus
    Department of Experimental Pneumology, Hannover Medical School , Hannover 30625,

書誌事項

公開日
2012-09
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.1201399
公開者
Oxford University Press (OUP)

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説明

<jats:title>Abstract</jats:title> <jats:p>The role of macrophage-inducible C-type lectin Mincle in lung innate immunity against mycobacterial infection is incompletely defined. In this study, we show that wild-type (WT) mice responded with a delayed Mincle induction on resident alveolar macrophages and newly immigrating exudate macrophages to infection with Mycobacterium bovis bacillus Calmette-Guérin (BCG), peaking by days 14–21 posttreatment. As compared with WT mice, Mincle knockout (KO) mice exhibited decreased proinflammatory mediator responses and leukocyte recruitment upon M. bovis BCG challenge, and they demonstrated increased mycobacterial loads in pulmonary and extrapulmonary organ systems. Secondary mycobacterial infection on day 14 after primary BCG challenge led to increased cytokine gene expression in sorted alveolar macrophages of WT mice, but not Mincle KO mice, resulting in substantially reduced alveolar neutrophil recruitment and increased mycobacterial loads in the lungs of Mincle KO mice. Collectively, these data show that WT mice respond with a relatively late Mincle expression on lung sentinel cells to M. bovis BCG infection. Moreover, M. bovis BCG-induced upregulation of C-type lectin Mincle on professional phagocytes critically shapes antimycobacterial responses in both pulmonary and extrapulmonary organ systems of mice, which may be important for elucidating the role of Mincle in the control of mycobacterial dissemination in mice.</jats:p>

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