Autophagosomes can support Yersinia pseudotuberculosis replication in macrophages

Authors

  • Kevin Moreau,

    1. Cellular Microbiology of Infectious Pathogens – Center of Infection and Immunity of Lille – Institut Pasteur de Lille, Lille F-59019, France.
    2. CNRS UMR 8204, Lille F-59046, France.
    3. INSERM U1019, Lille F-59008, France.
    4. Univ. Lille Nord de France, Lille F-59044, France.
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  • Sandra Lacas-Gervais,

    1. Cellular Microbiology of Infectious Pathogens – Center of Infection and Immunity of Lille – Institut Pasteur de Lille, Lille F-59019, France.
    2. CNRS UMR 8204, Lille F-59046, France.
    3. INSERM U1019, Lille F-59008, France.
    4. Univ. Lille Nord de France, Lille F-59044, France.
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  • Naonobu Fujita,

    1. Department of Cellular Regulation, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan.
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  • Florent Sebbane,

    1. CNRS UMR 8204, Lille F-59046, France.
    2. INSERM U1019, Lille F-59008, France.
    3. Univ. Lille Nord de France, Lille F-59044, France.
    4. Plague and Yersinia pestis – Center of Infection and Immunity of Lille – Institute Pasteur de Lille, Lille F-59019, France.
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  • Tamotsu Yoshimori,

    1. Department of Cellular Regulation, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan.
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  • Michel Simonet,

    1. CNRS UMR 8204, Lille F-59046, France.
    2. INSERM U1019, Lille F-59008, France.
    3. Univ. Lille Nord de France, Lille F-59044, France.
    4. Plague and Yersinia pestis – Center of Infection and Immunity of Lille – Institute Pasteur de Lille, Lille F-59019, France.
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  • Frank Lafont

    Corresponding author
    1. Cellular Microbiology of Infectious Pathogens – Center of Infection and Immunity of Lille – Institut Pasteur de Lille, Lille F-59019, France.
    2. CNRS UMR 8204, Lille F-59046, France.
    3. INSERM U1019, Lille F-59008, France.
    4. Univ. Lille Nord de France, Lille F-59044, France.
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E-mail frank.lafont@pasteur-lille.fr; Tel. (+33) 320 871 136; Fax (+33) 320 871 135.

Summary

Yersinia pseudotuberculosis is able to replicate inside macrophages. However, the intracellular trafficking of the pathogen after its entry into the macrophage remains poorly understood. Using in vitro infected bone marrow-derived macrophages, we show that Y. pseudotuberculosis activates the autophagy pathway. Host cell autophagosomes subverted by bacteria do not become acidified and sustain bacteria replication. Moreover, we report that autophagy inhibition correlated with bacterial trafficking inside an acidic compartment. This study indicates that Y. pseudotuberculosis hijacks the autophagy pathway for its replication and also opens up new opportunities for deciphering the molecular basis of the host cell signalling response to intracellular Yersinia infection.

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