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Inhibition of inflammasome activation by Coxiella burnetii type IV secretion system effector IcaA

Author

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  • Larissa D. Cunha

    (Medical School of Ribeirão Preto, University of São Paulo (FMRP/USP)
    Present address: Department of Immunology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA.)

  • Juliana M. Ribeiro

    (Medical School of Ribeirão Preto, University of São Paulo (FMRP/USP))

  • Talita D. Fernandes

    (Medical School of Ribeirão Preto, University of São Paulo (FMRP/USP))

  • Liliana M. Massis

    (Medical School of Ribeirão Preto, University of São Paulo (FMRP/USP))

  • Chen Ai Khoo

    (University of Melbourne at the Peter Doherty Institute for Infection and Immunity)

  • Jennifer H. Moffatt

    (University of Melbourne at the Peter Doherty Institute for Infection and Immunity)

  • Hayley J. Newton

    (University of Melbourne at the Peter Doherty Institute for Infection and Immunity)

  • Craig R. Roy

    (Yale University School of Medicine)

  • Dario S. Zamboni

    (Medical School of Ribeirão Preto, University of São Paulo (FMRP/USP))

Abstract

Coxiella burnetii is a highly infectious bacterium that promotes its own replication in macrophages by inhibiting several host cell responses. Here, we show that C. burnetii inhibits caspase-1 activation in primary mouse macrophages. By using co-infection experiments, we determine that the infection of macrophages with C. burnetii inhibits the caspase-11-mediated non-canonical activation of the NLRP3 inflammasome induced by subsequent infection with Escherichia coli or Legionella pneumophila. Genetic screening using flagellin mutants of L. pneumophila as a surrogate host, reveals a novel C. burnetii gene (IcaA) involved in the inhibition of caspase activation. Expression of IcaA in L. pneumophila inhibited the caspase-11 activation in macrophages. Moreover, icaA- mutants of C. burnetii failed to suppress the caspase-11-mediated inflammasome activation induced by L. pneumophila. Our data reveal IcaA as a novel C. burnetii effector protein that is secreted by the Dot/Icm type IV secretion system and interferes with the caspase-11-induced, non-canonical activation of the inflammasome.

Suggested Citation

  • Larissa D. Cunha & Juliana M. Ribeiro & Talita D. Fernandes & Liliana M. Massis & Chen Ai Khoo & Jennifer H. Moffatt & Hayley J. Newton & Craig R. Roy & Dario S. Zamboni, 2015. "Inhibition of inflammasome activation by Coxiella burnetii type IV secretion system effector IcaA," Nature Communications, Nature, vol. 6(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms10205
    DOI: 10.1038/ncomms10205
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    Cited by:

    1. Ordu J I & Amajuo N F, 2024. "Evaluation Of Python Fat-Based Topical Formulation For Enhanced Furuncles (Boils) Management," International Journal of Research and Scientific Innovation, International Journal of Research and Scientific Innovation (IJRSI), vol. 11(2), pages 283-294, February.

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