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CD200R deletion promotes a neutrophil niche for Francisella tularensis and increases infectious burden and mortality

Author

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  • J. Casulli

    (Lydia Becker Institute for Immunology and Inflammation
    Wellcome Trust Centre for Cell-Matrix Research
    University of Manchester)

  • M. E. Fife

    (Lydia Becker Institute for Immunology and Inflammation
    University of Manchester)

  • S. A. Houston

    (Lydia Becker Institute for Immunology and Inflammation
    Wellcome Trust Centre for Cell-Matrix Research
    University of Manchester)

  • S. Rossi

    (Lydia Becker Institute for Immunology and Inflammation
    Wellcome Trust Centre for Cell-Matrix Research
    University of Manchester)

  • J. Dow

    (Lydia Becker Institute for Immunology and Inflammation
    Wellcome Trust Centre for Cell-Matrix Research
    University of Manchester)

  • E. D. Williamson

    (Defence Science and Technology Laboratory (Dstl), Porton Down)

  • G. C Clark

    (Defence Science and Technology Laboratory (Dstl), Porton Down)

  • T. Hussell

    (Lydia Becker Institute for Immunology and Inflammation
    University of Manchester)

  • R. V. D’Elia

    (Defence Science and Technology Laboratory (Dstl), Porton Down)

  • M. A Travis

    (Lydia Becker Institute for Immunology and Inflammation
    Wellcome Trust Centre for Cell-Matrix Research
    University of Manchester)

Abstract

Pulmonary immune control is crucial for protection against pathogens. Here we identify a pathway that promotes host responses during pulmonary bacterial infection; the expression of CD200 receptor (CD200R), which is known to dampen pulmonary immune responses, promotes effective clearance of the lethal intracellular bacterium Francisella tularensis. We show that depletion of CD200R in mice increases in vitro and in vivo infectious burden. In vivo, CD200R deficiency leads to enhanced bacterial burden in neutrophils, suggesting CD200R normally limits the neutrophil niche for infection. Indeed, depletion of this neutrophil niche in CD200R−/− mice restores F. tularensis infection to levels seen in wild-type mice. Mechanistically, CD200R-deficient neutrophils display significantly reduced reactive oxygen species production (ROS), suggesting that CD200R-mediated ROS production in neutrophils is necessary for limiting F. tularensis colonisation and proliferation. Overall, our data show that CD200R promotes the antimicrobial properties of neutrophils and may represent a novel antibacterial therapeutic target.

Suggested Citation

  • J. Casulli & M. E. Fife & S. A. Houston & S. Rossi & J. Dow & E. D. Williamson & G. C Clark & T. Hussell & R. V. D’Elia & M. A Travis, 2019. "CD200R deletion promotes a neutrophil niche for Francisella tularensis and increases infectious burden and mortality," Nature Communications, Nature, vol. 10(1), pages 1-9, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-10156-6
    DOI: 10.1038/s41467-019-10156-6
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    Cited by:

    1. Nicolaj S. Hackert & Felix A. Radtke & Tarik Exner & Hanns-Martin Lorenz & Carsten Müller-Tidow & Peter A. Nigrovic & Guido Wabnitz & Ricardo Grieshaber-Bouyer, 2023. "Human and mouse neutrophils share core transcriptional programs in both homeostatic and inflamed contexts," Nature Communications, Nature, vol. 14(1), pages 1-21, December.

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