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Nlrp12 mutation causes C57BL/6J strain-specific defect in neutrophil recruitment

Author

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  • Tyler K. Ulland

    (Inflammation Program, University of Iowa Carver College of Medicine
    Interdisciplinary Program in Molecular and Cellular Biology, University of Iowa Carver College of Medicine)

  • Nidhi Jain

    (Inflammation Program, University of Iowa Carver College of Medicine
    Cedars-Sinai Medical Center)

  • Emma E. Hornick

    (Inflammation Program, University of Iowa Carver College of Medicine
    Interdisciplinary Program in Immunology, University of Iowa Carver College of Medicine)

  • Eric I. Elliott

    (Inflammation Program, University of Iowa Carver College of Medicine
    Interdisciplinary Program in Molecular and Cellular Biology, University of Iowa Carver College of Medicine
    Cedars-Sinai Medical Center
    Medical Scientist Training Program, University of Iowa Carver College of Medicine)

  • Gwendolyn M. Clay

    (Interdisciplinary Program in Molecular and Cellular Biology, University of Iowa Carver College of Medicine
    Medical Scientist Training Program, University of Iowa Carver College of Medicine)

  • Jeffrey J. Sadler

    (Inflammation Program, University of Iowa Carver College of Medicine)

  • Kathleen A. M. Mills

    (Inflammation Program, University of Iowa Carver College of Medicine)

  • Ann M. Janowski

    (Inflammation Program, University of Iowa Carver College of Medicine
    Interdisciplinary Program in Immunology, University of Iowa Carver College of Medicine)

  • A. Paige Davis Volk

    (Inflammation Program, University of Iowa Carver College of Medicine
    University of Iowa Carver College of Medicine)

  • Kai Wang

    (University of Iowa College of Public Health)

  • Kevin L. Legge

    (Interdisciplinary Program in Immunology, University of Iowa Carver College of Medicine
    Medical Scientist Training Program, University of Iowa Carver College of Medicine
    University of Iowa Carver College of Medicine)

  • Lokesh Gakhar

    (University of Iowa Carver College of Medicine
    Protein Crystallography Facility, University of Iowa Carver College of Medicine)

  • Mohammed Bourdi

    (Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health)

  • Polly J. Ferguson

    (University of Iowa Carver College of Medicine)

  • Mary E. Wilson

    (Interdisciplinary Program in Molecular and Cellular Biology, University of Iowa Carver College of Medicine
    Interdisciplinary Program in Immunology, University of Iowa Carver College of Medicine
    Medical Scientist Training Program, University of Iowa Carver College of Medicine
    University of Iowa Carver College of Medicine)

  • Suzanne L. Cassel

    (Inflammation Program, University of Iowa Carver College of Medicine
    Cedars-Sinai Medical Center
    Interdisciplinary Program in Immunology, University of Iowa Carver College of Medicine
    University of Iowa Carver College of Medicine)

  • Fayyaz S. Sutterwala

    (Inflammation Program, University of Iowa Carver College of Medicine
    Interdisciplinary Program in Molecular and Cellular Biology, University of Iowa Carver College of Medicine
    Cedars-Sinai Medical Center
    Interdisciplinary Program in Immunology, University of Iowa Carver College of Medicine)

Abstract

The inbred mouse strain C57BL/6J is widely used in models of immunological and infectious diseases. Here we show that C57BL/6J mice have a defect in neutrophil recruitment to a range of inflammatory stimuli compared with the related C57BL/6N substrain. This immune perturbation is associated with a missense mutation in Nlrp12 in C57BL/6J mice. Both C57BL/6J and NLRP12-deficient mice have increased susceptibility to bacterial infection that correlates with defective neutrophil migration. C57BL/6J and NLRP12-deficient macrophages have impaired CXCL1 production and the neutrophil defect observed in C57BL/6J and NLRP12-deficient mice is rescued by restoration of macrophage NLRP12. These results demonstrate that C57BL/6J mice have a functional defect in NLRP12 and that macrophages require NLRP12 expression for effective recruitment of neutrophils to inflammatory sites.

Suggested Citation

  • Tyler K. Ulland & Nidhi Jain & Emma E. Hornick & Eric I. Elliott & Gwendolyn M. Clay & Jeffrey J. Sadler & Kathleen A. M. Mills & Ann M. Janowski & A. Paige Davis Volk & Kai Wang & Kevin L. Legge & Lo, 2016. "Nlrp12 mutation causes C57BL/6J strain-specific defect in neutrophil recruitment," Nature Communications, Nature, vol. 7(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13180
    DOI: 10.1038/ncomms13180
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