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Decreased maternal serum acetate and impaired fetal thymic and regulatory T cell development in preeclampsia

Author

Listed:
  • Mingjing Hu

    (The University of Sydney
    The University of Sydney)

  • David Eviston

    (The University of Sydney)

  • Peter Hsu

    (The University of Sydney
    The Children’s Hospital at Westmead)

  • Eliana Mariño

    (Monash University)

  • Ann Chidgey

    (Monash University)

  • Brigitte Santner-Nanan

    (The University of Sydney
    The University of Sydney)

  • Kahlia Wong

    (Monash University)

  • James L. Richards

    (Monash University)

  • Yu Anne Yap

    (Monash University)

  • Fiona Collier

    (Deakin University
    Barwon Health
    Murdoch Children’s Research Institute)

  • Ann Quinton

    (The University of Sydney
    Central Queensland University)

  • Steven Joung

    (The University of Sydney
    Nepean Hospital)

  • Michael Peek

    (The University of Sydney
    The Australian National University)

  • Ron Benzie

    (Nepean Hospital
    The University of Sydney)

  • Laurence Macia

    (The University of Sydney)

  • David Wilson

    (AITHM, James Cook University)

  • Ann-Louise Ponsonby

    (Murdoch Children’s Research Institute
    The Australian National University)

  • Mimi L. K. Tang

    (Murdoch Children’s Research Institute
    The Royal Children’s Hospital, Parkville
    University of Melbourne)

  • Martin O’Hely

    (Deakin University
    Murdoch Children’s Research Institute)

  • Norelle L. Daly

    (AITHM, James Cook University)

  • Charles R. Mackay

    (Monash University)

  • Jane E. Dahlstrom

    (The Australian National University)

  • Peter Vuillermin

    (Deakin University
    Barwon Health
    Murdoch Children’s Research Institute
    Centre for Food and Allergy Research)

  • Ralph Nanan

    (The University of Sydney
    The University of Sydney)

Abstract

Maternal immune dysregulation seems to affect fetal or postnatal immune development. Preeclampsia is a pregnancy-associated disorder with an immune basis and is linked to atopic disorders in offspring. Here we show reduction of fetal thymic size, altered thymic architecture and reduced fetal thymic regulatory T (Treg) cell output in preeclamptic pregnancies, which persists up to 4 years of age in human offspring. In germ-free mice, fetal thymic CD4+ T cell and Treg cell development are compromised, but rescued by maternal supplementation with the intestinal bacterial metabolite short chain fatty acid (SCFA) acetate, which induces upregulation of the autoimmune regulator (AIRE), known to contribute to Treg cell generation. In our human cohorts, low maternal serum acetate is associated with subsequent preeclampsia, and correlates with serum acetate in the fetus. These findings suggest a potential role of acetate in the pathogenesis of preeclampsia and immune development in offspring.

Suggested Citation

  • Mingjing Hu & David Eviston & Peter Hsu & Eliana Mariño & Ann Chidgey & Brigitte Santner-Nanan & Kahlia Wong & James L. Richards & Yu Anne Yap & Fiona Collier & Ann Quinton & Steven Joung & Michael Pe, 2019. "Decreased maternal serum acetate and impaired fetal thymic and regulatory T cell development in preeclampsia," Nature Communications, Nature, vol. 10(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-10703-1
    DOI: 10.1038/s41467-019-10703-1
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