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

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 Peek, Ron Benzie, Laurence Macia, David Wilson, Ann-Louise Ponsonby, Mimi L. K. Tang, Martin O’Hely, Norelle L. Daly, Charles R. Mackay, Jane E. Dahlstrom, Peter Vuillermin and Ralph Nanan ()
Additional contact information
Mingjing Hu: The University of Sydney
David Eviston: The University of Sydney
Peter Hsu: The University of Sydney
Eliana Mariño: Monash University
Ann Chidgey: Monash University
Brigitte Santner-Nanan: The University of Sydney
Kahlia Wong: Monash University
James L. Richards: Monash University
Yu Anne Yap: Monash University
Fiona Collier: Deakin University
Ann Quinton: The University of Sydney
Steven Joung: The University of Sydney
Michael Peek: The University of Sydney
Ron Benzie: Nepean Hospital
Laurence Macia: The University of Sydney
David Wilson: AITHM, James Cook University
Ann-Louise Ponsonby: Murdoch Children’s Research Institute
Mimi L. K. Tang: Murdoch Children’s Research Institute
Martin O’Hely: Deakin University
Norelle L. Daly: AITHM, James Cook University
Charles R. Mackay: Monash University
Jane E. Dahlstrom: The Australian National University
Peter Vuillermin: Deakin University
Ralph Nanan: The University of Sydney

Nature Communications, 2019, vol. 10, issue 1, 1-13

Abstract: 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.

Date: 2019
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DOI: 10.1038/s41467-019-10703-1

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