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


Hu, M; Eviston, D; Hsu, P; Marino, E; Chidgey, A; Santner-Nanan, B; Wong, K; Richards, JL; Yap, YA; Collier, F; Quinton, A; Joung, S; Peek, M; Benzie, R; Macia, L; Wilson, D; Ponsonby, AL; Tang, MLK; O'Hely, M; Daly, NL; Mackay, CR; Dahlstrom, JE; BISInvestigator Group,; includes Harrison, LC; Vuillermin, P; Nanan, R
2019-07-10
Nature Communications
Journal Article
10
1
3031
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.
Springer Nature
Population Health and Immunity
10.1038/s41467-019-10703-1
31292453
Refer to copyright notice on published article.

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Creation Date 2019-07-26 09:44:15 Last Modified 2019-07-26 11:52:44