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Pulmonary maternal immune activation does not cross the placenta but leads to fetal metabolic adaptation

Author

Listed:
  • Signe Schmidt Kjølner Hansen

    (University of Copenhagen
    University of Copenhagen
    National Research Centre for the Working Environment)

  • Robert Krautz

    (University of Copenhagen)

  • Daria Rago

    (University of Copenhagen
    University of Copenhagen)

  • Jesper Havelund

    (University of Southern Denmark)

  • Arnaud Stigliani

    (University of Copenhagen
    University of Copenhagen)

  • Nils J. Færgeman

    (University of Southern Denmark)

  • Audrey Prézelin

    (BREED
    BREED)

  • Julie Rivière

    (GABI
    Micalis Institute)

  • Anne Couturier-Tarrade

    (BREED
    BREED)

  • Vyacheslav Akimov

    (University of Southern Denmark)

  • Blagoy Blagoev

    (University of Southern Denmark)

  • Betina Elfving

    (Aarhus University)

  • Ditte Neess

    (University of Southern Denmark)

  • Ulla Vogel

    (National Research Centre for the Working Environment)

  • Konstantin Khodosevich

    (University of Copenhagen)

  • Karin Sørig Hougaard

    (National Research Centre for the Working Environment
    University of Copenhagen)

  • Albin Sandelin

    (University of Copenhagen
    University of Copenhagen)

Abstract

The fetal development of organs and functions is vulnerable to perturbation by maternal inflammation which may increase susceptibility to disorders after birth. Because it is not well understood how the placenta and fetus respond to acute lung- inflammation, we characterize the response to maternal pulmonary lipopolysaccharide exposure across 24 h in maternal and fetal organs using multi-omics, imaging and integrative analyses. Unlike maternal organs, which mount strong inflammatory immune responses, the placenta upregulates immuno-modulatory genes, in particular the IL-6 signaling suppressor Socs3. Similarly, we observe no immune response in the fetal liver, which instead displays metabolic changes, including increases in lipids containing docosahexaenoic acid, crucial for fetal brain development. The maternal liver and plasma display similar metabolic alterations, potentially increasing bioavailability of docosahexaenoic acid for the mother and fetus. Thus, our integrated temporal analysis shows that systemic inflammation in the mother leads to a metabolic perturbation in the fetus.

Suggested Citation

  • Signe Schmidt Kjølner Hansen & Robert Krautz & Daria Rago & Jesper Havelund & Arnaud Stigliani & Nils J. Færgeman & Audrey Prézelin & Julie Rivière & Anne Couturier-Tarrade & Vyacheslav Akimov & Blago, 2024. "Pulmonary maternal immune activation does not cross the placenta but leads to fetal metabolic adaptation," Nature Communications, Nature, vol. 15(1), pages 1-24, December.
  • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-48492-x
    DOI: 10.1038/s41467-024-48492-x
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    References listed on IDEAS

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    1. Florian Rohart & Benoît Gautier & Amrit Singh & Kim-Anh Lê Cao, 2017. "mixOmics: An R package for ‘omics feature selection and multiple data integration," PLOS Computational Biology, Public Library of Science, vol. 13(11), pages 1-19, November.
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