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

Signe Schmidt Kjølner Hansen (), Robert Krautz, Daria Rago, Jesper Havelund, Arnaud Stigliani, Nils J. Færgeman, Audrey Prézelin, Julie Rivière, Anne Couturier-Tarrade, Vyacheslav Akimov, Blagoy Blagoev, Betina Elfving, Ditte Neess, Ulla Vogel, Konstantin Khodosevich, Karin Sørig Hougaard () and Albin Sandelin ()
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Signe Schmidt Kjølner Hansen: University of Copenhagen
Robert Krautz: University of Copenhagen
Daria Rago: University of Copenhagen
Jesper Havelund: University of Southern Denmark
Arnaud Stigliani: University of Copenhagen
Nils J. Færgeman: University of Southern Denmark
Audrey Prézelin: BREED
Julie Rivière: GABI
Anne Couturier-Tarrade: 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
Albin Sandelin: University of Copenhagen

Nature Communications, 2024, vol. 15, issue 1, 1-24

Abstract: 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.

Date: 2024
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DOI: 10.1038/s41467-024-48492-x

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