Hofbauer cell function in the term placenta associates with adult cardiovascular and depressive outcomes

Eamon Fitzgerald (), Mojun Shen, Hannah Ee Juen Yong, Zihan Wang, Irina Pokhvisneva, Sachin Patel, Nicholas O’Toole, Shiao-Yng Chan, Yap Seng Chong, Helen Chen, Peter D. Gluckman, Jerry Chan, Patrick Kia Ming Lee and Michael J. Meaney ()
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Eamon Fitzgerald: McGill University
Mojun Shen: Singapore Institute for Clinical Sciences, Agency for Science, Technology & Research
Hannah Ee Juen Yong: Singapore Institute for Clinical Sciences, Agency for Science, Technology & Research
Zihan Wang: McGill University
Irina Pokhvisneva: McGill University
Sachin Patel: McGill University
Nicholas O’Toole: McGill University
Shiao-Yng Chan: Singapore Institute for Clinical Sciences, Agency for Science, Technology & Research
Yap Seng Chong: Singapore Institute for Clinical Sciences, Agency for Science, Technology & Research
Helen Chen: KK Women’s and Children’s Hospital
Peter D. Gluckman: Singapore Institute for Clinical Sciences, Agency for Science, Technology & Research
Jerry Chan: KK Women’s and Children’s Hospital
Patrick Kia Ming Lee: Brain – Body Initiative, Agency for Science, Technology & Research
Michael J. Meaney: McGill University

Nature Communications, 2023, vol. 14, issue 1, 1-11

Abstract: Abstract Pathological placental inflammation increases the risk for several adult disorders, but these mediators are also expressed under homeostatic conditions, where their contribution to adult health outcomes is unknown. Here we define an inflammation-related expression signature, primarily expressed in Hofbauer cells of the term placenta and use expression quantitative trait loci to create a polygenic score (PGS) predictive of its expression. Using this PGS in the UK Biobank we conduct a phenome-wide association study, followed by Mendelian randomization and identify protective, sex-dependent effects of the placental module on cardiovascular and depressive outcomes. Genes differentially regulated by intra-amniotic infection and preterm birth are over-represented within the module. We also identify aspirin as a putative modulator of this inflammation-related signature. Our data support a model where disruption of placental Hofbauer cell function, due to preterm birth or prenatal infection, contributes to the increased risk of depression and cardiovascular disease observed in these individuals.

Date: 2023
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DOI: 10.1038/s41467-023-42300-8

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