The maternal microbiome promotes placental development in mice

The maternal microbiome is an important regulator of gestational health, but how it affects the placenta as the interface between mother and fetus remains unexplored. Here, we show that the maternal gut microbiota supports placental development in mice. Depletion of the maternal gut microbiota restr...

Full description

Saved in:
Bibliographic Details
Published inScience advances Vol. 9; no. 40; p. eadk1887
Main Authors Pronovost, Geoffrey N, Yu, Kristie B, Coley-O'Rourke, Elena J L, Telang, Sahil S, Chen, Angela S, Vuong, Helen E, Williams, Drake W, Chandra, Anisha, Rendon, Tomiko K, Paramo, Jorge, Kim, Reuben H, Hsiao, Elaine Y
Format Journal Article
LanguageEnglish
Published United States American Association for the Advancement of Science 06.10.2023
Subjects
Animals
Biomedicine and Life Sciences
Developmental Biology
Female
Fetus
Gastrointestinal Microbiome
Mice
Microbiology
Microbiota
Placenta - metabolism
Placentation
Pregnancy
SciAdv r-articles
Online AccessGet full text

Cover

More Information
Summary:The maternal microbiome is an important regulator of gestational health, but how it affects the placenta as the interface between mother and fetus remains unexplored. Here, we show that the maternal gut microbiota supports placental development in mice. Depletion of the maternal gut microbiota restricts placental growth and impairs feto-placental vascularization. The maternal gut microbiota modulates metabolites in the maternal and fetal circulation. Short-chain fatty acids (SCFAs) stimulate cultured endothelial cell tube formation and prevent abnormalities in placental vascularization in microbiota-deficient mice. Furthermore, in a model of maternal malnutrition, gestational supplementation with SCFAs prevents placental growth restriction and vascular insufficiency. These findings highlight the importance of host-microbial symbioses during pregnancy and reveal that the maternal gut microbiome promotes placental growth and vascularization in mice.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Present address: Oral Immunity and Inflammation Section, NIDCR, NIH, Bethesda, MD, USA.
Present address: Department of Pediatrics, University of Minnesota Medical School, Minneapolis, MN, USA.
ISSN:2375-2548
2375-2548
DOI:10.1126/sciadv.adk1887