# Host–gut microbiota interactions during pregnancy

**Authors:** Katherine R Amato, Priyanka Pradhan, Elizabeth K Mallott, Wesley Shirola, Amy Lu

PMC · DOI: 10.1093/emph/eoae001 · Evolution, Medicine, and Public Health · 2024-01-06

## TL;DR

This paper explores how changes in gut microbiota during pregnancy interact with maternal hormones and immunity to influence mother and offspring health.

## Contribution

The paper introduces a mechanistic model linking maternal hormonal, immune, and metabolic changes to gut microbiota dynamics during pregnancy.

## Key findings

- Maternal hormonal changes directly and indirectly alter gut microbiome composition and function.
- Gut microbiota feedback influences maternal immunity and metabolism during pregnancy.
- These interactions likely mediate maternal and offspring fitness trade-offs.

## Abstract

Mammalian pregnancy is characterized by a well-known suite of physiological changes that support fetal growth and development, thereby positively affecting both maternal and offspring fitness. However, mothers also experience trade-offs between current and future maternal reproductive success, and maternal responses to these trade-offs can result in mother–offspring fitness conflicts. Knowledge of the mechanisms through which these trade-offs operate, as well as the contexts in which they operate, is critical for understanding the evolution of reproduction. Historically, hormonal changes during pregnancy have been thought to play a pivotal role in these conflicts since they directly and indirectly influence maternal metabolism, immunity, fetal growth and other aspects of offspring development. However, recent research suggests that gut microbiota may also play an important role. Here, we create a foundation for exploring this role by constructing a mechanistic model linking changes in maternal hormones, immunity and metabolism during pregnancy to changes in the gut microbiota. We posit that marked changes in hormones alter maternal gut microbiome composition and function both directly and indirectly via impacts on the immune system. The gut microbiota then feeds back to influence maternal immunity and metabolism. We posit that these dynamics are likely to be involved in mediating maternal and offspring fitness as well as trade-offs in different aspects of maternal and offspring health and fitness during pregnancy. We also predict that the interactions we describe are likely to vary across populations in response to maternal environments. Moving forward, empirical studies that combine microbial functional data and maternal physiological data with health and fitness outcomes for both mothers and infants will allow us to test the evolutionary and fitness implications of the gestational microbiota, enriching our understanding of the ecology and evolution of reproductive physiology.

## Full-text entities

- **Genes:** CD79A (CD79a molecule) [NCBI Gene 973] {aka IGA, IGAlpha, MB-1, MB1}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}, CRH (corticotropin releasing hormone) [NCBI Gene 1392] {aka CRF, CRH1}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, OXT (oxytocin/neurophysin I prepropeptide) [NCBI Gene 5020] {aka OT, OT-NPI, OXT-NPI}, Mucin [NCBI Gene 100508689], CGB5 (chorionic gonadotropin subunit beta 5) [NCBI Gene 93659] {aka CGB, HCG}, PRL (prolactin) [NCBI Gene 5617] {aka GHA1, pPRL}
- **Diseases:** MODEL (MESH:D004195), gestational diabetes (MESH:D016640), intrauterine growth restriction (MESH:D005317), metabolic and cardiovascular disease (MESH:D002318), bacterial (MESH:D001424), metabolic disorders (MESH:D008659), viral (MESH:D014777), and parasitic infections (MESH:D010272), miscarriage (MESH:D000022), EFFECTS (MESH:D065606), HOST (MESH:D006086), autoimmune disease (MESH:D001327), pre-eclampsia (MESH:D011225), HPA (MESH:D010661), Roseburia intestinalis (MESH:D005873), infection (MESH:D007239), CHANGES (MESH:D009402), infectious disease (MESH:D003141), hypoxia (MESH:D000860), metabolic dysregulation (MESH:D021081), inflammation (MESH:D007249), EFFECTS OF MATERNAL (MESH:D000079262), weight gain (MESH:D015430), insulin insensitivity (MESH:D007333), adipose tissue (MESH:D018205)
- **Chemicals:** propionate (MESH:D011422), fatty acid (MESH:D005227), serotonin (MESH:D012701), glucose (MESH:D005947), estrone (MESH:D004970), lactose (MESH:D007785), starch (MESH:D013213), 17B-estradiol (-), estradiol (MESH:D004958), cortisol (MESH:D006854), acetate (MESH:D000085), Butyrate (MESH:D002087), soy isoflavones (MESH:D007529), SCFA (MESH:D005232), choline (MESH:D002794), lipid (MESH:D008055), bile acids (MESH:D001647), progesterone (MESH:D011374)
- **Species:** Roseburia intestinalis (species) [taxon 166486], Lacticaseibacillus paracasei (species) [taxon 1597], Sus scrofa (pig, species) [taxon 9823], Anaerobutyricum hallii (species) [taxon 39488], Trachypithecus phayrei (Phayre's leaf monkey, species) [taxon 61618], Propionibacterium sp. (species) [taxon 1977903], Bifidobacterium (genus) [taxon 1678], Homo sapiens (human, species) [taxon 9606], Streptococcus (genus) [taxon 1301], Bacteroides fragilis (species) [taxon 817], Lactiplantibacillus plantarum (species) [taxon 1590], Blautia sp. (species) [taxon 1955243], Clostridium perfringens (species) [taxon 1502], Faecalibacterium sp. (species) [taxon 1971605], Ruminococcus bromii (species) [taxon 40518], Thomasclavelia ramosa (species) [taxon 1547], Lepidosauria (lepidosaurs, class) [taxon 8504], Akkermansia (genus) [taxon 239934], Sciuromorpha (squirrels, suborder) [taxon 33553], Ligilactobacillus salivarius (species) [taxon 1624], Agathobacter rectalis (species) [taxon 39491], Mus musculus (house mouse, species) [taxon 10090], Enterococcus faecalis (species) [taxon 1351]

## Full text

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## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC10824165/full.md

## References

146 references — full list in the complete paper: https://tomesphere.com/paper/PMC10824165/full.md

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Source: https://tomesphere.com/paper/PMC10824165