# Intersections between the maternal microbiome, placental immunity, vasculature and fetal growth

> **NIH NIH F31** · UNIVERSITY OF CALIFORNIA LOS ANGELES · 2021 · $40,145

## Abstract

PROJECT SUMMARY
The World Health Organization identifies intrauterine growth restriction (IUGR) as a primary risk factor for
adverse perinatal outcomes and long-term health consequences. It afflicts an estimated 100,000 children born
each year in the United States, with even higher prevalence in developing countries and socioeconomic groups
with limited access to healthcare. IUGR is commonly associated with poor maternal nutrition and placental
insufficiencies, including immune dysfunction and impaired vascular growth, but how environmental factors
regulate these processes is not completely understood. The gut microbiome mediates environmental
contributions to host immune function and angiogenesis, and microbiota composition is markedly influenced by
dietary intake. This warrants investigation of the microbiome as a critical regulator of placental homeostasis,
opening the possibility for microbiota-based therapeutic strategies to treat IUGR. Indeed, this novel approach
to improve maternal health during gestation and treat IUGR aligns with the NICHD mission, specifically to
ensure “…that women suffer no harmful effects from reproductive processes, and that all children have the
chance to achieve their full potential for healthy and productive lives.”
My preliminary data supports the central hypothesis that dysbiosis of the maternal microbiome during
pregnancy impairs placental angiogenic immune cells and vasculature, leading to downstream abnormalities in
fetal development. Further, my data supports the presumption that the microbiome regulates circulating
metabolites that have known immunoregulatory and angiogenic potential that can act systemically throughout
the host. My rationale is that disrupting the maternal microbiome, whether through bacterial depletion or
through maternal nutrition, alters bioavailability of circulating biochemicals that are critical for maternal and fetal
health during pregnancy. I propose to test my central hypothesis with the following aims: Aim 1: Investigate
effects of the maternal microbiome on placental immune homeostasis; Aim 2: Examine how the maternal
microbiome regulates placental vascular development; Aim 3: Determine mechanistic influences of the
maternal microbiome on fetal growth. Upon completion, I will provide novel insights into how the maternal
microbiome regulates placental immune and vascular homeostasis through specific molecular interactions.
This mechanistic approach is significant because it sheds light on a causal role of the microbiome as a
regulator of IUGR, and opens the potential for microbiome-based therapeutic targets to markedly improve
maternal and fetal health on a global scale.
The proposed research is of critical importance for my predoctoral training, as I will develop and refine my
technical skills, experimental design and analysis, and critical review of scientific literature from multiple fields.

## Key facts

- **NIH application ID:** 10049188
- **Project number:** 5F31HD101270-02
- **Recipient organization:** UNIVERSITY OF CALIFORNIA LOS ANGELES
- **Principal Investigator:** Geoffrey Nathan Pronovost
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $40,145
- **Award type:** 5
- **Project period:** 2019-11-01 → 2021-10-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10049188

## Citation

> US National Institutes of Health, RePORTER application 10049188, Intersections between the maternal microbiome, placental immunity, vasculature and fetal growth (5F31HD101270-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10049188. Licensed CC0.

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