# Host genetics, early-life microbiome, and childhood asthma: MARC-43 Boston

> **NIH NIH UG3** · MASSACHUSETTS GENERAL HOSPITAL · 2024 · $832,707

## Abstract

Project Abstract
Recent studies report probabilistic associations between the early-life microbiome and various child health
outcomes (e.g., obesity, asthma), suggesting potential insights into pathogenesis and subsequent, targeted
development of preventive interventions. However, the causal role of the early-life microbiome on child health
remains unclear. Our preliminary work has applied state-of-art statistical genetics and causal inference
approaches to large genetics and microbiome data in our ECHO-supported cohorts, demonstrating: 1) host
genetic loci for airway Streptococcus across racial/ethnic populations, 2) host genetic loci for gut microbiome
and significantly enriched biological pathways (e.g., regulation of neuron development, glucuronate
interconversions), and 3) relationship of gut Bacteroides with obesity and asthma risk. Our central hypothesis
is that the genetically driven gut and upper airway microbiome in the first two years of life has a causal role in
the development of child health outcomes, such as obesity and airway outcomes. This UG3/UH3 project will
test this innovative hypothesis by applying the latest statistical genetics and epidemiological methods—e.g.,
microbiome genome-wide association study (mGWAS)— to large ECHO genetics, microbiome, and extensive
clinical and environmental data. By using ECHO core data elements, Aim 1 will generate mGWAS summary
statistics to enable researchers to examine the causal role of the early-life microbiome on child health
outcomes. For example, by using the mGWAS and Mendelian randomization approaches, we will determine
the causal role of the gut and nasal airway microbiome (during age 0-1.9 years) in the risk of developing
childhood obesity. By using specialized airway outcome data, Aim 2 will determine whether the genetically
driven gut and nasal microbiome has a causal effect on the development of asthma (and its major phenotypes)
and on lower lung function in later childhood. Aim 3 will maximize the retention of existing ECHO Cohort
Protocol (ECP) participants, with emphasis on diversity, and implement the ECP with high fidelity. (To date, in
MARC-43 Boston participants, ECP retention is 100%, with >80% data completeness.) The proposed project
will serve as a national research resource for examining the causal role of early-life microbiome in various
childhood health outcomes. Furthermore, the project will provide a robust evidence base for the future
development of targeted microbiome interventions to prevent childhood obesity and asthma. The investigators
are NIH-funded researchers with international expertise in all relevant fields (e.g., epidemiology, statistical
genetics, microbiome, childhood obesity, asthma). The project matches well with the goals of the ECHO
Program.

## Key facts

- **NIH application ID:** 10906958
- **Project number:** 5UG3OD023253-09
- **Recipient organization:** MASSACHUSETTS GENERAL HOSPITAL
- **Principal Investigator:** CARLOS ARTURO CAMARGO
- **Activity code:** UG3 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $832,707
- **Award type:** 5
- **Project period:** 2016-09-21 → 2025-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10906958

## Citation

> US National Institutes of Health, RePORTER application 10906958, Host genetics, early-life microbiome, and childhood asthma: MARC-43 Boston (5UG3OD023253-09). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10906958. Licensed CC0.

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