# Maternal exposures modify offspring allergic airway disease risk via epigenetic reprogramming

> **NIH NIH F31** · JOHNS HOPKINS UNIVERSITY · 2020 · $45,520

## Abstract

PROJECT SUMMARY
Asthma is the most common chronic disease among children in the US and globally, and its prevalence is
increasing. In utero exposures have been shown to alter offspring asthma risk, but the mechanisms governing
this effect are unclear. Compelling data has demonstrated that the structure and function of the fetal lung may
be altered by maternal exposures and thus predisposed to asthma before birth. Our previous work has
demonstrated that prenatal exposure to house dust mite (HDM) extract, a ubiquitous indoor allergen, increases
offspring lung reactivity in the absence of a secondary exposure in mice. In offspring exposed prenatally and
then later exposed in adulthood, airway reactivity was further increased. These changes were accompanied
by genome wide and gene-specific changes in DNA methylation in the lung, implying that epigenetic alterations
may play a role in this phenomenon. The objective of this research is to investigate the effects of maternal
exposures on offspring lung health throughout development. We hypothesize that maternal allergen
exposure alters the fetal methylome, leading to dysregulated fetal lung growth and development,
resulting in increased airway hyperresponsiveness in later life, and that concurrent exposure with a
methyl donor enriched diet may alter the effect of maternal allergen exposure on offspring. This
phenomenon will be investigated via two specific aims. Specific aim 1: examine the effects of maternal
house dust mite and/or methyl-enriched diet exposure on lung function and epigenetic markers of lung
growth, development, and defense from the fetal lung to the adult lung. Additionally, we hypothesize that
the effects of maternal exposures on the fetus are mediated by the placenta, thus placental dysregulation
induced by maternal exposures can result in altered fetal growth and function. To investigate this, we propose
Specific aim 2: investigate the influence of the maternal/fetal interface on fetal epigenetic regulation of
fetal lung development in offspring. We will examine the effect of maternal house dust mite exposure on
maternal oxidative stress, inflammation, and placental function. The completion of these aims will offer insight
into how maternal exposures alter offspring asthma risk, including whether allergen exposure directly target
and modify lung development, and/or indirectly affect offspring asthma risk by altering placenta functions.

## Key facts

- **NIH application ID:** 9992489
- **Project number:** 1F31HL152594-01
- **Recipient organization:** JOHNS HOPKINS UNIVERSITY
- **Principal Investigator:** Jairus C Pulczinski
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $45,520
- **Award type:** 1
- **Project period:** 2020-05-01 → 2022-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9992489

## Citation

> US National Institutes of Health, RePORTER application 9992489, Maternal exposures modify offspring allergic airway disease risk via epigenetic reprogramming (1F31HL152594-01). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9992489. Licensed CC0.

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