# Epigenomics of mononuclear phagocytes in prematurity associated lung disease

> **NIH NIH K08** · UNIVERSITY OF CALIFORNIA, SAN DIEGO · 2020 · $177,120

## Abstract

PROJECT SUMMARY/ABSTRACT
Medical advances have made it possible for premature infants to survive in increasing numbers. However, the
increased survival at early gestational ages is accompanied with increased morbidity. Bronchopulmonary
dysplasia (BPD) is the most prevalent major complication of premature birth affecting at least one quarter of
infants born with a birth weight less than 1500g. Alarmingly, the rate of BPD is increasing, while rates of
several other in-hospital complications of premature birth have dropped. BPD predisposes premature infants to
a higher mortality and morbidity risk both in the immediate neonatal period as well as after discharge form the
neonatal intensive care unit. Many survivors of premature birth will continue to have persistent respiratory
symptoms and decreased lung function into adulthood. In addition to the respiratory complications, BPD is also
one of the strongest predictors of neurodevelopmental impairment. These life-long complications of BPD
create significant health burden and necessitate extensive health care utilization. Currently, there is no
effective treatment for BPD. Key pathogenic mechanisms of the disease are not completely understood and
therefore we lack a clear path for development of new therapies. One factor that plays a central role in the
pathogenesis of BPD is oxygen administration, used as a life-saving intervention after premature birth.
Exposure of the immature lung to increased levels of oxygen results in a profound inflammatory response that
permanently disrupts normal lung development. However, not every premature infant is equally sensitive to
oxygen-induced injury. Therefore, identifying the cellular and molecular mechanisms leading to oxygen
induced inflammation and variance in individual susceptibility has the potential to establish new therapeutic
targets. I propose to build on recent conceptual, technical and computational advances to identify the innate
immune cells that initiate and maintain the pathologic inflammatory response in BPD. After identifying the
disease-relevant cells, I will apply state of the art sequencing techniques to study their gene expression and
the epigenetic mechanisms that regulate gene expression. Using computational analysis I will integrate the
genetic and epigenetic data to identify candidate genes that are likely to drive the pathology in BPD and
contribute to individual differences in disease susceptibility. Understanding the fundamental biology of gene
expression and regulation in innate immune cells in the developing lung will not only benefit premature infants
with BPD, but could be harnessed for therapeutic purposes in several other respiratory diseases.

## Key facts

- **NIH application ID:** 9843725
- **Project number:** 5K08HL140198-03
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN DIEGO
- **Principal Investigator:** Eniko Sajti
- **Activity code:** K08 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $177,120
- **Award type:** 5
- **Project period:** 2018-01-15 → 2022-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9843725

## Citation

> US National Institutes of Health, RePORTER application 9843725, Epigenomics of mononuclear phagocytes in prematurity associated lung disease (5K08HL140198-03). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/9843725. Licensed CC0.

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