# Genetic and microbial modifiers of Atopic Dermatitis (AD): Mechanisms of increased AD severity in patients with the R576 polymorphism in IL-4Ra and impact of S aureus skin decolonization on AD

> **NIH NIH U01** · BOSTON CHILDREN'S HOSPITAL · 2024 · $526,128

## Abstract

This ADRN-CRC application brings together seasoned clinical and laboratory investigators in atopic
dermatitis (AD), with expertise in clinical research, immunology, S aureus biology, dermatology, and statistics.
The investigators have long track records in implementing multi-center and single-center clinical trials and
observational studies in allergic diseases, including AD, to the standards of NIH funded clinical research
networks, in conducting NIH fundamental research on disease mechanisms in AD and in training generations
of investigators in AD research
 In part A we demonstrate that we have the personnel and facilities to conduct ADRN network-wide and
CRC center-specific research on pediatric and adult AD patient populations recruited from the allergy and
dermatology clinics at Boston Children's Hospital and collaborating adult centers at the Brigham and Women's
Hospital Mas General Hospital and Boston University Medical Center and Hospital, and from our just
completed, as well as ongoing, NIH-funded studies of schoolchildren with allergic diseases. We have a highly
experienced team, IRB-approved protocols for recruitment and clinical characterization of AD patients, an
infrastructure which includes clinical research facilities, investigational pharmacy services, a laboratory facility
capable of processing, storing and shipping human samples, a state-of-the-art immunology research laboratory
with a 25 year focus on AD, and a data management facility with quality control plans, and capability to upload
data into the NIAID designated repositories and biostatistical support.
 Project I in part B will draw on an already genotyped local population of AD patients to test the
hypothesis that the IL-4Rα R576 polymorphism is associated with increased AD severity and alterations in the
function and gene expression of epidermal and immune cells. We will also use a mouse model of AD to test
the hypothesis that both epidermal and immune cells contribute to the increased antigen allergic skin
inflammation observed in mice with the IL-4Rα R576R polymorphism.
 Project II in part B will test the hypothesis that S. aureus skin decolonization in AD will reduce disease
severity and favorably alter the function and gene expression of epidermal and immune cells that contribute to
disease severity. We will also test the hypothesis that S. aureus skin colonization promotes the development of
antigen-driven allergic skin inflammation, and its reactivation, using a mouse model of AD.
 Our proposal will contribute extensively to the ADRN as a Clinical Research Unit and, as an ADRN-CRC will
help elucidate the role of genetic and microbial modifiers in AD.
!

## Key facts

- **NIH application ID:** 10808171
- **Project number:** 5U01AI152033-05
- **Recipient organization:** BOSTON CHILDREN'S HOSPITAL
- **Principal Investigator:** RAIF SALIM GEHA
- **Activity code:** U01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $526,128
- **Award type:** 5
- **Project period:** 2020-04-01 → 2027-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10808171

## Citation

> US National Institutes of Health, RePORTER application 10808171, Genetic and microbial modifiers of Atopic Dermatitis (AD): Mechanisms of increased AD severity in patients with the R576 polymorphism in IL-4Ra and impact of S aureus skin decolonization on AD (5U01AI152033-05). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10808171. Licensed CC0.

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