# Epithelial Genes in Allergic Inflammation

> **NIH NIH U19** · CINCINNATI CHILDRENS HOSP MED CTR · 2020 · $252,416

## Abstract

Allergic disorders are a major global health concern affecting 150 million people worldwide.
Recently, epithelial cells have emerged as central participants in the pathogenesis of allergic
inflammation. Defining the key epithelial drivers of the development, persistence, and progression
of allergic inflammation is the focus of this application. Although epithelial cells are increasingly
recognized as critical participants in the initiation and propagation of allergic inflammation,
therapies that specifically target the epithelium are lacking. There are substantial gaps in
understanding the mechanisms by which epithelial pathways converge to promote allergic
inflammation that must be filled before interventions can be designed. Our U19 AADCRC proposal
is designed to help fill this critical knowledge gap. We are uniquely poised for the proposed studies
because of resources and collaborations that we have developed over the past 2 decades.
Through the synergistic projects, we will explore the immunological mechanisms, which underpin
initiation, persistence, and progression of allergic disease and provide novel insights into a key
unanswered question in the allergy field: Why is allergic inflammation restricted to one tissue in
some cases, while it progresses to involve additional tissues in other individuals? The projects
are:
Project 1 – To elucidate endotypes of AD that are predictive of progression to asthma and dissect
the mechanistic basis of the contribution of epithelial kinesin family member 3A (KIF3A) to allergic
inflammation and disease persistence/progression.
Project 2 – To determine how protease/protease inhibitor imbalance promotes allergic
inflammation – dissect the mechanistic basis by which the epithelial-derived protease inhibitor
serine protease inhibitor Kazal-type 7 (SPINK7) promotes allergic inflammation.
Project 3 –To determine whether specific heterophilic protein adhesion events between
Staphylococcus spp colonizing AD but not normal skin facilitate inter-species synergism, leading
to strong mixed biofilms, which promote inflammation, compromise skin barrier function, and
result in more severe AD and progression to asthma.

## Key facts

- **NIH application ID:** 10146526
- **Project number:** 3U19AI070235-14S1
- **Recipient organization:** CINCINNATI CHILDRENS HOSP MED CTR
- **Principal Investigator:** Gurjit K. Khurana Hershey
- **Activity code:** U19 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $252,416
- **Award type:** 3
- **Project period:** 2020-05-07 → 2021-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10146526

## Citation

> US National Institutes of Health, RePORTER application 10146526, Epithelial Genes in Allergic Inflammation (3U19AI070235-14S1). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10146526. Licensed CC0.

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