# Innate immune mechanisms of periodontal disease and inflammatory bowel disease

> **NIH NIH R21** · UNIVERSITY OF MISSISSIPPI MED CTR · 2020 · $230,468

## Abstract

Abstract
Crohn's disease (CD) is a chronic inflammatory disease of the intestinal tissue that affects over 3 million people
in the US. Periodontal disease (PD) is a chronic inflammation of the gingival epithelium, ultimately leading to the
destruction of the supporting tissues of the teeth and loss of alveolar bone, that affects over 45% of older adults
in the US. Patients with CD have a significantly higher incidence of PD than the general population (up to 90%),
and the severity and extent of PD is greater in CD patients than in intestinally healthy individuals. While there
are similarities between the two diseases with respect to mediators of immunity and bacterial growth and
colonization, the link between the two is unknown. Elucidation of this relationship can lead to a more effective
personalized medicine approach to treat these two diseases. It is clear that innate immunity plays an important
role in the pathogenesis of both CD and PD. A major regulator of innate immunity is the innate lymphoid cell
(ILC). There are three types of ILC (ILC1, ILC2 and ILC3), based on the cytokines they express. Mucosal tissues
are generally populated by ILC2 and ILC3, with ILC1 being present at low frequency. In CD lesions, however,
there is a phenotype switch leading to a shift from ILC3 to ILC1. While only recently discovered in periodontal
tissues, a similar identification of ILC1 was observed in the gingiva. Therefore, it is hypothesized that patients
with both CD and PD suffer from the same immune dysfunction, which is related to the regulation of ILC
phenotype. The purpose of this exploratory proposal is to obtain sufficient data to support an in-depth study to
address this hypothesis, and ultimately identify the mechanism that underlies the pathogenesis of these two
disorders. To this end, two aims are proposed: 1) Define the ILC phenotype in diseased and healthy sites in
patients with CD and PD; and 2) Characterize the change in ILC phenotype in mouse models of CD and PD.
Successful completion of these aims will demonstrate a role for ILC plasticity in the interrelationship between CD
and PD. This will then provide a strong foundation upon which to develop an in-depth study to define the
mechanism which underlies the susceptibility to both CD and PD.

## Key facts

- **NIH application ID:** 10007789
- **Project number:** 5R21DE028378-02
- **Recipient organization:** UNIVERSITY OF MISSISSIPPI MED CTR
- **Principal Investigator:** GILL DIAMOND
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $230,468
- **Award type:** 5
- **Project period:** 2019-09-04 → 2022-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10007789

## Citation

> US National Institutes of Health, RePORTER application 10007789, Innate immune mechanisms of periodontal disease and inflammatory bowel disease (5R21DE028378-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10007789. Licensed CC0.

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