# Exploring roles of protein deamidation in oral inflammation

> **NIH NIH R35** · UNIVERSITY OF SOUTHERN CALIFORNIA · 2020 · $1,024,914

## Abstract

Abstract
Inflammation is the body's response to damage induced by physical injury or pathogen infection. The oral
cavity, gastrointestinal track, skin, lung and urogenital track represent distinct anatomical sites where host cells
interface extensively with diverse microbes, presenting ample opportunities for infection and inflammation.
Recent advances have uncovered pivotal roles of microbiota, primarily from the gut, in human health and
disease. Our understanding in mucosal immunity of the other sites, particularly the oral cavity, is extremely
limited. How viruses, in addition to the microbiome, contribute to oral inflammation and diseases thereof
remains unknown.
Emerging clinical studies revealed that human herpesviruses (e.g., Epstein-Barr virus and cytomegalovirus)
were frequently detected in the oral cavity of patients with severe forms of inflammatory diseases, such as
periodontitis, peri-implantitis and mucositis. Other studies also suggest that inflammation can promote
herpesvirus reactivation and replication in the oral cavity. However, how herpesviruses contribute to oral
inflammation and the underlying molecular mechanisms have never been explored. Built on our recent
discovery that herpesviruses deploy protein deamidation to manipulate host immune response, this study will
directly address the above knowledge gap with research answering the following questions: 1) What is the role
of herpesvirus infection in oral inflammatory diseases; 2) How do nucleic acid sensing pathways operate in oral
immune defense and impact oral inflammatory disease; 3) How does herpesviral evasion of nucleic acid-
sensing pathways impinge on oral inflammation; 4) What are the regulatory role of protein deamidation in viral
infection and immune defense in the oral cavity; and 5) Can we leverage protein deamidation to tame oral
inflammation and treat oral inflammatory diseases. This work will illuminate the role and molecular basis of
innate immune sensing, herpesvirus infection and protein deamidation in oral inflammation. Harnessing our
knowledge of protein deamidation, we will develop key reagents to rectify chronic inflammation and treat oral
inflammatory diseases.

## Key facts

- **NIH application ID:** 9969074
- **Project number:** 5R35DE027556-04
- **Recipient organization:** UNIVERSITY OF SOUTHERN CALIFORNIA
- **Principal Investigator:** Casey CHEN
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $1,024,914
- **Award type:** 5
- **Project period:** 2017-09-14 → 2021-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9969074

## Citation

> US National Institutes of Health, RePORTER application 9969074, Exploring roles of protein deamidation in oral inflammation (5R35DE027556-04). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9969074. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*