# Defining the role of sphingolipids on Porphyromonas gingivalis outer membrane vesicle uptake and elicited inflammation

> **NIH NIH F31** · UNIVERSITY OF FLORIDA · 2024 · $39,047

## Abstract

ABSTRACT
The proposed work outlined in the training plan for this NRSA Individual Predoctoral Fellowships to Promote
Diversity in Health-Related Research (F31) Award will support fourth year pre-doctoral candidate Zavier Eure
throughout his graduate program at University of Florida. Mr. Eure has displayed phenomenal excellence in his
academics and his learning of new lab techniques while being in the UF BMS program and currently supported
by the Oral Biology Department R90/T90 Training Grant. The research and training plan for Mr. Eure will provide
him a repertoire of skills needed to matriculate to the next level of his pre-doctoral training and also opportunities
to further advance his career and professional development. Being awarded this F31 will offer Mr. Eure the ability
to achieve his long-term goal of becoming a leader in science and provide a significant contribution to the field
of biomedical research.
Periodontal disease is a highly prevalent chronic inflammatory disease affecting up to 42% of adults in the US
over the age of 30. Periodontal disease is orchestrated by various microorganisms that make up the subgingival
microbiota. In susceptible individuals, dysbiosis of the subgingival microbiota promotes a dysregulated
inflammation that causes an irreversible destruction of the soft and hard tissues supporting the teeth.
Porphyromonas gingivalis (Pg) is an oral bacterium commonly associated with the microbial dysbiosis leading
to periodontal disease. Pg is referred to as a pathobiont because its known to manipulate the host inflammatory
milieu to facilitate disease states, however Pg can also remain in the oral cavity during healthy states. The
various mechanisms behind how Pg contributes to the changing inflammatory milieu is yet to be
identified.
Our lab has discovered Pg sphingolipids (SLs) limit host inflammation and host cell SL transfer via outer
membrane vesicles is a potential transport mechanism for Pg. The mechanism of OMV uptake by host cells is
known to impact elicited inflammation and OMV composition (SL+ or SL-) plays an important role in the route for
OMV uptake. Myeloid differentiation factor 88 (MyD88) is also known to be involved in the innate immune sensing
of Pg OMVs and has been found to be a target for immunomodulation by Pg. I hypothesize Pg SLs facilitates an
OMV uptake mechanism that limits inflammation and that SLs promote an immunomodulatory mechanism linked
to targeting of MyD88. I plan to use the THP-1 human cell line and primary human macrophages to characterize
the uptake mechanism of SL-containing Pg OMVs (Aim 1) and to determine the role of MyD88 in Pg SL-mediated
immunomodulation (Aim 2).

## Key facts

- **NIH application ID:** 10895305
- **Project number:** 5F31DE033255-02
- **Recipient organization:** UNIVERSITY OF FLORIDA
- **Principal Investigator:** Zavier G Eure
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $39,047
- **Award type:** 5
- **Project period:** 2023-08-16 → 2025-05-15

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10895305

## Citation

> US National Institutes of Health, RePORTER application 10895305, Defining the role of sphingolipids on Porphyromonas gingivalis outer membrane vesicle uptake and elicited inflammation (5F31DE033255-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10895305. Licensed CC0.

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