Date Available

3-9-2022

Year of Publication

2021

Degree Name

Master of Science (MS)

Document Type

Master's Thesis

College

Medicine

Department/School/Program

Medical Sciences

First Advisor

Dr. Octavio Gonzalez

Abstract

The mechanisms through which a persistent recognition of commensal bacteria by oral epithelial cells (OECs) mitigates an uncontrolled inflammatory response of the oral mucosa remain unknown. CCL20 secretion by OECs in response to pathogenic bacteria is regulated by S. gordonii (Sg)-induced miR-663a; nevertheless, the mechanisms involved in these Sg-modulated responses remain to be elucidated. Since Sg is a hydrogen peroxide (H2O2) producer, and H2O2 has been shown to stimulate miRNA expression, we hypothesized that H2O2 could be involved in Sg-induced miR663a and CCL20 responses. Expression of miR663a was stimulated by Sg and H2O2 in a dose-dependent manner. Response was significantly attenuated by catalase. Strong miR663a up-regulation was associated with H2O2-producing oral streptococci. Catalase treatment rescued An-induced CCL20 expression attenuated by Sg and Ss. Here we showed that H2O2 produced by Sg and other oral streptococcal species is involved in miR663a up-regulation and regulation of CCL20 secretion by OECs. H2O2-producing oral streptococci could represent a group of commensal bacteria contributing to attenuating oral inflammation and dysbiosis.

Digital Object Identifier (DOI)

https://doi.org/10.13023/etd.2021.372

Funding Information

National Institutes of Health/National Institutes of Dental and Craniofacial Research Grant no.: DE024586 in 2015

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