Date Available
3-9-2022
Year of Publication
2021
Document Type
Master's Thesis
Degree Name
Master of Science (MS)
College
Medicine
Department/School/Program
Medical Sciences
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
Recommended Citation
Maynard, Marshall Houston, "S. gordonii-PRODUCED HYDROGEN PEROXIDE MODULATES miR-663A AND CCL20 EXPRESSION IN ORAL EPITHELIAL CELLS" (2021). Theses and Dissertations--Medical Sciences. 17.
https://uknowledge.uky.edu/medsci_etds/17
Included in
Medical Immunology Commons, Medical Microbiology Commons, Oral Biology and Oral Pathology Commons, Periodontics and Periodontology Commons
