Role of Oral Epithelial Cell Toll-Like Receptors in the Onset and Progression of Periodontal Disease

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Material Information

Title:
Role of Oral Epithelial Cell Toll-Like Receptors in the Onset and Progression of Periodontal Disease
Physical Description:
1 online resource (45 p.)
Language:
english
Creator:
Rasmussen, Richard Allyn III
Publisher:
University of Florida
Place of Publication:
Gainesville, Fla.
Publication Date:

Thesis/Dissertation Information

Degree:
Master's ( M.S.)
Degree Grantor:
University of Florida
Degree Disciplines:
Dental Sciences, Dentistry
Committee Chair:
WALLET,SHANNON MARGARET
Committee Co-Chair:
KOUTOUZIS,THEOFILOS
Committee Members:
LAKSHMYYA,KESAVALU NAIDU
YILMAZ,OZLEM

Subjects

Subjects / Keywords:
epithelial-cells -- inflammation -- myd88 -- periodontitis -- toll-like
Dentistry -- Dissertations, Academic -- UF
Genre:
Dental Sciences thesis, M.S.
bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

Abstract:
The oral cavity is a gateway for a wide array of antigenic challenges where alterations in oral mucosal homeostasis can lead to inflammatory diseases such as periodontitis. Epithelial barrier function and mucosal immunity depend on interactions between commensal microbiota and pathogens respectively with toll-like receptors (TLRs) on epithelial cells. Here we wanted to determine if TLR induced oral epithelial cell responses contribute to periodontal disease. Myeloid differentiation factor 88 (MyD88) is a required signaling adaptor protein for most TLRs and is expressed in oral epithelium and resident immune cell populations. In mice, expression of dominant- negative MyD88 in intestinal epithelial cells causes spontaneous intestinal inflammation. In contrast, ubiquitous MyD88 deficiency prevents induced intestinal inflammation. These data support the hypothesis that MyD88-dependent signaling plays distinct roles in epithelial cells versus resident innate immune cells. The purpose of this research is to evaluate the role(s) of TLR oral epithelial cell specific responses in the progression of periodontal disease. A well described poly-microbial model of periodontal disease induction and inducible epithelial cell specific MyD88 knockout mice (B6K5Cre.MyD88plox) were utilized. Following knockdown of MyD88 in the oral epithelium, mice were infected with Porphorymonas gingivalis and Aggregatibacter actinomycetemcomitans by oral lavage 4 times per week, every other week for 12 weeks, after which maxillae and mandibles were subjected to bone morphometric and histological analysis. An increase in total bone loss and soft tissue changes were observed in the epithelial cell specific MyD88 deficient mice compared to infected controls. A difference in the level of local inflammation was also observed. These results indicate that oral epithelial cell MyD88-dependent TLR signaling is responsible for tolerogenic immune tuning which counteracts otherwise inflammatory responses and that oral epithelial cells can be a target for periodontal therapies aimed at controlling inflammation.
General Note:
In the series University of Florida Digital Collections.
General Note:
Includes vita.
Bibliography:
Includes bibliographical references.
Source of Description:
Description based on online resource; title from PDF title page.
Source of Description:
This bibliographic record is available under the Creative Commons CC0 public domain dedication. The University of Florida Libraries, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.
Statement of Responsibility:
by Richard Allyn III Rasmussen.
Thesis:
Thesis (M.S.)--University of Florida, 2014.
Local:
Adviser: WALLET,SHANNON MARGARET.
Local:
Co-adviser: KOUTOUZIS,THEOFILOS.
Electronic Access:
RESTRICTED TO UF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE UNTIL 2015-05-31

Record Information

Source Institution:
UFRGP
Rights Management:
Applicable rights reserved.
Classification:
lcc - LD1780 2014
System ID:
UFE0046779:00001