Investigating the Role of MyD88 in the Evolution of Porphyromonas gingivalis-induced Experimental Periodontitis in Mice

碩士 === 國防醫學院 === 微生物及免疫學研究所 === 102 === Periodontitis can be characterized by the accumulation of a specific gram-negative periodontopathogens (i.e., Porphyromonas gingivalis), but progression of the disease is dependent on the host response to these pathogenic bacteria. As the number of microbial...

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Main Authors: Lin Wei Huang, 黃琳惟
Other Authors: Ren-Yeong Huang
Format: Others
Language:zh-TW
Published: 2014
Online Access:http://ndltd.ncl.edu.tw/handle/44095253977136769176
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spelling ndltd-TW-102NDMC03800092015-10-13T23:37:37Z http://ndltd.ncl.edu.tw/handle/44095253977136769176 Investigating the Role of MyD88 in the Evolution of Porphyromonas gingivalis-induced Experimental Periodontitis in Mice 探討MyD88在Porphyromonas gingivalis誘導之實驗型牙周炎過程中所扮演之角色 Lin Wei Huang 黃琳惟 碩士 國防醫學院 微生物及免疫學研究所 102 Periodontitis can be characterized by the accumulation of a specific gram-negative periodontopathogens (i.e., Porphyromonas gingivalis), but progression of the disease is dependent on the host response to these pathogenic bacteria. As the number of microbial factors, such as lipopolysaccharide (LPS) from P. gingivalis (P.g), increases surface receptors known as Toll-like receptors (TLR) in the oral cavity function to recognize and respond to this change. This interaction leads to the production of inflammatory cytokines by myeloid differentiation primary response protein 88 (MyD88)-dependent and -independent pathways, which may in turn initiate a local immune response, release of inflammatory mediators, and activation of osteoclasts responsible for bone resorption. Moreover, the T helper 17 (Th17)/ regulatory T (Treg) imbalance has recently been suggested to play a role in the development of periodontitis. Although the role of adapter molecule MyD88 in controlling infection and immune system activation has been examined, its function/involvement in the development and progression of periodontal destruction has not been investigated. The aim of current study was to assess the involvement of MyD88 in alveolar bone loss (ABL) induced by P.g in mice, to investigate whether Th17/Treg imbalance plays a role in the development of experimental periodontitis, and to examine the role of MyD88 in osteoclast differentiation and function in vitro. Experimental periodontitis will be induced in C57BL/6 wild-type 1 and MyD88 KO mice by oral infection with P. gingivalis. Animals will be sacrificed at indicated time points (D14-D60) and the maxillae removed for micro-CT analyses. ABL will be assessed by measuring the distance from the cemento-enamel junction (CEJ) to the alveolar bone crest (ABC). CD4+ T cell subsets (Th17 and Treg cells)in the cervical lymph nodes (CLNs) and spleen will be analyzed by flow cytometry. Bone marrow-derived osteoclasts will be isolated, tartrate resistant acid phosphate (TRAP) staining and TRAP activity will be measured in vitro. Our data showed that increased CEJ-ABC distance was observed in WT mice at 42 days post infection, Th17/Treg imbalance in the CLNs, and blunted osteoclast differentiation of hematopoietic bone marrow cells from MyD88 KO mice was also noted when compared with WT mice after P. gingivalis LPS stimulation. Ren-Yeong Huang 黃仁勇 2014 學位論文 ; thesis 80 zh-TW
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description 碩士 === 國防醫學院 === 微生物及免疫學研究所 === 102 === Periodontitis can be characterized by the accumulation of a specific gram-negative periodontopathogens (i.e., Porphyromonas gingivalis), but progression of the disease is dependent on the host response to these pathogenic bacteria. As the number of microbial factors, such as lipopolysaccharide (LPS) from P. gingivalis (P.g), increases surface receptors known as Toll-like receptors (TLR) in the oral cavity function to recognize and respond to this change. This interaction leads to the production of inflammatory cytokines by myeloid differentiation primary response protein 88 (MyD88)-dependent and -independent pathways, which may in turn initiate a local immune response, release of inflammatory mediators, and activation of osteoclasts responsible for bone resorption. Moreover, the T helper 17 (Th17)/ regulatory T (Treg) imbalance has recently been suggested to play a role in the development of periodontitis. Although the role of adapter molecule MyD88 in controlling infection and immune system activation has been examined, its function/involvement in the development and progression of periodontal destruction has not been investigated. The aim of current study was to assess the involvement of MyD88 in alveolar bone loss (ABL) induced by P.g in mice, to investigate whether Th17/Treg imbalance plays a role in the development of experimental periodontitis, and to examine the role of MyD88 in osteoclast differentiation and function in vitro. Experimental periodontitis will be induced in C57BL/6 wild-type 1 and MyD88 KO mice by oral infection with P. gingivalis. Animals will be sacrificed at indicated time points (D14-D60) and the maxillae removed for micro-CT analyses. ABL will be assessed by measuring the distance from the cemento-enamel junction (CEJ) to the alveolar bone crest (ABC). CD4+ T cell subsets (Th17 and Treg cells)in the cervical lymph nodes (CLNs) and spleen will be analyzed by flow cytometry. Bone marrow-derived osteoclasts will be isolated, tartrate resistant acid phosphate (TRAP) staining and TRAP activity will be measured in vitro. Our data showed that increased CEJ-ABC distance was observed in WT mice at 42 days post infection, Th17/Treg imbalance in the CLNs, and blunted osteoclast differentiation of hematopoietic bone marrow cells from MyD88 KO mice was also noted when compared with WT mice after P. gingivalis LPS stimulation.
author2 Ren-Yeong Huang
author_facet Ren-Yeong Huang
Lin Wei Huang
黃琳惟
author Lin Wei Huang
黃琳惟
spellingShingle Lin Wei Huang
黃琳惟
Investigating the Role of MyD88 in the Evolution of Porphyromonas gingivalis-induced Experimental Periodontitis in Mice
author_sort Lin Wei Huang
title Investigating the Role of MyD88 in the Evolution of Porphyromonas gingivalis-induced Experimental Periodontitis in Mice
title_short Investigating the Role of MyD88 in the Evolution of Porphyromonas gingivalis-induced Experimental Periodontitis in Mice
title_full Investigating the Role of MyD88 in the Evolution of Porphyromonas gingivalis-induced Experimental Periodontitis in Mice
title_fullStr Investigating the Role of MyD88 in the Evolution of Porphyromonas gingivalis-induced Experimental Periodontitis in Mice
title_full_unstemmed Investigating the Role of MyD88 in the Evolution of Porphyromonas gingivalis-induced Experimental Periodontitis in Mice
title_sort investigating the role of myd88 in the evolution of porphyromonas gingivalis-induced experimental periodontitis in mice
publishDate 2014
url http://ndltd.ncl.edu.tw/handle/44095253977136769176
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