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Involvement of PGE2, IL-1β, and TNF-α in RANKL-dosteoclastogenesis induced by Porphyromonas gingivalis, Treponema denticola and Treponema socranskii

Other Titles
 Porphyromonas gingivalis, Treponema denticola, 
Authors
 김기환 
Issue Date
2003
Description
Dept. of Dentistry/석사
Abstract
[한글] 치주염은 치조골의 흡수를 동반하는 염증성 질환으로 치은연하 치태내의 여러 종류의 미생물이 치조골 흡수에 영향을 준다. 이러한 여러 종류의 치주병인체로 인하여 발생하는 여러 파골세포형성 인자 중에서 공통된 인자를 찾기 위해, 마우스 두개골 기원의 조골세포와 골수 세포의 혼합배양에서 세 종류의 치주병인체, 즉, Porphyromonas gingivalis, Treponema denticola 및 Treponema socranskii에 의한 파골세포형성 기전을 관찰하였다. 조골세포의 interleukin (IL)-1b, tumor necrosis factor (TNF)-a, receptor activator of NF-kB ligand (RANKL) 및 prostaglandin E2 (PGE2)의 발현은 reverse transcriptase polymerase chain reaction (RT-PCR) 및 면역분석법을 통하여 관찰하였다. 세 종의 세균 분쇄액은 혼합배양에서 파골세포형성을 촉진하였고, 조골세포의 RANKL, IL-1b 및 TNF-a의 mRNA 발현 그리고 PGE2 의 생성을 증가시켰다. RANKL의 억제 인자인 osteopotegerin (OPG)는 각 세균 분쇄액에 의한 파골세포형성을 완전히 억제하였다. 또한 PGE2 형성 억제 인자인 indomethacin, anti-IL-1b antibody (Ab), 및 anti-TNF-a Ab가 더해졌을 때 각각의 미세균 분쇄액의 파골세포 형성능이 저하되었다. 또한, indomethacin, anti-IL-1b Ab, 또는 anti-TNF-a Ab는 P. gingivalis, T. denticola, 및 T. socranskii 분쇄액 으로 처리된 조골 세포내에서 RANKL 발현을 저하시켰다. 이는 P. gingivalis, T. denticola, 및 T. socranskii가 조골세포의 RANKL의 발현을 증가시켜 파골세포 형성을 촉진하며, 이러한 세 종의 미생물에 의한 RANKL 발현에 IL-1b, TNF-a 및 PGE2 가 중간 매개체로 작용한다는 것을 보여주고 있다.
[영문] Periodontitis is an inflammatory disease that often leads to destruction of alveolar bone. Multiple species of bacteria in subgingival plaque are associated with bone destruction in periodontitis. In this kind of bone destruction, the osteoclast is known to play a key role. To determine the mediators which are involved in osteoclastogenesis by periodontopathogens, we studied the effect of three periodontopathogens, Porphyromonas gingivalis, Treponema denticola, and Treponema socranskii on osteoclastogenesis in coculture system of mouse calvaria derived osteoblastic cells and bone marrow cells. The expression of interleukin (IL)-1b, tumor necrosis factor (TNF)-a, receptor activator of NF-kB ligand (RANKL) and prostaglandin E2 (PGE2) in mouse calvaria cells was determined by reverse transcriptase-polymerase chain reaction (RT-PCR) or immunoassay. Sonicates of three bacteria induced osteoclast formation in coculture systems and the mRNA expression of IL-1b, TNF-a, and RANKL in osteoblastic cells. The production of PGE2 was increased by three bacteria sonicates. Addition of osteoprotegerin (OPG), which is an inhibitor of RANKL, in the cocultures resulted in the complete suppression of the induction of the osteoclast formation. Anti-IL-1b antibody (Ab), anti-TNF-a Ab and indomethacin, which is an inhibitor of PGE2, partially inhibited the induction of the osteoclast formation by each bacteria. In addition, indomethacin, anti-IL-1b Ab, or anti-TNF-a Ab decreased RANKL expression of osteoblastic cells treated with bacterial sonicates of P. gingivalis, T. denticola, and T. socranskii. These findings suggest that increased RANKL expression of osteoblastic cells may play an important role in the osteoclast formation induced by P. gingivalis, T. denticola, and T. socranskii and that PGE2, IL-1b, and TNF-a are mediators for the induction of RANKL expression by these bacteria.
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/128386
Appears in Collections:
2. Thesis / Dissertation (학위논문) > 2. College of Dentistry (치과대학) > Master's Degree (석사)
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