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Responsiveness to Lipopolysaccharide Changes According to the Aging of Periodontal Ligament Fibroblasts
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  • Responsiveness to Lipopolysaccharide Changes According to the Aging of Periodontal Ligament Fibroblasts
  • Responsiveness to Lipopolysaccharide Changes According to the Aging of Periodontal Ligament Fibroblasts
저자명
Jun. Ji-Hae,Kim. Gwan-Shik,Woo. Kyung-Mi,Min. Byung-Moo,Baek. Jeong-Hwa
간행물명
International journal of oral biology : official journal of the Korean Academy of Oral Biology and the UCLA Dental Research Institute
권/호정보
2005년|30권 1호|pp.1-8 (8 pages)
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대한구강생물학회
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

The elderly suffer from an impaired immune function being obvious in a higher susceptibility to infections. Although the inflammatory cells are the major immunomodulatory cells, fibroblasts also secrete a variety of inflammatory cytokines and chemokines. Therefore periodontal tissue aging might playa role in development and progress of periodontitis. In this study, we investigated the effect of in vitro periodontal ligament cellular aging on the inflammatory cytokines, chemokines, and matrix metalloprotease(MMP)-2 expression induced by lipopolysaccharide(LPS) treatment. Three different cell populations were used; passages 4-5, 14-15, and 24-25 (at passage 27, more than 90% cells were replicative senescent). LPS increased the expression of interleukin(IL)-1${eta}$, IL-6, and tumor necrosis factor-${alpha}$, IL-8, RANTES, and MMP-2. However, the order of induction folds were passages 14-15 > 4-5 > 24-25. While the expression level of Toll-like receptor(TLR) 4 decreased according to the increase in passage number, the level of TLR2 was highest at passages 14-15 and then decreased at passages 24-25. While the spontaneous expression of IL-8 decreased according to the increase in passage number, that of RANTES and proMMP-2 increased according to the increase in passage number. These results suggest that the aging of periodontal ligament fibroblasts differentially affect the role as immunomodulatory cells in response to periodontopathic bacteria and therefore might be another risk factor of periodontitis progression.