牙龈卟啉单胞菌
TLR2型
TLR4型
TLR9型
牙周炎
慢性牙周炎
Toll样受体
肿瘤坏死因子α
微生物学
下调和上调
先天免疫系统
逆转录聚合酶链式反应
生物
受体
免疫系统
免疫学
基因表达
化学
医学
基因
内科学
DNA甲基化
生物化学
作者
Nawarat Wara‐aswapati,Anek Chayasadom,Rudee Surarit,Waranuch Pitiphat,Jason A. Boch,Toshiyuki Nagasawa,Isao Ishikawa,Yuichi Izumi
标识
DOI:10.1902/jop.2012.120362
摘要
Background: Toll‐like receptors (TLRs) play pivotal roles in host immune responses and have been suggested to be involved in the development of many infectious diseases. In this study, the mRNA expression levels of TLR2, TLR4, and TLR9 and their relationship with periodontopathic bacteria in periodontal tissue are examined. Furthermore, the mechanism of TLR induction by Porphyromonas gingivalis is investigated in human gingival fibroblasts (HGFs). Methods: Gingival tissue and subgingival plaque samples were collected from 19 patients with chronic periodontitis (CP) and 16 control individuals without periodontitis. Gene expression levels in the tissues and in HGFs were analyzed by reverse transcription‐polymerase chain reaction (RT‐PCR). The numbers of periodontopathic bacteria were determined by quantitative real‐time PCR. Results: The expression levels of TLR2 and TLR9 were significantly higher in the tissues of patients with CP compared to the tissues of control individuals. The mRNA levels of TLR2 and TLR9, but not TLR4, were positively correlated with the number of P. gingivalis in subgingival plaque. P. gingivalis sonicated extract, P. gingivalis lipopolysaccharide, P. gingivalis DNA, and tumor necrosis factor‐α(TNF‐α) could significantly upregulate the mRNA expression of TLR2 in HGFs. Furthermore, P. gingivalis –mediated TLR2 expression was suppressed by TNF‐α antibody. Conclusions: This study suggests that P. gingivalis infection induces TLR2 and TLR9 upregulation in patients with CP. P. gingivalis –induced TLR2 expression in HGFs is partially dependent on TNF‐α and may lead to sensitization of HGFs to bacterial components encountered in the periodontal microenvironment.
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