Induction of Toll‐Like Receptor Expression by Porphyromonas gingivalis

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
出处
期刊:Journal of Periodontology [Wiley]
卷期号:84 (7): 1010-1018 被引量:52
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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