Department of Periodontology, Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
J Periodontol. 2010 Oct;81(10):1488-96. doi: 10.1902/jop.2010.100004.
Periodontitis is a bacterially induced chronic inflammatory disease. Toll-like receptors (TLRs), which could recognize microbial pathogens, are important components in the innate and adaptive immune systems. Both qualitatively and quantitatively distinct immune responses might result from different bacteria stimulation and the triggering of different TLRs. This study explores the interaction of Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum, and Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) with TLR2 and TLR4.
We studied the gene expression changes of TLR2 and TLR4 and cytokine production (interleukin-1β, -6, -8, -10, and tumor necrosis factor-alpha) in human periodontal ligament cells (HPDLCs) stimulated with heat-killed bacteria or P. gingivalis lipopolysaccharide (LPS) in the presence or absence of monoclonal antibodies to TLR2 or TLR4 (anti-TLR2/4 mAb).
Both test bacteria and 10 microg/ml P. gingivalis LPS treatment increased the gene expression of TLR2 and TLR4 and cytokine production in HPDLCs. In addition, these upregulations could be blocked by anti-TLR2/4 mAb. However, the expression of TLR4 mRNA in HPDLCs stimulated with 1 microg/ml P. gingivalis LPS was not increased. No differences were found in the cytokine production caused by 1 microg/ml P. gingivalis LPS treatment in the presence or absence of anti-TLR4 mAb.
These patterns of gene expression and cytokine production indicate that Gram-negative periodontal bacteria or their LPS might play a role in triggering TLR2 and/or TLR4, and be of importance for the immune responses in periodontitis.
牙周炎是一种由细菌引起的慢性炎症性疾病。Toll 样受体（TLR）能够识别微生物病原体，是先天和适应性免疫系统的重要组成部分。不同的细菌刺激和不同 TLR 的触发可能导致不同的免疫反应，无论是在质量上还是在数量上。本研究探讨了牙龈卟啉单胞菌、中间普氏菌、核梭杆菌和伴放线放线杆菌（以前称为伴放线放线杆菌）与 TLR2 和 TLR4 的相互作用。
我们研究了热灭活细菌或牙龈卟啉单胞菌脂多糖（LPS）刺激下人牙周韧带细胞（HPDLC）中 TLR2 和 TLR4 的基因表达变化以及细胞因子（白细胞介素-1β、-6、-8、-10 和肿瘤坏死因子-α）的产生，同时存在或不存在 TLR2 或 TLR4 的单克隆抗体（抗 TLR2/4 mAb）。
两种试验细菌和 10μg/ml 牙龈卟啉单胞菌 LPS 处理均增加了 HPDLC 中 TLR2 和 TLR4 的基因表达和细胞因子产生。此外，这些上调可以被抗 TLR2/4 mAb 阻断。然而，1μg/ml 牙龈卟啉单胞菌 LPS 刺激下 HPDLC 中 TLR4 mRNA 的表达没有增加。在存在或不存在抗 TLR4 mAb 的情况下，1μg/ml 牙龈卟啉单胞菌 LPS 处理引起的细胞因子产生没有差异。
这些基因表达和细胞因子产生模式表明革兰氏阴性牙周细菌或其 LPS 可能在触发 TLR2 和/或 TLR4 中起作用，对牙周炎的免疫反应很重要。
