Sun Ying, Shu Rong, Zhang Ming-Zhu, Wu An-Ping
Department of Periodontology, Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
FEMS Immunol Med Microbiol. 2008 Apr;52(3):362-9. doi: 10.1111/j.1574-695X.2008.00386.x. Epub 2008 Mar 6.
Toll-like receptors (TLRs) are a group of sensors on the surface of antigen-presenting cells, such as dendritic cells and macrophages, which recognize microbial pathogens and induce innate and adaptive immune responses. Periodontitis is an inflammatory disease characterized by the destruction of tooth-supporting structures. In order to address whether TLR4 signaling plays a role in periodontitis, we studied the gene expression change in human periodontal ligament cells (HPDLCs) in response to TLR4 ligand, lipopolysaccharide treatment by microarray analysis. Expression of TLR4 was detected in HPDLCs. Lipopolysaccharide treatment increased the expression of 12 genes (more than twofold), including TLR4, TLR5, TLR7, Pellino 1, colony stimulating factor 2 (CSF2) and IL-6. In addition, the expression of 15 genes (less than equal to twofold) was decreased, including Fos, LY64 and LY86. In addition, real-time PCR was used to confirm the change of gene expression of TLR4, IL-6 and Fos. We also showed that the upregulation of IL-6 by lipopolysaccharide treatment was TLR4-dependent. This pattern of gene expression indicates that pathogens may trigger TLR4 signaling and cause periodontitis. Manipulating TLR4 signaling may potentially become one of the recognized therapies for periodontitis.
Toll样受体（TLRs）是抗原呈递细胞（如树突状细胞和巨噬细胞）表面的一组传感器，可识别微生物病原体并诱导先天性和适应性免疫反应。牙周炎是一种以牙齿支持结构破坏为特征的炎症性疾病。为了探究TLR4信号通路是否在牙周炎中起作用，我们通过微阵列分析研究了人牙周膜细胞（HPDLCs）在TLR4配体脂多糖处理后的基因表达变化。在HPDLCs中检测到TLR4的表达。脂多糖处理增加了12个基因（超过两倍）的表达，包括TLR4、TLR5、TLR7、pellino 1、集落刺激因子2（CSF2）和IL-6。此外，15个基因（小于或等于两倍） 的表达下降，包括Fos、LY64和LY86。此外，使用实时PCR来确认TLR4、IL-6和Fos基因表达的变化。我们还表明，脂多糖处理引起的IL-6上调是TLR4依赖性的。这种基因表达模式表明病原体可能触发TLR4信号通路并导致牙周炎。操纵TLR4信号通路可能会成为牙周炎公认的治疗方法之一。
