Toll-like receptor 4 signaling plays a role in triggering periodontal infection

被引:56
作者
Sun, Ying [1 ,2 ]
Shu, Rong [1 ,2 ]
Zhang, Ming-Zhu [1 ,2 ]
Wu, An-Ping [3 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, Ninth Peoples Hosp, Dept Periodontol, Shanghai 200011, Peoples R China
[2] Shanghai Jiao Tong Univ, Sch Med, Ninth Peoples Hosp, Shanghai Key Lab Stomatol,Shanghai Res Inst Stoma, Shanghai 200011, Peoples R China
[3] Xuhui Stomatol Hosp, Shanghai, Peoples R China
来源
FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY | 2008年 / 52卷 / 03期
关键词
toll-like receptor 4; lipopolysaccharide; human periodontal ligament cell;
D O I
10.1111/j.1574-695X.2008.00386.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
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.
引用
收藏
页码:362 / 369
页数:8
相关论文
共 30 条
[1]
Toll-like receptors in the induction of the innate immune response [J].
Aderem, A ;
Ulevitch, RJ .
NATURE, 2000, 406 (6797) :782-787
[2]
Gamma interferon and granulocyte/monocyte colony-stimulating factor prevent endotoxin tolerance in human monocytes by promoting interleukin-1 receptor-associated kinase expression and its association to MyD88 and not by modulating TLR4 expression [J].
Adib-Conquy, M ;
Cavaillon, JM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (31) :27927-27934
[3]
1-methyl-tryptophan can interfere with TLR signaling in dendritic cells independently of IDO activity [J].
Agaugue, Sophie ;
Perrin-Cocon, Laure ;
Coutant, Frederic ;
Andre, Patrice ;
Lotteau, Vincent .
JOURNAL OF IMMUNOLOGY, 2006, 177 (04) :2061-2071
[4]
BEGUM NA, 1999, J IMMUNOL, V161, P1348
[5]
Bitzer M, 2000, GENE DEV, V14, P187
[6]
Cutting edge:: TLR2 is required for the innate response to Porphyromonas gingivalis:: activation leads to bacterial persistence and TLR2 deficiency attenuates induced alveolar bone resorption [J].
Burns, Elia ;
Bachrach, Gilad ;
Shapira, Lior ;
Nussbaum, Gabriel .
JOURNAL OF IMMUNOLOGY, 2006, 177 (12) :8296-8300
[7]
Modulation of the innate immune response within the periodontium [J].
Dixon, DR ;
Bainbridge, BW ;
Darveau, RP .
PERIODONTOLOGY 2000, 2004, 35 :53-74
[8]
Role of bacteria in health and disease of periodontal tissues [J].
Feng, ZM ;
Weinberg, A .
PERIODONTOLOGY 2000, 2006, 40 :50-76
[9]
LPS induction of gene expression in human monocytes [J].
Guha, M ;
Mackman, N .
CELLULAR SIGNALLING, 2001, 13 (02) :85-94
[10]
Hoshino K, 1999, J IMMUNOL, V162, P3749