Intracellular Adhesion Molecule-1 Is Regulated by Porphyromonas gingivalis Through Nucleotide Binding Oligomerization Domain-Containing Proteins 1 and 2 Molecules in Periodontal Fibroblasts
Intracellular Adhesion Molecule-1 Is Regulated by Porphyromonas gingivalis Through Nucleotide Binding Oligomerization Domain-Containing Proteins 1 and 2 Molecules in Periodontal Fibroblasts
复制标题
牙周成纤维细胞中，细胞内粘附分子 1 由牙龈卟啉单胞菌通过含有核苷酸结合寡聚结构域的蛋白 1 和 2 分子进行调节。
DOI：
10.1902/jop.2013.130152
复制
发表时间：
2014-02-01
影响因子：
4.3
通讯作者：
Ouyang, Xiangying
中科院分区：
文献类型：
--
作者：
Liu, Jianru;Duan, Jinyu;Ouyang, Xiangying
背景
牙龈卟啉单胞菌调控人牙周膜细胞（hPDLCs）和人牙龈成纤维细胞（hGFs）细胞内粘附分子1（ICAM-1）表达的机制尚不清楚。本研究的目的是探讨含核苷酸结合寡聚化结构域蛋白（NOD）1和NOD 2是否参与这一过程以及ICAM-1在牙周炎中的临床意义。
方法
用牙龈卟啉单胞菌、1-Ala-γ-d-谷氨酰基-内二氨基庚二酸（NOD 1的激动剂）和胞壁酰二肽（NOD 2的激动剂）处理hPDLC和hGF。或者，用牙龈卟啉单胞菌处理用靶向NOD 1和NOD 2的小干扰RNA转染的细胞。在mRNA和蛋白水平检测ICAM-1、NOD 1和NOD 2。另外，对30例健康对照组和40例慢性牙周炎（CP）患者治疗前后进行临床检查，并采用酶联免疫吸附法（ELISA）检测血清可溶性细胞间粘附分子-1（sICAM-1）水平。
结果
这项研究表明，牙龈卟啉单胞菌引起牙周成纤维细胞中ICAM-1，NOD 1和NOD 2表达增加。ICAM-1与NOD 1、NOD 2水平呈直线相关。特异性激动剂激活NOD 1和NOD 2导致ICAM-1的上调，而敲低NOD 1和NOD 2导致牙龈卟啉单胞菌诱导的ICAM-1产生减少。此外，sICAM-1水平在CP患者高于健康对照组，并与牙周临床参数呈正相关。牙周治疗后sICAM-1水平明显下降。
结论
提示sICAM-1水平与牙周炎的严重程度有关。NOD 1和NOD 2介导牙龈卟啉单胞菌诱导的牙周成纤维细胞ICAM-1的产生。NOD 1和NOD 2可能被认为是牙周治疗的潜在靶点。
BACKGROUND
The mechanism by which Porphyromonas gingivalis regulates intracellular adhesion molecule 1 (ICAM-1) expression in human periodontal ligament cells (hPDLCs) and human gingival fibroblasts (hGFs) is unknown. The aim of this study is to investigate whether nucleotide binding oligomerization domain-containing protein (NOD) 1 and NOD2 are involved in this process and the clinical significance of ICAM-1 in periodontitis.
METHODS
hPDLCs and hGFs were treated with P. gingivalis, l-Ala-γ-d-glutamyl-mesodiaminopimelic acid (an agonist for NOD1), and muramyl dipeptide (an agonist for NOD2). Alternatively, cells transfected with small interfering RNA targeting NOD1and NOD2 were treated with P. gingivalis. ICAM-1, NOD1, and NOD2 were detected at mRNA and protein levels. In addition, clinical examinations were performed in 30 healthy controls and 40 patients with chronic periodontitis (CP) before and after treatment, and serum-soluble ICAM-1 (sICAM-1) levels in these individuals were detected by enzyme-linked immunosorbent assay.
RESULTS
This study shows that P. gingivalis caused an increase in ICAM-1, NOD1, and NOD2 expression in periodontal fibroblasts. There was a linear correlation between ICAM-1 and NOD1 and NOD2 levels. Activation of NOD1 and NOD2 by the specific agonist led to the upregulation of ICAM-1, whereas knocking down NOD1 and NOD2 caused a reduction in P. gingivalis-induced ICAM-1 production. Furthermore, sICAM-1 levels were higher in patients with CP than in healthy controls and were positively related to the clinical periodontal parameters. After periodontal treatment, sICAM-1 levels decreased significantly.
CONCLUSIONS
The present results indicate that sICAM-1 levels are correlated to the severity of periodontitis. NOD1 and NOD2 mediate P. gingivalis-induced ICAM-1 production in periodontal fibroblasts. NOD1 and NOD2 could be considered potential targets for periodontal therapy.