Laboratory of Molecular Biology, Department of Oral Surgery and Pathology, School of Dentistry, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Immunobiology. 2013 Jul;218(7):1012-7. doi: 10.1016/j.imbio.2012.12.001. Epub 2012 Dec 13.
Periodontitis is considered an inflammatory disorder of bacterial etiology that results in periodontal tissue destruction, as a result of complex interactions between periodontal pathogens, host and immune response. Genetic and epigenetic mechanisms may modulate the individual response since it is able to influence the gene expression. The aim of this study was to evaluate the impact of -174 G/C polymorphism and the methylation status of the promoter region of IL-6 gene on the expression of IL-6 in gingival samples from individuals with chronic periodontitis. Gingival biopsies were collected from 21 patients with chronic periodontitis and 21 controls. Histologic sections stained by hematoxylin-eosin were used for histopathological evaluation. The IL-6 gene expression was assessed by quantitative real-time PCR. The polymorphism IL-6 -174 C/G was studied by polymerase chain reaction (PCR) amplification and restriction endonuclease digestion (HspII). Methylation-specific polymerase chain reaction was used to verify the DNA methylation pattern. The number of inflammatory cells in tissue fragments from individuals with chronic periodontitis was higher than in the control group and the inflammatory infiltrate was predominantly mononuclear. The expression of IL-6 was higher in the group with periodontitis. In polymorphism assay, no statistical difference in the distribution of genotypes and alleles in both groups were observed. The most of samples were partially methylated. No difference was observed in methylation pattern from two different regions of the IL-6 gene among groups. The high expression of IL-6 is an important factor related to chronic periodontitis, but was not associated with methylation status or the -174 (G/C) genetic polymorphism, suggesting that other mechanisms are involved in this gene transcription regulation.
牙周炎被认为是一种细菌性病因的炎症性疾病，导致牙周组织破坏，这是由于牙周病原体、宿主和免疫反应之间的复杂相互作用。遗传和表观遗传机制可能调节个体反应，因为它能够影响基因表达。本研究旨在评估 IL-6 基因启动子区域-174 G/C 多态性和甲基化状态对慢性牙周炎患者牙龈样本中 IL-6 表达的影响。从 21 例慢性牙周炎患者和 21 例对照中采集牙龈活检组织。苏木精-伊红染色的组织学切片用于组织病理学评估。通过定量实时 PCR 评估 IL-6 基因表达。通过聚合酶链反应 (PCR) 扩增和限制性内切酶消化 (HspII) 研究 IL-6-174C/G 多态性。甲基化特异性聚合酶链反应用于验证 DNA 甲基化模式。慢性牙周炎患者组织碎片中的炎症细胞数量高于对照组，炎症浸润主要为单核细胞。牙周炎组的 IL-6 表达更高。在多态性检测中，两组基因型和等位基因的分布均无统计学差异。大多数样本呈部分甲基化。三组之间 IL-6 基因的两个不同区域的甲基化模式没有差异。IL-6 的高表达是与慢性牙周炎相关的重要因素，但与甲基化状态或-174（G/C）遗传多态性无关，提示其他机制参与了该基因的转录调控。
