Schulz Susanne, Immel Uta Dorothee, Just Louise, Schaller Hans-Günter, Gläser Christiane, Reichert Stefan
University School of Dental Medicine, Department of Operative Dentistry and Periodontology, Martin-Luther University Halle-Wittenberg, Germany.
Institute of Legal Medicine, Martin-Luther-University Halle-Wittenberg, Germany.
Hum Immunol. 2016 Jan;77(1):71-75. doi: 10.1016/j.humimm.2015.10.007. Epub 2015 Oct 21.
Periodontitis is a chronic inflammatory disease triggered by the host immune response. Epigenetic modifications also affect the immune response. We assessed CpG methylation in 22 inflammatory candidate genes (ATF2, CCL25, CXCL14, CXCL3, CXCL5, CXCL6, FADD, GATA3, IL10RA, IL12A, IL12B, IL13, IL13RA1, IL15, IL17C, IL17RA, IL4R, IL6R, IL6ST, IL7, INHA, and TYK2) with respect to the occurrence of aggressive periodontitis (AgP).
In this study 15 AgP patients (53.3% males, 41.4±10.5 years) and 10 controls (40.0% males, 36.9±17.5 years) were included. The methylation patterns of gingival biopsies were quantified using EpiTect® Methyl Signature PCR Array Human Inflammatory Response.
In gingival biopsies taken from patients with AgP, CpG methylation of CCL25 (1.73% vs. 2.59%, p=0.015) and IL17C (6.89% vs. 19.27%, p=0.002) was significantly reduced as compared with periodontally healthy tissues.
We showed for the first time a differential methylation pattern for CCL25 and IL17C in periodontitis. CCL25 plays an important role in T-cell development, whereas IL17C regulates innate epithelial immune responses. The decrease in CpG methylation is presumably accompanied by an increase in gene expression. This could lead to a greater availability of CCL25 and interleukin 17C and support periodontal loss of attachment.
牙周炎是一种由宿主免疫反应引发的慢性炎症性疾病。表观遗传修饰也会影响免疫反应。我们评估了22个炎症候选基因（ATF2、CCL25、CXCL14、CXCL3、CXCL5、CXCL6、FADD、GATA3、IL10RA、IL12A、IL12B、IL13、IL13RA1、IL15、IL17C、IL17RA、IL4R、IL6R、IL6ST、IL7、INHA和TYK2）的CpG甲基化与侵袭性牙周炎（AgP）发生的关系。
本研究纳入了15例AgP患者（男性占53.3%，年龄41.4±10.5岁）和10例对照者（男性占40.0%，年龄36.9±17.5岁）。使用EpiTect®甲基化特征PCR阵列人类炎症反应对牙龈活检组织的甲基化模式进行定量分析。
与牙周健康组织相比，取自AgP患者的牙龈活检组织中，CCL25的CpG甲基化（1.73%对2.59%，p = 0.015）和IL17C的CpG甲基化（6.89%对19.27%，p = 0.002）显著降低。
我们首次在牙周炎中发现了CCL25和IL17C的差异甲基化模式。CCL25在T细胞发育中起重要作用，而IL17C调节先天性上皮免疫反应。CpG甲基化的降低可能伴随着基因表达的增加。这可能导致CCL25和白细胞介素17C的可用性增加，并支持牙周附着丧失。
