Bobetsis Y A, Barros S P, Lin D M, Weidman J R, Dolinoy D C, Jirtle R L, Boggess K A, Beck J D, Offenbacher S
University of North Carolina at Chapel Hill, Center for Oral and Systemic Diseases, Department of Periodontology, UNC School of Dentistry, CB #7455, DRC Rm 222, Chapel Hill, NC 27599-7455, USA.
J Dent Res. 2007 Feb;86(2):169-74. doi: 10.1177/154405910708600212.
Maternal oral infection, caused by bacteria such as C. rectus or P. gingivalis, has been implicated as a potential source of placental and fetal infection and inflammatory challenge, which increases the relative risk for pre-term delivery and growth restriction. Intra-uterine growth restriction has also been reported in various animal models infected with oral organisms. Analyzing placental tissues of infected growth-restricted mice, we found down-regulation of the imprinted Igf2 gene. Epigenetic modification of imprinted genes via changes in DNA methylation plays a critical role in fetal growth and development programming. Here, we assessed whether C. rectus infection mediates changes in the murine placenta Igf2 methylation patterns. We found that infection induced hypermethylation in the promoter region-P0 of the Igf2 gene. This novel finding, correlating infection with epigenetic alterations, provides a mechanism linking environmental signals to placental phenotype, with consequences for development.
由直肠弯曲杆菌或牙龈卟啉单胞菌等细菌引起的母体口腔感染,被认为是胎盘和胎儿感染及炎症刺激的潜在来源,这会增加早产和生长受限的相对风险。在感染口腔微生物的各种动物模型中也报道了宫内生长受限。通过分析受感染的生长受限小鼠的胎盘组织,我们发现印记基因Igf2表达下调。通过DNA甲基化变化对印记基因进行表观遗传修饰在胎儿生长和发育编程中起关键作用。在此,我们评估了直肠弯曲杆菌感染是否介导了小鼠胎盘Igf2甲基化模式的变化。我们发现感染诱导了Igf2基因启动子区域-P0的高甲基化。这一将感染与表观遗传改变相关联的新发现,提供了一种将环境信号与胎盘表型联系起来的机制,并对发育产生影响。