Bacterial infection promotes DNA hypermethylation
Bacterial infection promotes DNA hypermethylation
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DOI：
10.1177/154405910708600212
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发表时间：
2007-02-01
影响因子：
7.6
通讯作者：
Offenbacher, S.
中科院分区：
文献类型：
--
作者：
Bobetsis, Y. A.;Barros, S. P.;Offenbacher, S.
由直肠弯曲杆菌或牙龈假单胞菌等细菌引起的母体口腔感染，已被认为是胎盘和胎儿感染和炎症挑战的潜在来源，从而增加了早产和生长受限的相对风险。在各种感染口腔微生物的动物模型中，也有宫内生长受限的报道。分析感染生长受限小鼠的胎盘组织，我们发现印记的Igf2基因下调。通过DNA甲基化改变对印记基因的表观遗传修饰在胎儿生长发育规划中起着至关重要的作用。在这里，我们评估了直肠弯曲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-P0的甲基化。这一新发现将感染与表观遗传学改变联系起来，提供了一种将环境信号与胎盘表型联系起来的机制，并对发育产生了影响。
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.