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Bacterial Infection Promotes DNA Hypermethylation

¹ 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, USA 27599-7455;
² Duke University Medical Center, Department of Radiation Oncology Environmental Safety, Durham, NC;
³ University of North Carolina at Chapel Hill, Center for Oral and Systemic Diseases, UNC School of Dentistry, and Department of Obstetrics and Gynecology, UNC School of Medicine, Chapel Hill, NC, USA 27599; and
⁴ University of North Carolina at Chapel Hill, Center for Oral and Systemic Diseases, Department of Dental Ecology, UNC School of Dentistry, Chapel Hill, NC, USA 27599

^* corresponding author, steve_offenbacher{at}dentistry.unc.edu

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.

KEY WORDS: epigenetics • chronic inflammation • oral pathogen • fetal growth