Porphyromonas gingivalis is considered a keystone pathogen that contributes to the initiation and progression of periodontitis in humans. P. gingivalis has also been detected in human placentas associated with adverse pregnancy outcomes. The spread of P. gingivalis from the oral cavity to the reproductive tract thus represents a potential mechanism whereby periodontitis can lead to adverse pregnancy outcomes. In a murine model of pregnancy and oral infection with P. gingivalis, C57BL/6J mice developed low fetal weight, whereas C57BL/6NCrl mice did not. Although C57BL/6NCrl mice harbor segmented filamentous bacteria that drive a Th17 response, fetal weight was independent of frequency of Th17 or Th1 in either substrain. Low fetal weight was instead correlated with increasing amounts of P. gingivalis DNA in the placentas of the C57BL/6J dams. In contrast, fetal weight in C57BL/6NCrl mice was independent of P. gingivalis in the placenta. Differences in genetics or microbiome that influence the ability of P. gingivalis to colonize the placenta may drive differential fetal weight outcomes between C57BL/6J and C57BL/6NCrl mice and, potentially, between diverse human populations.
Bibliographical noteFunding Information:
We thank Mark C. Herzberg and his team, Bryan Michalowicz, the University of Minnesota School of Dentistry Oral Biology Program, and Scott Lunos at the Biostatistic Core. This study was supported in part by NIH/NIDCR R21 grants DE022858 (M.C.) and DE026209 (M.C.) and the Schaffer Chair for Periodontal Research at the University of Minnesota. The funders had no role in the decision to submit the work for publication. We declare that we have no conflicts of interest.
Copyright © 2019 American Society for Microbiology. All Rights Reserved.
Copyright 2019 Elsevier B.V., All rights reserved.
- Placental immunology