Campylobacter rectus infection impairs placental function and development in mice.

摘要

In humans, periodontal disease has been associated with an increased risk for preterm and low birth weight deliveries. Among the periodontal pathogens, Campylobacter rectus (C. rectus) appears to play a key role in these processes. Several animal models have been developed to study the effects of periodontal bacteria on pregnancy outcomes, and demonstrate their deleterious consequences on fetal growth. Since the placenta is the organ where nutrient exchange takes place between the mother and the fetus, and since its normal development is considered of crucial importance for the normal growth and development of the fetus, our hypothesis is that maternal infection with C. rectus impairs placental function and development, which may contribute to intrauterine growth restriction (IUGR).; We used a pregnancy/infection mouse model and found that C. rectus infection leads to IUGR. Moreover, the bacteria not only disseminated to the placenta, but also translocated to fetal tissues where they have the capacity of invading host cells. The presence of C. rectus in the placenta may have mediated structural changes in this organ, with the most significant being the decrease of the labyrinth and the increase of the decidual layer. These alterations could have been induced by the down-regulation in the expression of genes important for placental and fetal growth and development. Among these genes several imprinted genes, such as Igf2, were included. Finally, we found that C. rectus infection induced hypermethylation of the promoter of Igf2. This may present a possible mechanism for the down-regulation of this gene and possibly of other imprinted genes.; The data from this study provide information about potential mechanisms that underlie the impaired fetal growth after maternal infection with the periodontal pathogen C. rectos. Moreover, since changes in the methylation patterns of genes are usually inherited in somatic cells, our data raise the possibility that infection-mediated epigenetic modifications of the DNA, that occur in utero, may predispose the individual for diseases that appear later in life.