A new study by researchers at Baylor College of Medicine and Texas Children’s Hospital, in collaboration with Cincinnati Children’s Hospital Medical Center and Queensland University of Technology, has shed new light on the role of bacteria in the placenta (or afterbirth) and its membranes that surround the fetus during pregnancy and preterm birth. This recent study builds on their prior research and compares the placental membrane microbiome in women who have an early preterm birth with and without any suggestion of an intrauterine (in the womb) infection.
The microbiome is the collection of trillions of bacteria and microscopic organisms that inhabit our bodies and the world around us. The placenta, once thought to be sterile, has its own unique microbiome community that can be detected both by microscopes and using bacterial DNA sequencing. The team of Baylor researchers, led by senior author Dr. Kjersti Aagaard, associate professor of obstetrics and gynecology in the section of maternal-fetal medicine at Baylor and the Texas Children’s Pavilion for Women, examined the differences in the microbiome in association with preterm birth in both the presence and absence of a relatively common clinical infection, called chorioamnionitis, of the placental membranes.
“In agreement with our previous studies, we found that the placental membrane microbiome was altered in association with preterm birth. We speculate those altered states may indicate risk of preterm birth,” said Dr. Amanda Prince, a postdoctoral associate in obstetrics and gynecology at Baylor and first author of the study. “Altogether, our current study demonstrates microbial compartmentalization of the placental microbiome that is associated with preterm birth and histological chorioamnionitis.”
Using advanced DNA sequencing approaches developed for the Human Microbiome Project, the team looked at the microbiome in the space between the placental membranes and the developing fetus in 71 pregnancies.
What they found was interesting. First, the most significant difference when comparing the women’s placental membrane microbiomes was based on whether or not they had a preterm birth. The second most significant difference was when that preterm birth was accompanied by histological signs of chorioamnionitis, or the infection and inflammation of the membranes and the placenta.
What was common was the overall groups of bacteria found in previous studies conducted by other institutions of women’s placental membranes in comparison to this current study. They included women from cities other than Houston and were collected using slightly different methods than the Aagaard team had used in their other work.
“These findings were very exciting to us since they support our earlier observations from 320 Houston area women’s placenta published in 2014,” Aagaard said. “More importantly, when combined with data coming out of other research teams in Finland and Europe, as well as the U.S., China and Central and South America, we are seeing an emerging picture of the consistent bacterial contributors to the non-sterile placenta and intrauterine environment, which changes first and foremost in association with preterm birth. We and others speculate that the placenta and its membrane microbiome may be the earliest contributors to both preterm and terms infants developing microbiome. Whether or not we can ultimately identify a predictor of preterm birth, and which body site in the mom it will arise from, remains to be seen. We have several studies presently underway that are attempting to do precisely this, but at this point, we just don’t yet know.”
The research appears in the American Journal of Obstetrics and Gynecology and is currently available on PubMed.
Other contributing authors to this study include Drs. Jun Ma and Alan Harris (Baylor College of Medicine and Texas Children’s Hospital), Paranthaman Kanna, Manuel Alvarez, Tate Gisslen, Alan Job, Claire Chougnet, and Suhas Kallapur (Cincinnati Children’s Hospital), Donna Lambers (Good Samaritan Hospital, Cincinnati), and Emma Sweeney and Christine Knox (Queensland University of Technology, Brisbane, Australia).
The effort and resources for this study was partially funded by the NIH (grant numbers R01NR014792 and DP2OD001500 to K.M.A., HL97064 to A.H.J. and S.G.K, 1F32HD082969-01A1 to A.L.P.), The Burroughs Welcome Fund Preterm Birth Initiative(s) (K.M.A. and S.G.K., C.A.C. and S.G.K.) and the March of Dimes Prematurity Research Initiative (K.M.A.).