It is well known that the early human embryo is free of microorganisms, whereas the postweaning infant hosts a community of
microbes — a microbiome — comparable in complexity to that in adults. How and when this symbiosis (system having mutual benefits) between newborns and their microbiota is established are subjects of active research. Authors [see attached article and editorial] provide convincing evidence that the placenta (which acts as the interface between the mother’s body and the fetus) does not have microorganisms in healthy pregnancies. Therefore, the placenta is unlikely to be the main gateway for development of the infant’s microbiota in utero [‘microbiota’ refers to bacteria (mostly), but keep in mind this also includes some viruses and fungi].
If microbial colonization of humans were to occur in the uterus, then this would have key implications for the shaping of the early immune system. An infant’s first stool is already populated with microorganisms, so it has been uncertain whether this is solely the result of [a] microbial acquisition during and after delivery, or [b] if microbes also reach and colonize the fetus before birth. Because sampling fetal gut content is much more difficult — than collecting placenta and amniotic fluid during (elective) caesarean delivery — authors focused on the latter two, as the interface between the maternal and fetal bodies.
Placental dysfunction is associated with common adverse pregnancy outcomes that lead to a substantial proportion of the global burden of disease. Several studies that applied sequencing-based methods — which acknowledge the potential for false-positive results due to contamination — have failed to detect a placental microbiome. Aims of the present study were: [a] to determine whether pre-eclampsia (condition during pregnancy characterized by high blood pressure, sometimes with fluid retention, and protein in the urine), delivery of a small for gestational age (SGA) newborn, and spontaneous pre-term birth (PTB) are each associated with presence (or a pattern) of bacterial DNA in the placenta; and [b] to determine whether there exists a placental microbiome. Authors used samples from a prospective cohort study of nulliparous (i.e. have never given birth to a child before) pregnant women and applied an experimental approach (that keeps in mind the substantial potential for false-positive results).
Authors [see attached article] studied placental biopsies from a total of 537 women — including 318 cases of adverse pregnancy outcome and 219 controls — using multiple methods of DNA extraction and detection [it was not made clear why no men were included in this study]. They found no evidence for presence of bacteria in the large majority of placental samples (from both complicated and uncomplicated pregnancies). Virtually all signals (from microbial ribosomal RNA) were related either to acquisition of bacteria during labor and delivery, or to contamination of laboratory reagents with bacterial DNA. One exception was Streptococcus agalactiae (group B Streptococcus), for which non-contaminant signals were detected in approximately 5% of samples collected before onset of labor. Authors conclude that bacterial infection of the placenta is not a common cause of adverse pregnancy outcome. Authors also conclude that the human placenta does not have a microbiome, but it does represent a potential site of perinatal acquisition of S. agalactiae — which is a major cause of neonatal sepsis.
Nature 15 Aug 2019; 572: 329-334 & editorial pp 317-318