Abstract:The placenta is the principal organ nurturing the fetus during pregnancy and was traditionally considered to be sterile. Recent work has suggested that the placenta harbours microbial communities, however the location and possible function of these microbes remain to be confirmed and elucidated. Here, we employed genomic DNA sequencing of multiple variable (V) regions of the bacterial 16S ribosomal gene, to interrogate microbial profiles in term pregnancies, from the basal plate, which is in direct contact wit… Show more
“…In addition to immune cells, the placenta harbors a low abundance but metabolically rich microbiome 147 that varies from the decidua to basal plates to the fetal membranes. 148 This microbial community is disrupted with preterm labor, 149 PE 150 and gestational weight gain, 151 and pregravid obesity. 126 Some of these studies were carried out using placenta samples of preterm births; therefore, our understanding of the impact of pregravid obesity on microbial communities within the term placental decidua remains limited.…”
Section: Pregravid Obesity and Immune Adaptations In The Placentamentioning
confidence: 99%
“…In addition to immune cells, the placenta harbors a low abundance but metabolically rich microbiome that varies from the decidua to basal plates to the fetal membranes . This microbial community is disrupted with preterm labor, PE and gestational weight gain, and pregravid obesity .…”
Maternal pregravid obesity results in several adverse health outcomes during pregnancy, including increased risk of gestational diabetes, preeclampsia, placental abruption, and complications at delivery. Additionally, pregravid obesity and in utero exposure to high fat diet have been shown to have detrimental effects on fetal programming, predisposing the offspring to adverse cardiometabolic, endocrine, and neurodevelopmental outcomes. More recently, a deeper appreciation for the modulation of offspring immunity and infectious disease‐related outcomes by maternal pregravid obesity has emerged. This review will describe currently available animal models for studying the impact of maternal pregravid obesity on fetal immunity and review the data from clinical and animal model studies. We also examine the burden of pregravid obesity on the maternal–fetal interface and the link between placental and systemic inflammation. Finally, we discuss future studies needed to identify key mechanistic underpinnings that link maternal inflammatory changes and fetal cellular reprogramming events.
“…In addition to immune cells, the placenta harbors a low abundance but metabolically rich microbiome 147 that varies from the decidua to basal plates to the fetal membranes. 148 This microbial community is disrupted with preterm labor, 149 PE 150 and gestational weight gain, 151 and pregravid obesity. 126 Some of these studies were carried out using placenta samples of preterm births; therefore, our understanding of the impact of pregravid obesity on microbial communities within the term placental decidua remains limited.…”
Section: Pregravid Obesity and Immune Adaptations In The Placentamentioning
confidence: 99%
“…In addition to immune cells, the placenta harbors a low abundance but metabolically rich microbiome that varies from the decidua to basal plates to the fetal membranes . This microbial community is disrupted with preterm labor, PE and gestational weight gain, and pregravid obesity .…”
Maternal pregravid obesity results in several adverse health outcomes during pregnancy, including increased risk of gestational diabetes, preeclampsia, placental abruption, and complications at delivery. Additionally, pregravid obesity and in utero exposure to high fat diet have been shown to have detrimental effects on fetal programming, predisposing the offspring to adverse cardiometabolic, endocrine, and neurodevelopmental outcomes. More recently, a deeper appreciation for the modulation of offspring immunity and infectious disease‐related outcomes by maternal pregravid obesity has emerged. This review will describe currently available animal models for studying the impact of maternal pregravid obesity on fetal immunity and review the data from clinical and animal model studies. We also examine the burden of pregravid obesity on the maternal–fetal interface and the link between placental and systemic inflammation. Finally, we discuss future studies needed to identify key mechanistic underpinnings that link maternal inflammatory changes and fetal cellular reprogramming events.
“…We found a high prevalence of R. insidiosa, a waterborne environmental bacterium, in human BPs using multi-variable region 16S sequencing approach 19 . Other investigators have also identified Ralstonia spp.…”
Section: Discussionmentioning
confidence: 88%
“…Whether there are microbiota (live or simply DNA signatures) in the maternal-fetal interface remains mired in controversy. In the recent years, there has been a large number of studies, providing both sequencing and histological evidence, indicating microbial signatures 3,11,18,19,22,23,29 , while other studies have reported these signatures as likely DNA contaminants originating from the sample collection and/or the DNA extraction process, rather than the placenta itself [54][55][56][57] . Placenta location remains a key variable in the aforementioned studies given that that BP, PV and FM have distinct physiology and function.…”
Section: Discussionmentioning
confidence: 99%
“…We found that Ralstonia insidiosa (R. insidiosa), a gram-negative, aerobic, motile bacillus, is most prevalent in the BP 19 . R. insidiosa was first isolated from the sputum of cystic fibrosis patients and can be isolated from immunocompromised patients in hospitals 31,32 .…”
Controversy about whether there are microbes in the placenta and if they have any functional importance during pregnancy and for neonatal health is ongoing. Previous work has demonstrated that the basal plate (BP), comprising maternal and fetal derived cells harbors intracellular bacteria. 16S sequencing and bacterial species-specific analysis of term placentas revealed that the gram-negative bacillus Ralstonia insidiosa, native to aqueous environments and an effective biofilm promoter, comprises the most abundant species in the BP. Here, we demonstrate whether R. insidiosa cells home to a particular niche in the BP, how they may arrive there, and whether they are associated with adverse outcomes. We developed methods to detect and study cell-specific localization of R.insidiosa using ex vivo and in vitro models. Additionally, we studied potential routes of R.insidiosa entry into the placenta. We show that R. insidiosa is a bona fide resident in human placental BP. It can access trophoblast cells in culture and within basal plate tissues where it localizes to intracellular single-membrane vacuoles and can replicate.However, the presence of R. insidiosa does not cause cell death and does not induce a pro-inflammatory immune response suggesting that it is not harmful in and of itself.Finally, we show that in a pregnant mouse model, R. insidiosa traffics to the placenta via the intrauterine route but does not induce preterm labor or preterm birth. Together, our findings provide a foundation for understanding non-pathogenic placental cell-microbe interactions and the functional importance of R. insidiosa in placental health and physiology.
Previously we have shown that the Japanese macaque gut microbiome differs not by obesity per se, but rather in association with high-fat diet (HFD) feeding. This held true for both pregnant dams, as well as their 1-year-old offspring, even when weaned onto a control diet. Here we aimed to examine the stability of the gut microbiome over time and in response to maternal and postweaning HFD feeding from 6 months of age, and at 1 and 3 years of age. In both cross-sectional and longitudinal specimens, we performed analysis of the V4 hypervariable region of the 16S rRNA gene on anus swabs collected from pregnant dams and their juveniles at age 6 months to 3 years (n = 55). Extracted microbial DNA was subjected to 16S-amplicon-based metagenomic sequencing on the Illumina MiSeq platform. We initially identified 272 unique bacterial genera, and multidimensional scaling revealed samples to cluster by age and diet exposures. Dirichlet multinomial mixture modeling of microbiota abundances enabled identification of two predominant enterotypes to which samples sorted, characterized primarily by Treponema abundance, or lack thereof. Approximating the time of initial weaning (6 months), the Japanese macaque offspring microbiome underwent a significant state type transition which stabilized from 1 to 3 years of age. However, we also found the low abundance Treponema enterotype to be strongly associated with HFD exposure, be it during gestation/lactation or in the postweaning interval. Examination of taxonomic co-occurrences revealed samples within the low Treponema cluster were relatively permissive (allowing for increased interactions between microbiota) whereas samples within the high Treponema cluster were relatively exclusionary (suggesting decreased interactions amongst microbiota). Taken together, these findings suggest that Treponemes are keystone species in the developing gut microbiome of the gut, and susceptible to HFD feeding in their relative abundance. K E Y W O R D S early development, high-fat diet (HFD), macaque, microbiome Am J Primatol. 2019;81:e22980.wileyonlinelibrary.com/journal/ajp
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