Intrauterine Microbiota: Missing, or the Missing Link?

Chen, Helen J.; Gur, Tamar L.

doi:10.1016/j.tins.2019.03.008

Cited by 63 publications

(43 citation statements)

References 90 publications

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“…Furthermore, using a number of microbiological and molecular methods, researchers could not identify a microbiota in human placentas delivered at term from women who underwent caesarean delivery . Finally, recently published reviews have concluded that there is no compelling evidence to date for the existence of a universal mammalian placental or fetal microbiota …”

Section: Introductionmentioning

confidence: 99%

Deep microbial analysis of multiple placentas shows no evidence for a placental microbiome

Kuperman

Zimmerman

Hamadia

et al. 2019

BJOG

106

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Objectives To resolve the controversy regarding the presence of a microbiota in the placenta.Design Classical and molecular microbiological study.Setting All samples were collected during caesarean section.Population A total of 28 human placentas and six murine placentas.Methods All 28 human placentas were checked for 16S rRNA gene amplification products. Three locations from four selected human placentas and three 'environmental controls' for each placenta were placed in seven culture media. The four selected human placentas were further analysed using Gram stain, immunohistochemistry for bacteria, electron microscopy, and TaqMan RT-qPCR. Six placentas from three SPF mice were cut into four pieces each, and further analysed for 16S rRNA gene amplification.Main outcome measures Microbiological and molecular evidence of bacteria.Results None of the placental cultures used for the full analysis, or their environmental cultures, was positive for bacterial growth. None of the other methods showed any evidence of bacteria. Immunohistochemistry showed negligible bacterial counts. None of the murine placentas showed evidence of 16S rRNA gene amplification.Conclusions Our results support that the fetal environment in the womb is sterile. Based on the immunohistochemistry and the limit of detection of the other methods used, if a placental microbiome exists, it is of extreme low biomass, and thus its effect on clinical phenotypes is probably minor, if it exists at all.Tweetable abstract Using several microbiological and molecular methods in parallel, we found no compelling evidence of bacteria in human and mouse placentas.

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Section: Introductionmentioning

confidence: 99%

Deep microbial analysis of multiple placentas shows no evidence for a placental microbiome

Kuperman

Zimmerman

Hamadia

et al. 2019

BJOG

106

View full text Add to dashboard Cite

show abstract

“…While there is a plethora of data demonstrating that gestational stressors affect placenta and fetal development (Brunton & Russell, 2011;Chen & Gur, 2019;Monk et al, 2012;St. Pierre et al, 2018), a stronger emphasis on identifying interventions to promote maternal/offspring protection from adverse experiences is needed (Kentner et al, 2019b;Shonkoff et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Environmental influences on placental programming and offspring outcomes following maternal immune activation

Estevez

Rondón-Ortiz

Nguyen

et al. 2019

Preprint

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Adverse experiences during pregnancy induce placental programming, affecting the fetus and its developmental trajectory. However, the influence of 'positive' maternal experiences on the placenta and fetus remain unclear. In animal models of early life stress, environmental enrichment (EE) has ameliorated and even prevented associated impairments in brain and behavior. Here, using a maternal immune activation (MIA) model in rats, we test whether EE attenuates maternal, placental and/or fetal responses to an inflammatory challenge, thereby offering a mechanism by which fetal programming may be prevented. Moreover, we evaluate life-long EE exposure on offspring development and examine a constellation of genes and epigenetic writers that may protect against MIA challenges. In our model, maternal plasma corticosterone and interleukin-1β were elevated 3 h after MIA, validating the maternal inflammatory response. Evidence for developmental programming was demonstrated by a simultaneous decrease in the placental enzymes Hsd11b2 and Hsd11b2/Hsd11b1, suggesting disturbances in glucocorticoid metabolism. Reductions of Hsd11b2 in response to challenge is thought to result in excess glucocorticoid exposure to the fetus and altered glucocorticoid receptor expression, increasing susceptibility to behavioral impairments later in life. The placental, but not maternal, glucocorticoid implications of MIA were attenuated by EE. There were also sustained changes in epigenetic writers in both placenta and fetal brain as a consequence of environmental experience and sex. Following MIA, both male and female juvenile animals were impaired in social discrimination ability. Life-long EE mitigated these impairments, in addition to the sex specific MIA associated disruptions in central Fkbp5 and Oprm1. These data provide the first evidence that EE protects placental functioning during stressor exposure, underscoring the importance of addressing maternal health and well-being throughout pregnancy. Future work must evaluate critical periods of EE use to determine if postnatal EE experience is necessary, or if prenatal exposure alone is sufficient to confer protection.

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“…Low levels associated with decreased alveolarization and susceptibility to injury [2] amnion is now challenged by the emergence of intrauterine microbiota influencing fetal programming and development [24] and its relation to premature birth and neonatal respiratory diseases [25,26]. Premature birth causes an interruption of lung development and maturation, and at the same time exposes the neonate to profound alterations of these systems.…”

Section: Vitaminsmentioning

confidence: 99%

Nutrients and Microbiota in Lung Diseases of Prematurity: The Placenta-Gut-Lung Triangle

et al. 2020

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Cardiorespiratory function is not only the foremost determinant of life after premature birth, but also a major factor of long-term outcomes. However, the path from placental disconnection to nutritional autonomy is enduring and challenging for the preterm infant and, at each step, will have profound influences on respiratory physiology and disease. Fluid and energy intake, specific nutrients such as amino-acids, lipids and vitamins, and their ways of administration —parenteral or enteral—have direct implications on lung tissue composition and cellular functions, thus affect lung development and homeostasis and contributing to acute and chronic respiratory disorders. In addition, metabolomic signatures have recently emerged as biomarkers of bronchopulmonary dysplasia and other neonatal diseases, suggesting a profound implication of specific metabolites such as amino-acids, acylcarnitine and fatty acids in lung injury and repair, inflammation and immune modulation. Recent advances have highlighted the profound influence of the microbiome on many short- and long-term outcomes in the preterm infant. Lung and intestinal microbiomes are deeply intricated, and nutrition plays a prominent role in their establishment and regulation. There is an emerging evidence that human milk prevents bronchopulmonary dysplasia in premature infants, potentially through microbiome composition and/or inflammation modulation. Restoring antibiotic therapy-mediated microbiome disruption is another potentially beneficial action of human milk, which can be in part emulated by pre- and probiotics and supplements. This review will explore the many facets of the gut-lung axis and its pathophysiology in acute and chronic respiratory disorders of the prematurely born infant, and explore established and innovative nutritional approaches for prevention and treatment.

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Intrauterine Microbiota: Missing, or the Missing Link?

Cited by 63 publications

References 90 publications

Deep microbial analysis of multiple placentas shows no evidence for a placental microbiome

Deep microbial analysis of multiple placentas shows no evidence for a placental microbiome

Environmental influences on placental programming and offspring outcomes following maternal immune activation

Nutrients and Microbiota in Lung Diseases of Prematurity: The Placenta-Gut-Lung Triangle

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