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3 results on '"Ratcliffe, Elyanne"'

1. Who's talking to whom: microbiome-enteric nervous system interactions in early life.

Author

Ganz J and Ratcliffe EM

Subjects
Humans, Mice, Animals, Zebrafish, Gastrointestinal Tract, Enteric Nervous System physiology, Microbiota, Gastrointestinal Microbiome physiology
Abstract

The enteric nervous system (ENS) is the intrinsic nervous system of the gastrointestinal tract (GI) and regulates important GI functions, including motility, nutrient uptake, and immune response. The development of the ENS begins during early organogenesis and continues to develop once feeding begins, with ongoing plasticity into adulthood. There has been increasing recognition that the intestinal microbiota and ENS interact during critical periods, with implications for normal development and potential disease pathogenesis. In this review, we focus on insights from mouse and zebrafish model systems to compare and contrast how each model can serve in elucidating the bidirectional communication between the ENS and the microbiome. At the end of this review, we further outline implications for human disease and highlight research innovations that can lead the field forward.

Published
2023
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2. Of the bugs that shape us: maternal obesity, the gut microbiome, and long-term disease risk.

Author

Gohir W, Ratcliffe EM, and Sloboda DM

Subjects
Female, Gastrointestinal Tract growth & development, Humans, Obesity microbiology, Pregnancy, Prenatal Exposure Delayed Effects immunology, Gastrointestinal Tract microbiology, Maternal Nutritional Physiological Phenomena, Maternal-Fetal Exchange, Microbiota, Obesity complications, Prenatal Exposure Delayed Effects microbiology
Abstract

Chronic disease risk is inextricably linked to our early-life environment, where maternal, fetal, and childhood factors predict disease risk later in life. Currently, maternal obesity is a key predictor of childhood obesity and metabolic complications in adulthood. Although the mechanisms are unclear, new and emerging evidence points to our microbiome, where the bacterial composition of the gut modulates the weight gain and altered metabolism that drives obesity. Over the course of pregnancy, maternal bacterial load increases, and gut bacterial diversity changes and is influenced by pre-pregnancy- and pregnancy-related obesity. Alterations in the bacterial composition of the mother have been shown to affect the development and function of the gastrointestinal tract of her offspring. How these microbial shifts influence the maternal-fetal-infant relationship is a topic of hot debate. This paper will review the evidence linking nutrition, maternal obesity, the maternal gut microbiome, and fetal gut development, bringing together clinical observations in humans and experimental data from targeted animal models.

Published
2015
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3. Influence of intestinal microbiota on the postnatal development of enterochromaffin cells and the enteric nervous system

Author

Mungovan, Kal A., Ratcliffe, Elyanne, Murphy, Kathryn, Jane Foster, Waliul Khan, and Neuroscience

Subjects
enteric nervous system, ENS, microbiota, Digestive, Oral, and Skin Physiology, enterochromaffin cells, dopamine, serotonin
Abstract

At birth the gastrointestinal (GI) tract is rapidly colonized by microbial organisms which exhibit considerable fluctuations in composition across the first two years of life. During this period, the enteric nervous system (ENS) continues to undergo significant structural and functional changes. In the present study, we investigated whether exposure to intestinal microbiota influences the postnatal development of the ENS. We focused our investigations on dopaminergic neurons as they are among the latest populations of neurons to differentiate during enteric development. The myenteric plexus of specific pathogen-free (SPF) and germ-free (GF) mice were examined in whole-mount preparations of the small and large intestine at three time-points: postnatal day 1 (P1), P7, and P28. The density of dopaminergic neurons did not differ significantly between SPF and GF mice in any region of the intestine examined at P1. However, at P7, GF mice had significantly fewer myenteric dopaminergic neurons in the ileum than did SPF mice, and this difference was maintained at P28. The proportion of enteric dopaminergic neurons has been shown to be dependent upon the availability of serotonin. In the GI tract, serotonin can be of neuronal or enterochromaffin (EC) cell origin. We therefore tested the hypothesis that reductions in myenteric dopaminergic neuron densities in the ileum of GF mice were secondary to changes in enteric serotonergic neuron densities or EC cell frequencies. Neither serotonergic neurons nor EC cell numbers were affected by GF status during the postnatal period. The reduction in dopaminergic neurons seen in GF mice must therefore be attributable to a mechanism that has yet to be determined. These findings are consistent with the notion that enteric microbiota can influence the development of late-born neuronal populations. The reduced proportion of dopaminergic neurons in the ileum of GF mice at P7 and P28 may contribute to the previously described altered motility patterns in postnatal GF mice. Master of Science (MSc)

Published
2013

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