Enteric glial cells and their role in the intestinal epithelial barrier

Yu, Yanbo; Li, Yanqing

doi:10.3748/wjg.v20.i32.11273

Cited by 118 publications

(102 citation statements)

References 87 publications

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“…This would be indicating that ATX/LPA could exert a necessary effect during the first month of life. Recent studies have shown that LPA has stimulatory effects on fluid absorption in the intestine [18] . On the other hand, it has been suggested that ATX/LPA signaling could negatively influence adipose tissue development [19] .…”

Section: Discussionmentioning

confidence: 99%

Bioactive Components in Human Milk Along the First Month of Life: Effects of Iodine Supplementation during Pregnancy

et al. 2016

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Background/Aims: Human milk is considered the most suitable food for infants. The potential benefits of breastfeeding can be explained by the presence of different growth and neurotrophic factors in human milk. This study was designed to detect some biomarkers in human milk, which could be involved in the infant neurodevelopment and in the regulation of the maturation of neonatal intestine (brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), glial fibrillary acidic protein (GFAP), fibroblast growth factor 21 (FGF21), lysophosphatidic acid (LPA) and autotaxin (ATX)), and compare them on the basis of the consumption of iodine supplements or multivitamins. Methods: A prospective study included 37 healthy breastfeeding mothers, divided into 3 different groups: (1) 10 mothers who did not take supplements, (2) 17 mothers who took potassium iodine (KI) 200 µg/day and (3) 10 mothers who took a multivitamin supplement. Results: The concentrations of BDNF, GDNF, GFAP, FGF21, LPA and ATX in human milk were not significantly different in women who took a multivitamin or KI supplement compared with those who did not take any supplement. Conclusions: The presence of neurotrophic factors in human milk is neither modified by the consumption of supplements nor by their type.

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Section: Discussionmentioning

confidence: 99%

Bioactive Components in Human Milk Along the First Month of Life: Effects of Iodine Supplementation during Pregnancy

et al. 2016

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“…Other factors contributing to homeostasis and maintenance of the permeability of the gut mucosa include the secretion of mucous and immunoglobulin cells, while pro-inflammatory cytokines secreted by inflammatory cells cause barrier disruption [97]. Inflammatory processes are known to facilitate destruction of the enteric glial cells which then leads to the breakdown of the epithelial lining [98]. More recently both preclinical and clinical studies have demonstrated an important role of the gut microbiota in maintaining the integrity of the intestinal epithelium.…”

Section: Candidate Mechanisms Underlying Gut Microbiota Induced Obesitymentioning

confidence: 99%

Gut Microbiome and Obesity: A Plausible Explanation for Obesity

2015

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Obesity is a multifactorial disorder that results in excessive accumulation of adipose tissue. Although obesity is caused by alterations in the energy consumption/expenditure balance, the factors promoting this disequilibrium are incompletely understood. The rapid development of new technologies and analysis strategies to decode the gut microbiota composition and metabolic pathways has opened a door into the complexity of the guest-host interactions between the gut microbiota and its human host in health and in disease. Pivotal studies have demonstrated that manipulation of the gut microbiota and its metabolic pathways can affect host’s adiposity and metabolism. These observations have paved the way for further assessment of the mechanisms underlying these changes. In this review we summarize the current evidence for possible mechanisms underlying gut microbiota induced obesity. The review addresses some well-known effects of the gut microbiota on energy harvesting and changes in metabolic machinery, on metabolic and immune interactions and on possible changes in brain function and behavior. Although there is limited understanding on the symbiotic relationship between us and our gut microbiome, and how disturbances of this relationship affects our health, there is compelling evidence for an important role of the gut microbiota in the development and perpetuation of obesity.

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“…As the intestinal mucosal barrier serves as the interface between vastly diverse external and internal environments, the maintenance of homeostasis is critical to its ability to respond to noxious or pathogenic stimuli. Intestinal epithelial cells, immune cells of the lamina propria, and enteric glial cells (EGCs) regulate mucosal barrier homeostasis though complex and dynamic interactions 16,17 .…”

Section: Introductionmentioning

confidence: 99%

Bidirectional brain-gut interactions and chronic pathological changes after traumatic brain injury in mice

Elise

Smith

Desai

et al. 2017

Brain, Behavior, and Immunity

128

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Objectives Traumatic brain injury (TBI) has complex effects on the gastrointestinal tract that are associated with TBI-related morbidity and mortality. We examined changes in mucosal barrier properties and enteric glial cell response in the gut after experimental TBI in mice, as well as effects of the enteric pathogen Citrobacter rodentium (Cr) on both gut and brain after injury. Methods Moderate-level TBI was induced in C57BL/6 mice by controlled cortical impact (CCI). Mucosal barrier function was assessed by transepithelial resistance, fluorescent-labelled dextran flux, and quantification of tight junction proteins. Enteric glial cell number and activation were measured by Sox10 expression and GFAP reactivity, respectively. Separate groups of mice were challenged with Cr infection during the chronic phase of TBI, and host immune response, barrier integrity, enteric glial cell reactivity, and progression of brain injury and inflammation were assessed. Results Chronic CCI induced changes in colon morphology, including increased mucosal depth and smooth muscle thickening. At day 28 post-CCI, increased paracellular permeability and decreased claudin-1 mRNA and protein expression were observed in the absence of inflammation in the colon. Colonic glial cell GFAP and Sox10 expression were significantly increased 28 days after brain injury. Clearance of Cr and upregulation of Th1/Th17 cytokines in the colon were unaffected by CCI; however, colonic paracellular flux and enteric glial cell GFAP expression were significantly increased. Importantly, Cr infection in chronically-injured mice worsened the brain lesion injury and increased astrocyte- and microglial-mediated inflammation. Conclusion These experimental studies demonstrate chronic and bidirectional brain-gut interactions after TBI, which may negatively impact late outcomes after brain injury.

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Enteric glial cells and their role in the intestinal epithelial barrier

Cited by 118 publications

References 87 publications

Bioactive Components in Human Milk Along the First Month of Life: Effects of Iodine Supplementation during Pregnancy

Bioactive Components in Human Milk Along the First Month of Life: Effects of Iodine Supplementation during Pregnancy

Gut Microbiome and Obesity: A Plausible Explanation for Obesity

Bidirectional brain-gut interactions and chronic pathological changes after traumatic brain injury in mice

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