Emerging roles for enteric glia in gastrointestinal disorders

Sharkey, Keith A.

doi:10.1172/jci76303

Cited by 161 publications

(141 citation statements)

References 88 publications

Supporting

Mentioning

131

Contrasting

Unclassified

Order By: Relevance

“…The clinical pathological intestinal characteristics of an hypoxic-ischemic neonate may that disruption of these cells altered the neurochemical phenotype of enteric neurons, reduced transmission to muscle and delayed gastrointestinal transit (65,66). In this study, global HI-induced distortion of enteric glial cells in the ganglia of the myenteric plexus in a similar pattern found in animal models of HI-induced intestinal injury (67) and in neonates with NEC (31).…”

Section: Resultssupporting

confidence: 68%

Global Hypoxia-Ischemia Induced Inflammation and Structural Changes in the Preterm Ovine Gut Which Were Not Ameliorated by Mesenchymal Stem Cell Treatment

Nikiforou

Willburger

Jong

et al. 2016

Mol Med

View full text Add to dashboard Cite

Perinatal asphyxia, a condition of impaired gas exchange during birth, leads to fetal hypoxia-ischemia (HI) and is associated with postnatal adverse outcomes including intestinal dysmotility and necrotizing enterocolitis. Evidence from adult animal models of transient, locally induced intestinal HI has shown that inflammation is essential in HI-induced injury of the gut. Importantly, mesenchymal stem cell (MSC) treatment prevented this HI-induced intestinal damage. We therefore assessed whether fetal global HI induced inflammation, injury and developmental changes in the gut and whether intravenous MSC administration ameliorated these HI-induced adverse intestinal effects. In a preclinical ovine model, fetuses were subjected to umbilical cord occlusion (UCO), with or without MSC treatment, and euthanized 7 d after UCO. Global HI increased the number of myeloperoxidase-positive cells in the mucosa, upregulated messenger RNA (mRNA) levels of interleukin (IL)-1b and IL-17 in gut tissue and caused T-cell invasion in the intestinal muscle layer. Intestinal inflammation following global HI was associated with increased Ki67 + cells in the muscularis and subsequent muscle hyperplasia. Global HI caused distortion of glial fibrillary acidic protein immunoreactivity in the enteric glial cells and increased synaptophysin and serotonin expression in the myenteric ganglia. Intravenous MSC treatment did not ameliorate these HI-induced adverse intestinal events. Global HI resulted in intestinal inflammation and enteric nervous system abnormalities, which are clinically associated with postnatal complications, including feeding intolerance, altered gastrointestinal transit and necrotizing enterocolitis. The intestinal histopathological changes were not prevented by intravenous MSC treatment directly after HI, indicating that alternative treatment regimens for cell-based therapies should be explored. online address: http://www.molmed.org

show abstract

Section: Resultssupporting

confidence: 68%

Global Hypoxia-Ischemia Induced Inflammation and Structural Changes in the Preterm Ovine Gut Which Were Not Ameliorated by Mesenchymal Stem Cell Treatment

Nikiforou

Willburger

Jong

et al. 2016

Mol Med

View full text Add to dashboard Cite

show abstract

“…Glial cells are closely associated with enteric neurons, in that they provide support for neuronal function (54). Recently, it has been demonstrated that enteric glia may be adversely affected in PD (55).…”

Section: Discussionmentioning

confidence: 99%

α-Synuclein in gut endocrine cells and its implications for Parkinson’s disease

Chandra

Hiniker²,

Kuo³

et al. 2017

JCI Insight

184

176

View full text Add to dashboard Cite

“…Of interest, some of these abnormalities seem to be related to a dysfunction of the enteric glial cells (EGC) [19][20][21], a key cell population involved in several gastrointestinal conditions, especially those characterized by abnormal motility and inflammation [22][23][24][25][26]. The important role of EGC, besides mechanical/trophic support function [27], involves regulation of gut barrier functions [28], maintenance and modulation of enteric neurotransmission [29], enteric neurons homeostasis [30], and acting as mediators of interactions between the enteric nervous system and the immune system [25,31].…”

Section: Pathophysiologic Aspectsmentioning

confidence: 99%

Clostridium difficile-related postinfectious IBS: a case of enteroglial microbiological stalking and/or the solution of a conundrum?

Bassotti

Macchioni

Corazzi

et al. 2017

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Post-infectious irritable bowel syndrome is a well-defined pathological entity that develops in about one-third of subjects after an acute infection (bacterial, viral) or parasitic infestation. Only recently it has been documented that an high incidence of post-infectious irritable bowel syndrome occurs after Clostridium difficile infection. However, until now it is not known why in some patients recovered from this infection the gastrointestinal disturbances persist for months or years. Based on our in vitro studies on enteric glial cells exposed to the effects of C. difficile toxin B, we hypothesize that persistence of symptoms up to the development of irritable bowel syndrome might be due to a disturbance/impairment of the correct functions of the enteroglial intestinal network.

show abstract

Emerging roles for enteric glia in gastrointestinal disorders

Cited by 161 publications

References 88 publications

Global Hypoxia-Ischemia Induced Inflammation and Structural Changes in the Preterm Ovine Gut Which Were Not Ameliorated by Mesenchymal Stem Cell Treatment

Global Hypoxia-Ischemia Induced Inflammation and Structural Changes in the Preterm Ovine Gut Which Were Not Ameliorated by Mesenchymal Stem Cell Treatment

α-Synuclein in gut endocrine cells and its implications for Parkinson’s disease

Clostridium difficile-related postinfectious IBS: a case of enteroglial microbiological stalking and/or the solution of a conundrum?

Contact Info

Product

Resources

About