• What do Enteric Glial Cells Do?

What do Enteric Glial Cells Do?

Enteric glial cells (EGCs) are important regulators of intestinal homeostasis—disruption of their activities can lead to digestive and extradigestive diseases.

Michael Neunlist et al describe the neuroprotective effects of EGCs, how they regulate expression of neuromediators, and their roles as neuronal and glial progenitors in the enteric nervous system in a review article in the December issue of Gastroenterology.

The enteric nervous system (ENS) is second largest nervous system of the human body, regulating almost all gut functions, including motility, nutrient absorption, immune responses, and blood flow.

EGCs are important members of the ENS, with morphological and functional similarities to astrocytes of the central nervous system. EGCs have been shown to promote neuron survival and reduce oxidative stress-induced cell death.

Loss of EGC function can affect gastrointestinal motility, leading to reduced gastric emptying, intestinal transit, and colonic transit. EGCs also help maintain the integrity of the intestinal epithelial barrier.

EGCs have neuroprotective effects and regulate neuromediator expression and neuron renewal via different mediators (A). EGCs also regulate intestinal epithelial barrier homeostasis via gliomediators. Under inflammatory conditions or following  or bacterial stimulation (B), enteric gliosis (similar to astrogliosis in the brain) can occur. This could lead to development of intestinal inflammation, or protection or repair of IEB/neuronal lesions induced by these processes. EGC death (induced by specific virus or pathogens) or altered enteric gliosis could contribute to neuronal degeneration or barrier dysfunctions observed in some chronic intestinal or extraintestinal diseases (C).

EGCs have neuroprotective effects and regulate neuromediator expression and neuron renewal via different mediators (A). EGCs also regulate intestinal epithelial barrier homeostasis via gliomediators. Under inflammatory conditions or following or bacterial stimulation (B), enteric gliosis (similar to astrogliosis in the brain) can occur. This could lead to development of intestinal inflammation, or protection or repair of IEB/neuronal lesions induced by these processes. EGC death (induced by specific virus or pathogens) or altered enteric gliosis could contribute to neuronal degeneration or barrier dysfunctions observed in some chronic intestinal or extraintestinal diseases (C).

ECGs can also contribute to inflammatory and other disease processes by secreting chemokines and cytokines. They might therefore be involved in development of digestive diseases such as post-operative ileus and inflammatory bowel diseases, as well as extra-digestive diseases, such as Parkinson’s disease or obesity.

Neunlist et al explain how tools such as lineage tracing and glial-specific gene targeting experiments, along with new in vivo imaging methods, are rapidly increasing in our understating of the role of EGCs in the control of gut functions and cell biology. EGC features might some day be used as biomarkers of disease progression, severity, or response to treatment.

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