Enteric neuroplasticity and dysmotility in inflammatory disease: Key players and possible therapeutic targets

25Citations
Citations of this article
28Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Intestinal functions, including motility and secretion, are locally controlled by enteric neural networks housed within the wall of the gut. The fidelity of these functions depends on the precision of intercellular signaling among cellular elements, including enteric neurons, epithelial cells, immune cells, and glia, all of which are vulnerable to disruptive influences during inflammatory events. This review article describes current knowledge regarding inflammation-induced neuroplasticity along key elements of enteric neural circuits, what is known about the causes of these changes, and possible therapeutic targets for protecting and/or repairing the integrity of intrinsic enteric neurotransmission. Changes that have been detected in response to inflammation include increased epithelial serotonin availability, hyperexcitability of intrinsic primary afferent neurons, facilitation of synaptic activity among enteric neurons, and attenuated purinergic neuromuscular transmission. Dysfunctional propulsive motility has been detected in models of colitis, where causes include the changes described above, and in models of multiple sclerosis and other autoimmune conditions, where autoantibodies are thought to mediate dysmotility. Other cells implicated in inflammation-induced neuroplasticity include muscularis macrophages and enteric glia. Targeted treatments that are discussed include 5-hydroxytryptamine receptor 4 agonists, cyclooxygenase inhibitors, antioxidants, B cell depletion therapy, and activation of anti-inflammatory pathways.

Cite

CITATION STYLE

APA

Spear, E. T., & Mawe, G. M. (2019). Enteric neuroplasticity and dysmotility in inflammatory disease: Key players and possible therapeutic targets. American Journal of Physiology - Gastrointestinal and Liver Physiology, 317(6), G853–G861. https://doi.org/10.1152/AJPGI.00206.2019

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free