Colitis-induced neuroplasticity disrupts motility in the inflamed and post-inflamed colon

Mawe, Gary M.

doi:10.1172/jci76306

Cited by 81 publications

(71 citation statements)

References 53 publications

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“…Transmitters that neurons secrete can positively (e.g., tachykinins/NK 1 receptors) or negatively (e.g., acetylcholine/α7 nicotinic receptors) affect the severity of inflammatory responses of the bowel, and thus neurons may not merely be passive bystanders in intestinal inflammation and IBD [10]. Certainly, the activity of neurons during inflammation has profound consequences for gastrointestinal (GI) secretion and motility [24]. …”

Section: Enteric Neuronal and Glial Regulation Of Immunitymentioning

confidence: 99%

Section: Changes In the Ens During Intestinal Inflammationmentioning

confidence: 99%

“…Inflammation also causes multiple changes in the intrinsic motor circuits of the intestine, including neuronal hyperexcitability, increased synaptic facilitation, and decreased descending inhibitory neuromuscular transmission that appears to be related to an attenuation of purinergic transmission [24, 40–46]. These changes are associated with a resultant loss of myenteric neurons_and can ultimately lead to long-lasting disruptions in colonic motor activity [24,47]. There are also data to suggest, however, that inflammation-induced neuroplasticity can increase the number of enteric neurons [48] and contribute to disrupted motility or, conversely, that a pre-existing excess of enteric neurons may actually predispose individuals to intestinal inflammatory disease [10].…”

Section: Changes In the Ens During Intestinal Inflammationmentioning

confidence: 99%

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Enteric Neuronal Regulation of Intestinal Inflammation

Margolis

Gershon

2016

Trends in Neurosciences

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Recent research has highlighted the importance of the two-way interaction between the nervous and immune systems. This interaction is particularly important in the bowel because of the unique properties of this organ. The lumen of the gut is lined by a very large but remarkably thin surface that separates the body from the enteric microbiome. Immune defenses against microbial invasion are thus well developed, and neuroimmune interactions are important in regulating and integrating these defenses. Important concepts in the phylogeny of neuroimmunity, enteric neuronal and glial regulation of immunity, changes that occur in the enteric nervous system during inflammation, the fundamental role of serotonin (5-HT) in enteric neuroimmune mechanisms, and future perspectives are reviewed.

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Section: Enteric Neuronal and Glial Regulation Of Immunitymentioning

confidence: 99%

Section: Changes In the Ens During Intestinal Inflammationmentioning

confidence: 99%

Section: Changes In the Ens During Intestinal Inflammationmentioning

confidence: 99%

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Enteric Neuronal Regulation of Intestinal Inflammation

Margolis

Gershon

2016

Trends in Neurosciences

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“…153 Inflammatory-induced neuroplasticity change can persist long after the inflammation subsides. 154 It should be noted that non-immune cells could also contribute signals to the process of sensitization. Enteric glial cells and smooth muscle cells produce GDNF and NGF, which in turn, promote neuropeptide Y and CGRP release from enteric neurons.…”

Section: Irritable Bowel Syndromementioning

confidence: 99%

Stem Cells in the Intestine: Possible Roles in Pathogenesis of Irritable Bowel Syndrome

Ratanasirintrawoot

Israsena

2016

J Neurogastroenterol Motil

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Irritable bowel syndrome is one of the most common functional gastrointestinal (GI) disorders that significantly impair quality of life in patients. Current available treatments are still not effective and the pathophysiology of this condition remains unclearly defined. Recently, research on intestinal stem cells has greatly advanced our understanding of various GI disorders. Alterations in conserved stem cell regulatory pathways such as Notch, Wnt, and bone morphogenic protein/TGF -β have been well documented in diseases such as inflammatory bowel diseases and cancer. Interaction between intestinal stem cells and various signals from their environment is important for the control of stem cell self-renewal, regulation of number and function of specific intestinal cell types, and maintenance of the mucosal barrier. Besides their roles in stem cell regulation, these signals are also known to have potent effects on immune cells, enteric nervous system and secretory cells in the gut, and may be responsible for various aspects of pathogenesis of functional GI disorders, including visceral hypersensitivity, altered gut motility and low grade gut inflammation. In this article, we briefly summarize the components of these signaling pathways, how they can be modified by extrinsic factors and novel treatments, and provide evidenced support of their roles in the inflammation processes. Furthermore, we propose how changes in these signals may contribute to the symptom development and pathogenesis of irritable bowel syndrome.

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“…Enteroendocrine cells are in direct contact with the gut lumen and express molecular receptors specifically activated by bacterial ligands (8). If the integrity of the epithelial barrier is compromised by infection, the function of the neural circuitry is affected, as discussed by Mawe (9).…”

mentioning

confidence: 99%