Role of Enteric Glia as Bridging Element between Gut Inflammation and Visceral Pain Consolidation during Acute Colitis in Rats
Acute inflammation is particularly relevant in the pathogenesis of visceral hypersensitivity associated with inflammatory bowel diseases. Glia within the enteric nervous system, as well as within the central nervous system, contributes to neuroplasticity during inflammation, but whether enteric glia...
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oai:doaj.org-article:c41ee61c78ce4f869de220d6a4220f7c2021-11-25T16:50:36ZRole of Enteric Glia as Bridging Element between Gut Inflammation and Visceral Pain Consolidation during Acute Colitis in Rats10.3390/biomedicines91116712227-9059https://doaj.org/article/c41ee61c78ce4f869de220d6a4220f7c2021-11-01T00:00:00Zhttps://www.mdpi.com/2227-9059/9/11/1671https://doaj.org/toc/2227-9059Acute inflammation is particularly relevant in the pathogenesis of visceral hypersensitivity associated with inflammatory bowel diseases. Glia within the enteric nervous system, as well as within the central nervous system, contributes to neuroplasticity during inflammation, but whether enteric glia has the potential to modify visceral sensitivity following colitis is still unknown. This work aimed to investigate the occurrence of changes in the neuron–glial networks controlling visceral perception along the gut–brain axis during colitis, and to assess the effects of peripheral glial manipulation. Enteric glia activity was altered by the poison fluorocitrate (FC; 10 µmol kg<sup>−1</sup> i.p.) before inducing colitis in animals (2,4-dinitrobenzenesulfonic acid, DNBS; 30 mg in 0.25 mL EtOH 50%), and visceral sensitivity, colon damage, and glia activation along the pain pathway were studied. FC injection significantly reduced the visceral hyperalgesia, the histological damage, and the immune activation caused by DNBS. Intestinal inflammation is associated with a parallel overexpression of TRPV1 and S100β along the gut–brain axis (colonic myenteric plexuses, dorsal root ganglion, and periaqueductal grey area). This effect was prevented by FC. Peripheral glia activity modulation emerges as a promising strategy for counteracting visceral pain induced by colitis.Elena LucariniLuisa SeguellaMartina VincenziCarmen ParisioLaura MicheliAlessandra TotiChiara CorpettiAlessandro Del ReSilvia SquillaceDaniela MafteiRoberta LattanziCarla GhelardiniLorenzo Di Cesare MannelliGiuseppe EspositoMDPI AGarticleinflammatory bowel diseaseS100βTRPV1 receptorsenteric gliaastrocytesmyenteric plexusBiology (General)QH301-705.5ENBiomedicines, Vol 9, Iss 1671, p 1671 (2021) |
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inflammatory bowel disease S100β TRPV1 receptors enteric glia astrocytes myenteric plexus Biology (General) QH301-705.5 |
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inflammatory bowel disease S100β TRPV1 receptors enteric glia astrocytes myenteric plexus Biology (General) QH301-705.5 Elena Lucarini Luisa Seguella Martina Vincenzi Carmen Parisio Laura Micheli Alessandra Toti Chiara Corpetti Alessandro Del Re Silvia Squillace Daniela Maftei Roberta Lattanzi Carla Ghelardini Lorenzo Di Cesare Mannelli Giuseppe Esposito Role of Enteric Glia as Bridging Element between Gut Inflammation and Visceral Pain Consolidation during Acute Colitis in Rats |
description |
Acute inflammation is particularly relevant in the pathogenesis of visceral hypersensitivity associated with inflammatory bowel diseases. Glia within the enteric nervous system, as well as within the central nervous system, contributes to neuroplasticity during inflammation, but whether enteric glia has the potential to modify visceral sensitivity following colitis is still unknown. This work aimed to investigate the occurrence of changes in the neuron–glial networks controlling visceral perception along the gut–brain axis during colitis, and to assess the effects of peripheral glial manipulation. Enteric glia activity was altered by the poison fluorocitrate (FC; 10 µmol kg<sup>−1</sup> i.p.) before inducing colitis in animals (2,4-dinitrobenzenesulfonic acid, DNBS; 30 mg in 0.25 mL EtOH 50%), and visceral sensitivity, colon damage, and glia activation along the pain pathway were studied. FC injection significantly reduced the visceral hyperalgesia, the histological damage, and the immune activation caused by DNBS. Intestinal inflammation is associated with a parallel overexpression of TRPV1 and S100β along the gut–brain axis (colonic myenteric plexuses, dorsal root ganglion, and periaqueductal grey area). This effect was prevented by FC. Peripheral glia activity modulation emerges as a promising strategy for counteracting visceral pain induced by colitis. |
format |
article |
author |
Elena Lucarini Luisa Seguella Martina Vincenzi Carmen Parisio Laura Micheli Alessandra Toti Chiara Corpetti Alessandro Del Re Silvia Squillace Daniela Maftei Roberta Lattanzi Carla Ghelardini Lorenzo Di Cesare Mannelli Giuseppe Esposito |
author_facet |
Elena Lucarini Luisa Seguella Martina Vincenzi Carmen Parisio Laura Micheli Alessandra Toti Chiara Corpetti Alessandro Del Re Silvia Squillace Daniela Maftei Roberta Lattanzi Carla Ghelardini Lorenzo Di Cesare Mannelli Giuseppe Esposito |
author_sort |
Elena Lucarini |
title |
Role of Enteric Glia as Bridging Element between Gut Inflammation and Visceral Pain Consolidation during Acute Colitis in Rats |
title_short |
Role of Enteric Glia as Bridging Element between Gut Inflammation and Visceral Pain Consolidation during Acute Colitis in Rats |
title_full |
Role of Enteric Glia as Bridging Element between Gut Inflammation and Visceral Pain Consolidation during Acute Colitis in Rats |
title_fullStr |
Role of Enteric Glia as Bridging Element between Gut Inflammation and Visceral Pain Consolidation during Acute Colitis in Rats |
title_full_unstemmed |
Role of Enteric Glia as Bridging Element between Gut Inflammation and Visceral Pain Consolidation during Acute Colitis in Rats |
title_sort |
role of enteric glia as bridging element between gut inflammation and visceral pain consolidation during acute colitis in rats |
publisher |
MDPI AG |
publishDate |
2021 |
url |
https://doaj.org/article/c41ee61c78ce4f869de220d6a4220f7c |
work_keys_str_mv |
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