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−1 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.

Role of enteric glia as bridging element between gut inflammation and visceral pain consolidation during acute colitis in rats / Lucarini E.; Seguella L.; Vincenzi M.; Parisio C.; Micheli L.; Toti A.; Corpetti C.; Del Re A.; Squillace S.; Maftei D.; Lattanzi R.; Ghelardini C.; Di Cesare Mannelli L.; Esposito G.. - In: BIOMEDICINES. - ISSN 2227-9059. - ELETTRONICO. - 9:(2021), pp. 1671-1671. [10.3390/biomedicines9111671]

Role of enteric glia as bridging element between gut inflammation and visceral pain consolidation during acute colitis in rats

Lucarini E.;Parisio C.;Micheli L.;Toti A.;Ghelardini C.;Di Cesare Mannelli L.;
2021

Abstract

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−1 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.
2021
9
1671
1671
Lucarini E.; Seguella L.; Vincenzi M.; Parisio C.; Micheli L.; Toti A.; Corpetti C.; Del Re A.; Squillace S.; Maftei D.; Lattanzi R.; Ghelardini C.; D...espandi
File in questo prodotto:
File Dimensione Formato  
biomedicines-09-01671.pdf

accesso aperto

Descrizione: pdf
Tipologia: Pdf editoriale (Version of record)
Licenza: Open Access
Dimensione 6.87 MB
Formato Adobe PDF
6.87 MB Adobe PDF

I documenti in FLORE sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificatore per citare o creare un link a questa risorsa: https://hdl.handle.net/2158/1254216
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 17
  • ???jsp.display-item.citation.isi??? 16
social impact