Neuropathic Pain Phenotype Does Not Involve the NLRP3 Inflammasome and Its End Product Interleukin-1β in the Mice Spared Nerve Injury Model.
Détails
Télécharger: BIB_DEBB7BE677C8.P001.pdf (787.52 [Ko])
Etat: Public
Version: de l'auteur⸱e
Etat: Public
Version: de l'auteur⸱e
ID Serval
serval:BIB_DEBB7BE677C8
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Neuropathic Pain Phenotype Does Not Involve the NLRP3 Inflammasome and Its End Product Interleukin-1β in the Mice Spared Nerve Injury Model.
Périodique
Plos One
ISSN
1932-6203 (Electronic)
ISSN-L
1932-6203
Statut éditorial
Publié
Date de publication
2015
Peer-reviewed
Oui
Volume
10
Numéro
7
Pages
e0133707
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: epublish
Résumé
The NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome is one of the main sources of interleukin-1β (IL-1β) and is involved in several inflammatory-related pathologies. To date, its relationship with pain has not been studied in depth. The aim of our study was to elucidate the role of NLRP3 inflammasome and IL-1β production on neuropathic pain. Results showed that basal pain sensitivity is unaltered in NLRP3-/- mice as well as responses to formalin test. Spared nerve injury (SNI) surgery induced the development of mechanical allodynia and thermal hyperalgesia in a similar way in both genotypes and did not modify mRNA levels of the NLRP3 inflammasome components in the spinal cord. Intrathecal lipopolysaccharide (LPS) injection increases apoptosis-associated speck like protein (ASC), caspase-1 and IL-1β expression in both wildtype and NLRP3-/- mice. Those data suggest that NLRP3 is not involved in neuropathic pain and also that other sources of IL-1β are implicated in neuroinflammatory responses induced by LPS.
Mots-clé
Animals, Behavior, Animal, Carrier Proteins/genetics, Carrier Proteins/metabolism, Disease Models, Animal, Female, Formaldehyde/toxicity, Inflammasomes/metabolism, Interleukin-1beta/metabolism, Lipopolysaccharides/pharmacology, Male, Mice, Inbred C57BL, Mice, Knockout, Neuralgia/chemically induced, Neuralgia/metabolism, Peripheral Nerve Injuries/physiopathology
Pubmed
Web of science
Open Access
Oui
Création de la notice
29/07/2015 9:46
Dernière modification de la notice
20/08/2019 16:03