Article: article from journal or magazin.
Neuropathic Pain Phenotype Does Not Involve the NLRP3 Inflammasome and Its End Product Interleukin-1β in the Mice Spared Nerve Injury Model.
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: epublish
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.
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
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