Targeting cryopyrin as a new therapeutic approach to control inflammation

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The mechanism by which inflammasome activation and following IL-1β induction in autoinflammation is not completely elucidated. We studied the role of serum amyloid A (SAA) in the regulation of IL-1β production and activation of inflammasome cascade in human rheumatoid synoviocytes. Rheumatoid synoviocytes stimulated with SAA express NLRP3 (cryopyrin) mRAN expression. MSU (modosodium urate), a ligand for NLRP3, stimulation did not induce IL-1β production in rheumatoid synoviocytes. Whereas, rheumatoid synoviocytes pretreated with low concentration (1-5μg/ml) of SAA produce IL-1β in response to MSU. These findings indicate that during systemic inflammation, SAA may promote the MSU-induced IL-1β induction through activating the NLRP3 inflammasome activation.