Abstract
The NLRP3 inflammasome is a vital component of the innate immune system that mediates caspase-1 activation and secretion of the proinflammatory cytokines, namely interleukins (IL-1/IL-18), in retort to microbial infection such as periodontal pathogens. Secretion of IL-1β is a major component of periodontal tissue inflammation and a crucial cause of periodontal disease. The conversion of pro-IL-1β into its biologically active form is controlled by inflammasomes such as NLRP3. Nevertheless, uncontrolled NLRP3 activation may cause several inflammatory disorders such as Alzheimer’s disease, periodontitis, diabetes, and atherosclerosis. NLRP3 activation may be caused due to various stimuli, leading to multiple molecular and cellular events. Drugs targeting the various steps in these events may provide a solution to the aberrant NLRP3 activation. In this review, we have investigated the various mechanisms of NLLRP3 activation and the various drugs which have exhibited its inhibition.
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