Inflammation is an important part of a host defense response against pathogens. Inflammasomes are intracellular mediators of inflammation through the activation of the cysteine protease caspase-1 and secretion of pro-inflammatory cytokines such as interleukin-1Î² (IL-1Î²). Among various inflammasomes, the NOD-, LRR- and pyrin domain-containing 3 (NLRP3) inflammasome senses not only pathogen-derived stimuli, but also senses cellular and homeostatic stress. As a result, NLRP3-driven inflammation is broadly implicated in pathogenic infections, as well as many sterile inflammatory conditions, including cardiovascular, neurodegenerative and metabolic diseases. This thesis aimed to further our understanding on the mode and regulation of NLRP3 inflammasome activation.