Fig. 1

NLRP3 inflammasome complex, as part of innate immunity, is activated upon exposure to viruses, bacteria, fungi, but also non-organic actors. Exposure engaging innate immunity occur through sensors called Toll-like receptor (TLR) and pattern recognition receptors (PRR). Agents activating these sensors are referred to as PAMPs or MAMPs (pathogen/microbial-associated molecular patterns), DAMPs (damage-generated molecular patterns) or LAMPs (lifestyle-associated molecular patterns). Cell response to PAMPS/MAMPS is mediated through the formation of the NLRP3 inflammasome complex. Upon engagement of pathogen, the NLRP3 inflammasome complex is formed directly or through priming via NFќB. Priming induces formation of precursors of the NLRP3 inflammasome complex including NLRP3, pro-IL-1ß & pro-IL-18. Besides pathogens, particles, toxins and ATP release secondary to cell damage have the ability to activate the NLRP3 inflammasome. Activated NLRP3 inflammasome complex results in conversion of pro-caspase 1, pro-IL-1ß & pro-IL-18 to caspase1, IL-1ß and IL-18 leading to pyroptosis and inflammation