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Inflammasomes, the cardinal pathology mediators are activated by pathogens, allergens and mutagens: A critical review with focus on NLRP3.

Inflammation is a pivotal defense system of body. Unfortunately, when homeostasis falters, the same inflammatory mechanism acts as a double-edged sword, and turns offensive, paving the path for a broad array of pathologies. A multi-protein complex termed as inflammasome perceives the PAMPs (pathogen associated molecular patterns) and DAMPs (danger associated molecular patterns), executing immune responses. This activation predominantly encompasses the elaboration of effector cytokines IL-1β, IL-18, and the cysteine proteases (caspase 1 and 11). Extensive study on an inflammasome NLRP3 has revealed its role in the onset and progression of pathogenic, metabolic, autoimmune, neural, and geriatric diseases. In this regard, this inflammasome's immune activation mechanisms and inhibition strategies have been discussed. Through this rigorous literature analysis, the superficial diversity between pathogens/allergens and mutagens, and NLRP3 activity towards them has been emphasized. Though there is a scope for inhibition of aberrant inflammasomes, including that of NLRP3, given their complexity and unpredictability, prevention of their activation by lifestyle correction has been suggested.

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