Chronic activation of inflammasome signaling complexes and enhancement of behavioral abnormalities

Introduction Inflammasomes are cytosolic multi-component signaling platforms critical to the innate immune response infectious diseases and dysregulation of their activation can lead development neurodegeneration cancer. Objectives We aim through this review ass a possible interplay between inflammasome activation, chronic inflammatory disease enhancement behavioral abnormalities. Methods comprehensively scientific literature using Pubmed database other search such as Google scholar assess role actors complexes establish potential association Results Our bibliographic revealed that is associated with onset progression several autoinflammatory autoimmune diseases, including cryopyrin-associated periodic fever syndrome, familial Mediterranean fever, rheumatoid arthritis, systemic lupus erythematosus. These multimeric form in molecular patterns unique pathogens cellular damage, triggering cascade downstream responses, induction pyroptotic cell death release proinflammatory cytokines. Some inflammasomes directly recognize these patterns, while others indirectly sense changes homeostatic environment cell. Moreover, although being normal part skin flora, yeasts genus Malassezia pityriasis versicolor (tinea versicolor), atopic eczema, psoriasis, folliculitis onychomycoses. In context tolerating fungi during colonization eliciting, complexes, has been identified an integral antifungal host defense. While mainly NLRP3 one, was shown be pivotal for immunity against pathogenic candida albicans, fungal remains imprecise. Even though, many observations suggest simultaneous NLRP3, NLRC4 AIM2 may play important role. Conclusions Whereas, by tied metabolic syndromes, neurodegenerative cancer progression, invasion Malassezia, vigorous eliminate invading pathogens, disruption sensors genotoxic stress, abnormalities new field researches. Disclosure Interest None Declared