Preventing NLRP3 inflammasome activation: Therapeutic atrategy and challenges in atopic dermatitis

Atopic dermatitis (AD) is a prevalent inflammatory skin disorder characterized by its chronic, persistent, and recurrent nature. The pathophysiology of this condition is complex, involving various factors including cell-mediated immune responses, compromised skin barrier function, and alterations in hypersensitivity reactions. These components synergistically contribute to the perpetuation of the bothersome "itch-scratch-itch" cycle. Recent research has highlighted the significant role of the NLRP3 inflammasome in the development of AD and other inflammatory conditions. Current research indicates that the NLRP3 inflammasome plays a pivotal role in both the acute and chronic phases of AD by modulating the Th2/Th1 immune deviation. Moreover, the pharmacological suppression of NLRP3 has shown promising results in mitigating the pathological aspects of AD. This review outlines potential drug development strategies that target the NLRP3 inflammasome as a therapeutic approach for AD and the challenges faced in this endeavor.