Abstract

Background and ObjectiveAcne vulgaris is a common skin disease around the world which affects the appearance of patients, as well as their physical and mental health. Cutibacterium acnes plays a vital role in the occurrence and development of acne vulgaris. Pattern recognition receptors (PRRs) are the first line of defense against external pathogens. The nucleotide oligomerization domain (NOD)-like receptor family pyrin containing 3 (NLRP3) inflammasome has recently been shown to contribute to the pathogenesis of acne vulgaris. The purpose of this review is to clarify the underlying mechanisms of NLRP3 inflammasome in the pathogenesis of acne vulgaris, and its potential as a therapeutic target for the condition.MethodsThe PubMed database was searched for relevant articles published in English between January 2003 to December 2021 using keywords “acne vulgaris”, “NLRP3 inflammasome”, and “Cutibacterium acnes”. The reference lists of retrieved articles were also reviewed to identify relevant articles.Key Content and FindingsCutibacterium acnes infection can lead to a series of inflammatory reactions and the production of inflammatory factors such as interleukin (IL)-1β. In vitro and in vivo studies demonstrated that the NLRP3 inflammasome plays essential roles in acne vulgaris. Further, innate immunity and adaptive immunity pervade the entire pathogenesis of acne vulgaris.ConclusionsThe NLRP3 inflammasome may be a potential therapeutic target for acne vulgaris. Future studies are needed to investigate the potential therapeutic effects of NLRP3 inhibitors on acne vulgaris.

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