Recent advances in understanding inflammatory acne: Deciphering the relationship between Cutibacterium acnes and Th17 inflammatory pathway.

Acne vulgaris is a common chronic inflammatory skin disease of the pilosebaceous units. Four factors contribute to acne: hyperseborrhea and dysseborrhea, follicular hyperkeratinisation, skin microbiome dysbiosis and local immuno-inflammation. Recent key studies have highlighted a better understanding of the important role of Cutibacterium acnes (C. acnes) in the development of acne. Three major findings in the last decade include: (1) the ability of C. acnes to self-organize in a biofilm associated with a more virulent activity, (2) the loss of the C. acnes phylotype diversity and (3) the central role of the Th17 pathway in acne inflammation. Indeed, there is a close link between C. acnes and the activation of the Th17 immuno-inflammatory pathway at the initiation of acne development. These mechanisms are directly linked to the loss of C. acnes phylotype diversity during acne, with a predominance of the pro-pathogenic phylotype IA1. This specifically contributes to the induction of the Th17-mediated immuno-inflammatory response involving skin cells, such as keratinocytes, monocytes and sebocytes. These advancements have led to new insights into the underlying mechanisms which can be harnessed to develop novel treatments and diagnostic biomarkers. A major disadvantage of traditional treatment with topical antibiotics is that they induce cutaneous dysbiosis and antimicrobial resistance. Thus, future treatments would no longer aim to 'kill' C. acnes, but to maintain the skin microbiota balance allowing for tissue homeostasis, specifically, the restoration of C. acnes phylotype diversity. Here, we provide an overview of some of the key processes involved in the pathogenesis of acne, with a focus on the prominent role of C. acnes and the Th17-inflammatory pathways involved.