The Skin Microbiome: A New Actor in Inflammatory Acne
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REVIEW ARTICLE
The Skin Microbiome: A New Actor in Inflammatory Acne Brigitte Dréno1,2 · Marie Ange Dagnelie2 · Amir Khammari1,2 · Stéphane Corvec3,4
© The Author(s) 2020
Abstract Our understanding of the role of Cutibacterium acnes in the pathophysiology of acne has recently undergone a paradigm shift: rather than C. acnes hyperproliferation, it is the loss of balance between the different C. acnes phylotypes, together with a dysbiosis of the skin microbiome, which results in acne development. The loss of diversity of C. acnes phylotypes acts as a trigger for innate immune system activation, leading to cutaneous inflammation. A predominance of C. acnes phylotype IA1 has been observed, with a more virulent profile in acne than in normal skin. Other bacteria, mainly Staphylococcus epidermis, are also implicated in acne. S. epidermidis and C. acnes interact and are critical for the regulation of skin homeostasis. Recent studies also showed that the gut microbiome is involved in acne, through interactions with the skin microbiome. As commonly used topical and systemic antibiotics induce cutaneous dysbiosis, our new understanding of acne pathophysiology has prompted a change in direction for acne treatment. In the future, the development of individualized acne therapies will allow targeting of the pathogenic strains, leaving the commensal strains intact. Such alternative treatments, involving modifications of the microbiome, will form the next generation of ‘ecobiological’ anti-inflammatory treatments.
Key Points
1 Introduction
Inflammatory acne is related to a loss of the diversity of phylotypes of Cutibacterium acnes.
Acne vulgaris (acne) is a highly prevalent inflammatory skin condition, involving an interplay of several factors. Besides increased sebum production by the sebaceous glands and follicular keratinization of the pilosebaceous ducts [1, 2], a third main actor in acne development has recently been uncovered: the microbiome and its interactions with the innate immune system. The term ‘microbiome’ refers to microorganisms (bacteria, viruses and fungi) and their environment. Further understanding of the role of the skin microbiome in acne development has been gained by characterizing the skin bacteria, with equal levels of diversity being obtained regardless of whether the sampling method retrieved bacteria located at the skin surface (swabbing) or in the follicle (cyanoacrylate skin surface stripping) [3]. The skin microbiome is divided into ‘normal’ commensal skin microbes, which live in homeostasis with the host and form the resident microbiome, and pathogen microbes from the environment, which temporarily live on the skin and form the transient microbiome [4]. In acne, the resident microbiome includes Cutibacterium acnes (formerly called Propionibacterium acnes) and Staphylococcus epidermidis, whereas the transient microbiome includes Staphylococcus aureus [5]. A microbial imbalance or ‘dysbiosis’, compared with the normal distribution in healthy tissues, has been
C. acnes and Staphylococcu
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