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 IA
1
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.