INTRODUCTION
Acne is a chronic inflammatory disease of the pilosebaceous unit with multifactorial etiology and a significant mental health component.1-3 Acne is the most common dermatological condition, affecting more than 85% of the population starting at adolescence.4,5 Although acne prevalence decreases with age, disease burden is high amongst young adults. The reported incidence of adult acne amongst women is as high as 54%.6
A key factor in acne pathogenesis is the skin bacterium Cutibacterium acnes (formerly Propionibacterium acnes), and it has been associated with acne for over a century.7 Acne pathogenesis is driven by follicular hyperkeratinization, excess sebum production, overgrowth of Cutibacterium acnes (C acnes), and inflammation.8 The spatio-temporal occurrence of C acnes on the skin coincides with the emergence of acne, as it is not a significant member of the skin microbiome of pre-pubescent children, and high levels of colonization occur on the face, upper neck, and back.9 C acnes can elicit inflammation via a number of pathways, including the expression of lipases, proteases, TLR agonists, and stimulating sebum production.10-12 C acnes levels vary by individual, and high levels of C acnes do not always correlate with acne incidence; different strains of C acnes can cause much more inflammation than others, and the carriage of pathogenic ribotypes of C acnes is highly correlated with the disease.9
A comparative analysis between healthy and acne skin microbiomes using ultra-deep shotgun metagenomics revealed the high relative abundance of C acnes bacteriophages on healthy skin compared to acneic skin.13 Bacteriophages
