Why should we consider the skin microbiota of acne patients in daily practice?

Acne is a chronic inflammatory disease that affects the pilosebaceous follicle.

Three main factors are involved in the development of acne¹:

Acne: dysbiosis of skin microbiota plays a key role

Altered bacterial colonization is believed to be one of the main elements contributing to the development of acne. This dysbiosis is associated with inflammation, one of the main factors in acne development.

Three-dimensional topography of the skin microbiome

P.acnes: there may be another bacterium involved!

P.acnes, the primary disease-associated bacterium, is an anaerobic commensal bacterium of the pilosebaceous follicle, growing particularly in the sebaceous areas of the forehead, retroauricular crease and back.³

It plays a well-known key role in inflammation.

Although it has been acknowledged that the sebaceous follicle microbiota is predominantly inhabited by P. acnes in acne patients, a recent study showed that their skin surface microbiota is dominated by Staphylococcus.¹
In addition, this study indicated that the concentration of Staphylococcus increases with acne severity.¹

Reducing Staphylococcus could be a new therapeutic approach.

Going further

The role of P.acnes in acne

P.acnes plays a physiological role by inhibiting the invasion of pathogenic bacteria such as S. aureus and S. pyogenes. It also maintains the acidic pH in the skin, including the sebaceous glands, by hydrolyzing triglycerides, releasing free fatty acids and secreting propionic acid.

P.acnes interacts with the innate immune system to promote inflammation in two ways.

• As a first-defense mechanism against infection, the skin acts as an immunological barrier, and P.acnes directly modulates innate immunity by identifying Pathogen Recognition Patterns (PRPs) and activating innate immune responses via toll-like receptors (TLRs), peroxisome-activated receptors (PARs), node-like intracellular receptors (NLRs 1-3), retinoic acid-inducible gene-like intracellular receptors (RLRs) and antimicrobial peptides (AMPs), thereby regulating cutaneous inflammation. Optimal skin health and innate immunity are maintained when the skin’s microbiota and immune system are balanced.
• The second mechanism by which P.acnes activates the skin's innate immunity is by quantitatively and qualitatively modifying the skin microbiota. Hyperseborrhea induces the proliferation of specific bacteria, creating changes in the skin microbiota that stimulate the activation of cutaneous innate immunity, including the secretion of interleukin-1β by keratinocytes and monocytes, and development of comedones and inflammatory lesions.³ A recent study has shown that acne is not necessarily the result of P.acnes proliferation alone as it predominates on both healthy and disease-associated skin⁴.

Genome comparison of P. acnes strains has identified different profiles of commensal P.acnes subtypes between healthy skin and acne lesions, demonstrating phenotypic and functional differences of P.acnes as a commensal in health and pathogen in acne.³