Acne and the life and survival of its prominent bacteria

There is still so much that is unknown about the skin microbiome, both in the healthy skin and skin with acne. Research has only just scratched the surface. This blog will discuss the recently published studies that offer a new perspective on the complexity of the role of bacteria in acne pathogenesis.

The reinvention of Propionibacterium acnes

Propionibacterium acnes (P. acnes), is a commensal bacterium active in the daily maintenance of healthy skin. It is also an opportunistic pathogen in acne. Not shy of reinvention, the bacterium has been renamed three times: Corynebacterium acnes, P. acnes, and finally Cutibacterium acnes.

“Contrary to previous belief and perhaps its bad reputation, the proliferation of P. acnes is not the trigger of acne”

Around the beginning of the nineteenth century, Corynebacterium acnes was isolated from lesions in acne patients, establishing the first link between bacterial infection and acne. The concept of seeing the bacterium as a pathogen greatly declined when the bacterium, now known as Propionibacterium acnes, was also isolated from normal, healthy skin. Even when later re-confirmed as a factor influencing acne inflammation through a wide range of pathways, the questions remain: Is this commensal bacterium capable of initiating inflammation in the sebaceous gland? If so, why does follicle colonization not always result in inflammation?[1]

Since 2018, we now understand that there is a fine balance between the members of P. acnes family members (phylotypes) as well as a wider balance within the entirety of the skin microbiome in skin health and diseases. There is also a new taxonomic classification of P. acnes, now named Cutibacterium acnes (C. acnes).

However, the role of its different phylotypes participating in the virulence and antimicrobial resistance of acne-associated strains is far from understood. Contrary to previous belief and perhaps its bad reputation, the proliferation of P. acnes is not the trigger of acne! People with acne do not have more P. acnes in their follicles compared to a normal population. It is now considered most likely to be the loss of the skin microbial diversity, together with the activation of the innate body immunity, that leads to the chronic inflammatory condition.[2]

Clinical success of topical acne therapies

In today’s clinical practice, dermatologists still rely on a limited number of therapeutics (antibiotics and benzoyl peroxide) to treat inflammatory acne. The strategy to target the environment in order to suppress the growth of P. acnes on the skin has been proposed in the past – altering the microenvironment within the follicle beyond the ‘boundaries for its growth and survival’. In doing so, several environmental parameters could be altered: pH, oxygen tension, ionic strength and water availability. The latter has been suggested as a safe therapeutic approach: preventing microbial growth and colonization by reducing water activity with small osmolytes, i.e. xylose or sucrose, non-fermentable by P.acnes.[3] In other words, dehydrating the skin to prevent P. acnes thriving.

Yet, targeting the environment as an approach to acne therapy has not taken off. The follicular niche in which P. acnes resides, as well as the bacterial attributes associated with its ability to thrive in this relatively “extreme” habitat, require more research. Despite new genome sequencing technology providing an array of answers, this technology alone cannot help to explain the exact role of the bacterium in acne since the environment in which it lives is also important. So, we look further afield to understand the link between acne and P. acnes.

Biofilm: A mode of bacterial growth

The main question surrounding the cause, and treatment, of acne remains: Is there a biofilm? In recent years there has been much interest in the ability of P. acnes to produce biofilms. Biofilms are the natural form of bacterial growth, different from planktonic, free-floating cells (see the UK National Biofilms Innovation Centre explainer)[4].

Any biofilm consists of three essential components: the microbial cells, a surface onto which these cells adhere, and an extracellular polymeric matrix, in which cells are embedded and can form larger communities. Biofilms are notoriously resistant to antimicrobial therapies due to restricted penetration of antimicrobials, decreased growth rate, expression of resistance genes and the presence of resistant cells.

Some P. acnes strains produce biofilms but does P. acnes form biofilm in acne? Unfortunately, biofilms without a clear-cut abiotic surface cannot be “explanted” and analyzed. Burkhart and Burkhart first suggested that P. acnes resides within the follicle as a biofilm based on circumstantial evidence. The failure of topical therapies could be explained by high resistance of sessile, or immobile, P. acnes cells; also demonstrated in in vitro studies.

In the end, the difference between P. acnes acting as a skin commensal in healthy skin or as a pathogen in acne, could be related to phylotypic differences associated with biofilm formation. However, the adaptation of P. acnes to its follicular niche, and understanding why it thrives in certain lesions is unclear.

It is plausible that cell-associated polysaccharides of some P. acnes strains, whether organized in biofilms or capsules, play a role in storing water and protecting the life of the bacteria in the acne follicle.

Science has many questions yet to be answered.

[1] https://link.springer.com/chapter/10.1007/978-3-540-69375-8_19

[2] https://www.ncbi.nlm.nih.gov/pubmed/29894579

[3]https://www.researchgate.net/publication/237200939_A_Honey_Trap_for_the_Treatment_of_Acne_Manipulating_the_Follicular_Microenvironment_to_Control_Propionibacterium_acnes

[4] https://biofilms.ac.uk/biofilms-explainer/

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