C. acnes: friend or foe?
Cutibacterium acnes (C. acnes), formerly known as Proprionibacterium acnes,is the most common strain of bacteria connected to the skin condition Acne Vulgaris. Acne is a very common skin condition, affecting up to 90% of teenagers (PMID: 31284694) Research into exactly how C. acnes bacteria play a role in Acne Vulgaris is still being explored. Here we will examine what we know so far about the many functions and facets of the C. acnes species, some of the challenges associated with Acne as a disease state, and why working towards a balanced skin microbiome is one of the best routes to healthy skin.
What is C. acnes?
C. acnes are an important part of a healthy skin microbiome. As a refresher, the skin microbiome is a collection of bacteria that lives in an ecosystem on the skin within a given microenvironment. These microenvironments are sebaceous, moist, and dry. The type of bacteria that resides on a particular area of skin varies depending on the microenvironment of that area.
Bacteria such as S. epidermidis and C. acnes are common species present within a healthy skin microbiome. C. acnes are a Gram-positive, facultative anaerobic bacterium that can be present in high numbers in lipid-rich (sebaceous) areas such as the scalp and face.
The composition of the skin microbiome plays an important role in defending against the colonization of pathogenic and opportunistic bacteria. While C. acnes is often considered a commensal bacteria, there are some strains that can be opportunistic and pose a threat to the ecosystem of our skin. So let’s discuss the intricacies of C. acnes and its role in acne.
C. acnes’ role in pathogenesis of acne
As discussed above, C. acnes is an important part of a healthy skin microbiome. The species C. acnes consists of different lineages, and this subdivision, to some extent, separates strains from healthy and acneic skin. Strains found on acneic skin most often belong to phylotype IA1, whereas strains not associated with acne or strains associated with healthy skin belong to other phylotypes such as IA2, IB, or II.
The effects of phylotype IA1 (acneic) C. acnes strains:
- Increases production of porphyrin: A substance that generates a substance that reacts to oxygen by creating inflammation in keratinocytes (building blocks of the skin barrier).
- Vitamin B12 reaction: This spikes porphyrin, again causing irritation and inflammation.
- Increases receptor for filligrin production: Filligrin helps bind the keratinocytes (building blocks). When too much of this is produced a commedogen forms.
- Hyperkeratinization: Sebum is digested by C. acnes lipase to free fatty acids, which causes a failure of the skin barrier function by hyperkeratinization (improper shedding of skin cells) and induces an increase in inflammatory cytokines.
- Other irritation: These strains are known to promote inflammation in sebocytes (oil production), keratinocytes (building blocks), and blood cells.
Commedogen: tending to clog pores or cause blackheads.
Why does some oil clog our pores and some does not?
Excessive Reactive Oxidative species have been found on patients with acne lesions.
In hamsters, it is found that certain strains of C. acnes change the type of sebum (oil) that our glands produce, making it comedogenic. This new oil is oxidized, meaning the amount of oxygen is lowered. Early sebum oxidation is the initial trigger for acne formations because the skin is no longer able to provide antioxidants (the fighting mechanism) to fend off the free radicals that are invading. This results in an immune response that presents as acne.
Balance is key
So, you may be wondering: why do we still need C. acnes? As mentioned before, C. acnes are a commensal organism on healthy skin. When the skin microbiome is in homeostasis, C. acnes outcompete other bacteria on the skin and colonizes the acidic, anaerobic environment of the sebaceous gland deep in the dermis. Through its digestion of the sebum, it produces free fatty acids, which are secreted with the sebum onto the skin. This helps regulate pH of the skin, keeping it at its mildly acidic state of 4.5-5.5, which inhibits pathogenic bacteria, such as Staphylococcus aureus (which causes atopic derm/ inflammation) and Streptococcus pyogenes, while favoring other commensal bacteria such as coagulase negative staphylococcus and corynebacteria. Essentially, when fighting for the right side, C.acnes are good soldiers for the skin.
This brings us to the problem with many popular acne treatments: topical and/or ingested antibiotics. These may work in the short term, but their success is not sustainable. Healthy levels of C. acnes keep the bacteria that causes dermatitis at bay, which is one of the reasons individuals report irritation, sensitivity, and dermatitis-like symptoms with many topical acne treatments, especially Benzoyl peroxide, which is one of the most effective killers of C. acnes bacteria.
Additionally, many of the acne-causing C. acnes strains are antibiotic resistant:
“Topical and oral antibiotics have been the center of acne treatment for a long time. C. acnes-resistance to antibiotics has increased over the years and become a worldwide problem in acne patients, with higher rates of resistance being reported for clindamycin (lincosamide) (36–90%) and erythromycin (macrolide) (21–98%) than for tetracyclines (4–16%). This is in line with the fact that topical macrolides and clindamycin are the most commonly used…The degree of antibiotic resistance varies among the different C. acnes strains. It is well known that acne-associated phylotype IA1 strains (ribotypes R4, R5) are most often antibiotic-resistant.
This suggests that these treatments may be killing the ‘good’ C. acnes strains while the ‘bad’ acne-causing strains are surviving.
While certain strains of C. acnes are implicated in the disease state of Acne Vulgaris, C. acnes are still an important commensal species in the skin microbiome of sebaceous skin sites. Essentially, balance is key. Getting rid of C. acnes completely is not a good long-term solution, as C. acnes strains perform many important functions for skin health such as regulating pH balance and keeping S. aureus at bay. With this in mind, the best thing we can do is encourage natural competition in the skin microbiome. This will allow for the good bacteria to survive and outcompete the bad. Balancing the skin microbiome sets the skin up for success in the long run because it allows for all necessary species to survive, which strengthens the immune system of skin and ultimately results in resilient, healthy skin.