Answer: Propionibacterium acnes (P. acnes) is a bacteria that can colonize the the skin and hair follicles. Excessive growth of this bacteria in the skin contributes to acne vulgaris.

Propionibacterium acnes – The Basics

Propionibacterium acnes (P. acnes) is a bacteria that grows deep inside of pores, where it feeds on the sebum that is produced by the sebaceous glands that surround the base of the hair shaft. Most individuals with acne symptoms have an overgrowth of P. acnes bacteria in their skin. Several research studies have indicated that specific strains of P. acnes bacteria are commonly associated with acne vulgaris. However, other bacteria (e.g. Staphylococcus and Corynebacterium) can also reside in the skin and contribute to acne.

Biology of Propionibacterium Acnes

P. acnes are a type of “gram-positive” bacteria. Gram-positive bacteria produce a positive result in the Gram stain test, which is a common way to test for bacterial infections. Gram positive bacteria have thick cell walls that that help protect them from their environment. There are many other types of gram-positive bacteria that cause infections, such as Staphylococcus (MRSA), Streptococcus (Strep Throat) and Listeria (food poisoning).

P. acnes is an oxygen-tolerant, anaerobic bacteria that prefers to grow in low oxygen environments (like deep within a plugged follicle). P. acnes bacteria can form sticky clumps of bacteria known as biofilms that help them to attach to surfaces and modulate their environment. In many cases, bacterial biofilms have been shown to contribute to long term infections, and may play a role in the persistence of P. acnes infection in some individuals.

The Relationship Between Sebum and Propionibacterium acnes

P. acnes bacteria use sebum as an energy source (food). Sebum production is partially controlled by hormones (androgens) and sebum production is elevated in many people with acne. The excess production of sebum increases the growth of P. acnes bacteria, causes oily skin and creates plugs that block the opening of the hair follicle. In a plugged follicle, the low oxygen levels and accumulating sebum create an excellent environment for the growth of P. acnes bacteria.

P. acnes bacteria produce specialized enzymes that help them digest the fatty acids and triglycerides that are abundant in sebum. In an anaerobic environment, P. acnes ferments the fatty acids and triglycerides, and releases short chain fatty acids and propionic acid as metabolic byproducts (that’s why it’s called Propionibacterium). Research indicates that the breakdown of sebum by P. acnes can create comedogenic byproducts, and this may be a contributing factor to the severity of acne symptoms. There is also some evidence that presence of P. acnes bacteria may directly stimulate the sebaceous glands to produce additional sebum. If this is true, it is possible that the bacteria has adapted to the environment of the follicle, and part of this adaptation includes a mechanism to get more food (sebum) from the surrounding tissue.

Propionibacterium acnes, Inflammation and Acne

The P. acnes bacteria itself does not directly cause significant damage to the skin. Instead, most of the damage caused by inflammation that results from the body’s own immune response to the presence of the P. acnes bacteria.

Particularly for individuals who suffer from inflammatory acne (Acne Types: 2-4), the immune system over-reacts to the presence of bacteria and sends in lots of white blood cells. Each person’s immune system is different, and some immune systems are more sensitive to P. acnes bacteria than others. People with a naturally strong immune response to P. acnes bacteria have an increased risk of developing acne symptoms.

Many of the individual components that make up the bacteria are easily recognized by the immune system as “foreign” molecules. This material includes components of the bacterial cell wall, like peptidoglycans, lipopolysacharides and proteins. Even the DNA from P. acnes bacteria is recognized as foreign by the immune system. The bacteria doesn’t even have to be alive to trigger a powerful immune response, dead bacteria can also set off alarms within the immune system.

Dysfunctional Immune Responses and Acne vulgaris

In some people who suffer from moderate to severe acne (Acne Types: 2-4), the root of the problem can be traced back to a faulty immune response. There are two main types of immune system malfunctions that can lead to acne symptoms:

Hyper-Sensitive Response

In a hyper-sensitive immune response, an individual’s immune system reacts over-aggressively to the presence of the bacteria and produces large amounts of inflammatory signals. These inflammatory cytokines induce white blood cells to release large amounts of digestive enzymes and free radicals into the site of infection.

For individuals with acne, this immune response is often poorly-targeted against the infectious agent and it causes a lot of unnecessary collateral damage to the surrounding tissue. This collateral damage can actually make it more difficult for the immune system to fight off the infection. The damage often stimulates the production of more inflammatory signals and this can become a vicious cycle. This type of inflammatory cycle is responsible for the symptoms observed in moderate-to-severe inflammatory acne. This inflammation can also permanently damage the skin and lead to acne scars.

Impaired Bacterial Killing Ability

Another type of dysfunctional immune response can occur when an individual’s white blood cells do not effectively destroy and process the bacteria that they encounter. In an ideal situation, white blood cells called Macrophages capture (phagocytose) all of the bacteria that they come in contact with. Once captured, the Macrophage isolates the bacteria into an special intracellular compartment called a phagosome. It then pumps antibacterial molecules and digestive enzymes into this compartment. These molecules and enzymes kill the bacteria and break it down into small pieces. Some of these pieces are then used by the immune system to design antibodies that target the bacteria and prevent future infections. The immune system uses certain pieces of the digested bacteria to train specialized white blood cells to identify and respond to infections caused by that bacteria.

Some individuals who suffer from chronic inflammatory infections (eg. acne) have white blood cells that are able to ingest bacteria normally, but are not able to efficiently kill certain types of bacteria that they ingest. In this situation, the white blood cell will often continue to secrete lots of inflammatory signals till it exhausts itself and dies in a process called apoptosis. After the white blood cell dies, the bacteria may not be dead, in which case it can sometimes escape and continue proliferating.

Genetics

Both of the above examples of immune system dysfunction are usually genetic in origin. The susceptibility to acne vulgaris is appears to be partially hereditary. Individuals whose parents experienced difficulty with acne have an increased risk of developing acne symptoms.

How to Treat P. acnes Bacteria

Antibiotics and Other Antibacterial Compounds

Extensive screening has been done to test the susceptibility of P. acnes bacteria to different classes of antibiotics. In general, what researchers have found is that P. acnes is moderately susceptible, when directly exposed, to many classes of antibiotics.

Researchers have also found that P. acnes bacteria is becoming increasingly resistant to some of the common antibiotics used to treat acne, like erythromycin and tetracycline family drugs (tetracycline, doxycycline and minocycline). Interestingly, numerous studies have shown that P. acnesbacteria is extremely sensitive to Penicillin, which was one of the first antibiotics ever developed.

It is important to keep in mind that these tests are primarily done on a Petri dish in a laboratory. When asking whether an antibiotic is effective when treating a clinical acne infection there are additional factors that need to be considered. The biggest question is whether the antibiotic makes it to the site of infection. Many antibiotics may be effective at killing P. acnes bacteria on a Petri dish, but they do not accumulate in sufficient concentration in the follicle and sebaceous glands to be effective at treating active acne infections.

Several Over-The-Counter medications, like benzoyl peroxide and triclosan, are also directly toxic to P. acnes bacteria. However, these topically applied medications have difficulty penetrating to the base of the hair follicle, which is where the P. acnes bacteria are causing problems.

Retinoids and Hormonal Treatments

P. acnes bacteria use the fatty acids and triglycerides found in sebum as its primary food source. Limiting the amount of sebum production can suppress the growth of P. acnes bacteria by reducing its food supply.

Treatment with retinoids can decrease the production of sebum in the skin. This is true for both oral retinoids (eg. Isotretinoin/Accutane) and topical retinoids (eg. Tretinoin/Retin-A, Adapalene/Differin). Hormonal treatments such as androgen inhibitors (eg. Spironolactone, Cyproterone) and birth control pills may also decrease sebum production.

Light and Laser Treatments

Certain light and laser therapies can also decrease the production of sebum. Diode lasers can be used to treat overactive sebaceous glands, thereby reducing the amount of sebum.

Blue light phototherapy and Photodynamic Therapy (PDT) can be used to directly kill P. acnes bacteria growing in the skin. These therapies work by using high intensity light of a specific color (wavelenght) to excite a bacterial molecule called a porphyrin. Porphyrin is produced in large quantities by P. acnes bacteria. Excitation of porphyrins with blue light causes them to release free radicals into the bacteria and killing them.

Essential Oils

Many essential oils have been shown to contain antibacterial molecules that are toxic to P. acnes bacteria. Some essential oils, such as Tea Tree Essential Oil and Thyme Essential Oil are commonly used as topical acne treatments.

Other Naturopathic Treatmens

Besides essential oil, many natural compounds (eg. Aloe vera gel and natural honey) have been shown to have antibacterial properties against P. acnes. Certain metals (eg. silver and copper) and other elements (eg. sulfur) are also toxic to P. acnes bacteria in pure form. There are numerous Naturopathic treatments for acne.

References

The complete genome sequence of Propionibacterium acnes, a commensal of human skin. Brüggemann, et al. 2004.

Acne and Propionibacterium acnes. Bojar, et al. 2004.

Induction of proinflammatory cytokines by a soluble factor of Propionibacterium acnes: implications for chronic inflammatory acne. Vowels, et al. 1995.

Propionibacterium acnes resistance: a worldwide problem. Eady, et al. 2003.

Eradication of Propionibacterium acnes by its endogenic porphyrins after illumination with high intensity blue light. Ashkenazi, et al. 2003.

Propionibacterium acnes strain populations in the human skin microbiome associated with acne. Fitz-Gibbon, et al. 2013.

Induction of toll‐like receptors by Propionibacterium acnes. Jugeau, et al. 2005.

Propionibacterium acnes and lipopolysaccharide induce the expression of antimicrobial peptides and proinflammatory cytokines/chemokines in human sebocytes. Nagy, et al. 2006.

Formation of Propionibacterium acnes biofilms on orthopaedic biomaterials and their susceptibility to antimicrobials. Ramage, et al. 2003.

Biofilm formation by Propionibacterium acnes is associated with increased resistance to antimicrobial agents and increased production of putative virulence factors. Coenye, et al. 2007.

The role of Propionibacterium acnes in acne pathogenesis: facts and controversies. Dessinioti, et al. 2010.

A comparative study of Cutibacterium (Propionibacterium) acnes clones from acne patients and healthy controls. Lomholt, et al. 2017.

Propionibacterium acnes: an update on its role in the pathogenesis of acne. Beylot, et al. 2014.

Antagonism between Staphylococcus epidermidis and Propionibacterium acnes and its genomic basis. Christensen, et al. 2016.