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The Role of Bacteria in Acne

Acne Bacteria May Turn a Clogged Pore into an Inflamed Pimple

By: Dan Kern, Acne.org Founder & CSO
Last updated: April 26, 2020

The Essential Information

Acne forms when a skin pore becomes clogged and skin oil that normally drains to the surface gets trapped inside. Living inside this skin oil is acne bacteria, called C. acnes. When skin oil gets trapped, C. acnes multiples. Research shows us that this bacteria then increases inflammation in the pore, leading to the characteristic redness and soreness that we see in acne lesions.

This is why medications that kill acne bacteria work well to combat acne, like benzoyl peroxide.

However, acne is not first-and-foremost a bacterial disease. As science marches on, researchers are realizing that acne is at its core an inflammatory disease, and bacteria is simply one component in its development.

The Science

Acne is a complex disease with many contributing factors, and the scientific community still does not understand its underlying causes. Researchers believe that a sequence of steps, including inflammation, excess production of sebum (skin oil), overgrowth of skin cells, and bacterial colonization all play a role in acne development. However, the order in which these steps occur, and the relationship between them, still is unclear and is a subject of scientific debate. Recently researchers have begun to study these steps in order to understand what causes acne.

In this article we will start by looking at the steps in acne development and then look more closely at the role of bacteria specifically.

The Underlying Causes of Acne

Steps in Acne Development

For years, scientists have used a classic model that explains the steps that lead to acne in the following order:

  • An overgrowth of skin cells and overproduction of sebum (skin oil) leads to the formation of a clogged pore
  • The clogged pore becomes colonized with acne bacteria (C. acnes)
  • Inflammation ensues

However, recent evidence indicates that this classic model that scientists have used for years may be incorrect and that inflammation may actually be the first step in acne development, and this inflammation leads to the initial clogged pore.1-3 Colonization of bacteria still comes later in the process, but instead of causing inflammation, it simply worsens already existing inflammation. In other words, acne is now viewed as a primarily inflammatory disease that becomes worse due to the presence of bacteria.4,5

The Role of Bacteria in Acne

A variety of different microorganisms, including the "acne bacteria" called C. acnes live on the skin of almost all adults.4 C. acnes is an anaerobic bacteria, which means it cannot live in the presence of oxygen. It lives mostly in the oily parts of the body where acne develops, such as the pores of the face and of the upper trunk (chest/back). According to a 2009 article in the journal, Science:

Science Journal

"[T]he [skin oil] glands of the face, scalp, chest and back produce large amounts of […] sebum and are the sites where […] Cutibacterium acnes predominates."6

The fact that C. acnes lives on normal skin and yet not all people develop acne indicates that its mere presence is not sufficient to cause acne. At the same time, C. acnes does indeed appear to contribute to acne, and scientists are still trying to determine exactly what role it plays and under what circumstances it transforms from a normal skin-microbe into one that contributes to disease.

To answer this perplexing question, scientists have studied acne lesions to determine whether C. acnes and/or other microorganisms must be present in a skin pore for an acne lesion to form. Investigations of inflamed acne lesions indicate a surprising finding: C. acnes and another strain of bacteria called S. epidermis are often, but not always, present in acne lesions. These results indicate that C. acnes and other microorganisms do not always appear in acne lesions, which means that the presence of these microorganisms is not always required in order for inflamed, red, and sore acne to occur.4

Even though bacteria is not always found in acne lesions, it usually is, and the presence of bacteria can make inflammation worse. In essence, bacteria likely make the redness and soreness of acne all the more red and sore. Let's look a bit more deeply into how this occurs.

How C. acnes Contributes to Inflammation of Acne

While the exact role of C. acnes or other bacteria in acne development remains unknown, and bacteria is not always necessary for acne lesions to occur, scientists do know that C. acnes bacteria contain genes that can activate the immune system and cause the immune system to then create inflammation.7 To put it simply, the immune system recognizes C. acnes bacteria as "invaders" and sends in troops of inflammatory molecules to attack these "invaders."

Now let's delve a bit deeper into how C. acnes can sometimes make inflammation worse. In addition to activating the immune system, studies show that C. acnes can also activate groups of proteins called inflammasome complexes in the skin, which stimulate the release of inflammatory molecules called cytokines.9,10 Previous research has linked activation of these inflammasome complexes to other inflammatory skin conditions, such as psoriasis.

Expand to read details of studies

Journal of Investigative Dermatology

A 2014 study in the Journal of Investigative Dermatology found that C. acnes interacted with a type of white blood-cell in the skin called a monocyte cell and "trigger[ed] a key inflammatory mediator, […], suggesting a role for inflammasome-mediated inflammation in acne pathogenesis."9

Journal of Investigative Dermatology

Another 2014 study in the Journal of Investigative Dermatology found that C. acnes also appeared to trigger an additional inflammatory immune response in cells called Th17 cells, which release inflammatory cytokines and create localized chronic inflammation. Previous research has shown that Th17 immune responses are associated with autoimmune inflammatory disorders, such as psoriasis, rheumatoid arthritis, Crohn's disease, and multiple sclerosis.10

As we can see from these studies, C. acnes appears to stimulate several different inflammatory mechanisms, including activating the immune system and creating inflammation directly in the skin, all of which ultimately contribute to the inflammatory redness and soreness of acne.

Cutibacterium acnes (C. acnes)

Potential New Therapeutic Options

As scientists gain a greater understanding of the role of bacteria, particularly C. acnes, in the processes underlying acne, new treatment options become possible, including medications that target particular parts of the immune system that are susceptible to activation by bacteria, and new vaccines that target C. acnes, to name just a few.7,10,11

Conclusion

New scientific research is steering researchers away from the traditional thinking that bacteria is the primary cause of acne. Acne is, first and foremost, an inflammatory disease. However, bacteria can contribute to the severity of acne by triggering an inflammatory response in the body's immune system as well as in the skin. As more research is done, new treatments aimed at addressing the bacterial component of acne formation may become available. Efforts to reduce inflammation in the body and using a reliable topical treatment that kills 99.9% all acne bacteria, such as The Acne.org Regimen, will go a long way toward reducing the incidence of acne in your skin.

References:

  1. Jeremy, A. H., Holland, D. B., Roberts, S. G., Thomson, K. F. & Cunliffe, W. J. Inflammatory events are involved in acne lesion initiation. J. Invest. Dermatol. 121, 20 - 27 (2003). https://www.ncbi.nlm.nih.gov/pubmed/12839559
  2. Do, T. T. et al. Computer-assisted alignment and tracking of acne lesions indicate that most inflammatory lesions arise from comedones and de novo. J Am. Acad. Dermatol. 58, 603 - 608 (2008). https://www.ncbi.nlm.nih.gov/pubmed/18249468
  3. Metiko, B., Brooks, K., Burkhart, C. G., Burkhart, C. N. & Morrell, D. Is the current model for acne pathogenesis backwards? J. Am. Acad. Dermatol. 72, e167 (2015). https://www.ncbi.nlm.nih.gov/pubmed/25981026
  4. Shaheen, B. & Gonzalez, M. A microbial aetiology of acne: what is the evidence? Br. J. Dermatol. 165, 474 - 485 (2011). https://www.ncbi.nlm.nih.gov/pubmed/21495996
  5. Suh, D. H. & Kwon, H. H. What's new in the physiopathology of acne? Br. J. Dermatol. 172 Suppl 1, 13 - 19 (2015). https://www.ncbi.nlm.nih.gov/pubmed/25645151
  6. Grice, E. A. et al. Topographical and temporal diversity of the human skin microbiome. Science 324, 1190 - 1192 (2009). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2805064/
  7. Beylot, C. et al. Propionibacterium acnes: an update on its role in the pathogenesis of acne. J. Eur. Acad. Dermatol. Venereol. 28, 271 - 278 (2014). https://www.ncbi.nlm.nih.gov/pubmed/23905540
  8. Contassot, E. & French, L. E. New insights into acne pathogenesis: propionibacterium acnes activates the inflammasome. J. Invest. Dermatol. 134, 310 - 313 (2014). https://www.ncbi.nlm.nih.gov/pubmed/24424454
  9. Qin, M. et al. Propionibacterium acnes Induces IL-1beta secretion via the NLRP3 inflammasome in human monocytes. J. Invest. Dermatol. 134, 381 - 388 (2014). https://www.ncbi.nlm.nih.gov/pubmed/23884315
  10. Agak, G. W. et al. Propionibacterium acnes Induces an IL-17 Response in Acne Vulgaris that Is Regulated by Vitamin A and Vitamin D. J. Invest. Dermatol. 134, 366 - 373 (2014). https://www.ncbi.nlm.nih.gov/pubmed/23924903
  11. Qin, M. et al. Nitric Oxide-Releasing Nanoparticles Prevent Propionibacterium acnes-Induced Inflammation by Both Clearing the Organism and Inhibiting Microbial Stimulation of the Innate Immune Response. J. Invest. Dermatol. 135, 2723 - 2731 (2015). https://www.ncbi.nlm.nih.gov/pubmed/26172313

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