The role of p.acnes bacteria in acne is well known. It inhabits your sebaceous glands and when overgrown, stimulates an immune system response which inflames and swells your pores. But up until twenty years ago there remained some mystery, since p.acnes is also a perfectly normal member of human skin flora.
You need p.acnes to prevent clogged pores and to kill infectious viruses. Even the most perfect skin pore in the world contains a bacterial composition of 87% p.acnes. What’s strangest is that occasionally, studies show that clear-skinned people and acne-ridden teenagers have virtually identical levels.
What’s the explanation? Like all infectious bacteria, such as the mostly benign E.coli where only a few subspecies actually kill people, Propionibacterium acnes has countless different strains, and some are much more involved with acne than others.
The truth about p.acnes bacteria
P.acnes bacteria is not one uniform microorganism, not even close. The strains share countless broad characteristics, such as feeding off sebum for their energy, but there’s 4 main subgroups of p.acnes, and over 11,000 different forms have been detected in human skin.
The recent illustration was a 2013 study where multiple strains of p.acnes were analysed, including 66 previously undetected ones. This alone shows how new strains are constantly being discovered.
The 10 most common ribotypes (strains) of p.acnes were analysed in detail. These bacteria samples were obtained from 52 clear-skinned people, and 49 people with moderate to severe acne.
Strains 1, 2, and 3 were found in equal amounts in healthy and acne-prone skin. Meanwhile, strains 4, 5, 7, 8, 9, and 10 were much more concentrated in acne-prone skin. Strain 6 was most prevalent in healthy skin
The most closely connected strains to acne were 4 and 5, as 20% of patients with severe acne had colonies of them, compared to almost zero for people with clear skin.
At one extreme, there was strain 4, where 84% of total samples came from acne patients, compared to only 16% from clear skinned humans. At the other, there was the beneficial strain 6, where a mere 1% was isolated from acne patients compared to 99% from healthy skin samples.
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Despite being deemed to be less to blame for acne than strain four, 100% of strain 8 and 10 samples were discovered in acne patients, while 0% were detected in healthy people.
A lot of people were shocked by this study, but research has been simmering away since the early 2000s, when p.acnes bacteria was separated into 4 broad subgroups: 1a, 1b, 2 and 3.
It’s now known that acne-prone skin is far more likely to contain subgroup 1a, and almost never subgroup 3. A gang of scientists once collected 106 strains of p.acnes from Danish skin. This included 25 from skin samples with severe acne, 42 from mild acne, and 39 from healthy skin.
Among the severe acne isolates, 22 belonged to p.acnes subgroup 1a. Three were from the combined subgroups of 1b and 2, while none were isolated from subgroup 3.
There’s even variation within the sinister 1a sect. One group called complex 18 found within subgroup 1a, a complex which itself contained a sizeable 46 strains, had 30% of its detected occurrences come from extreme acne. For complexes 27 and 28, also found within 1a, the figure was just 7.1%.
The conclusion is clear: some strains of p.acnes are much more troublesome than others.
But why?
The 2013 study found that the 10 main strains were 99% identical to strain 1 genetically. But that means little; remember that an Alaskan brown bear is almost 99% genetically identical to a polar bear. Genetic differences are already confirmed, as an aggressive type 1a strain called Sk137 had 64 unique genes, while a gentler strain called KPA171202 had 124 unique genes.
What we care about is the mechanism though, and summarised simply, the sinister strains such as group 1a stimulate a far stronger pro-inflammatory response. They stimulate the immune system far more than others, and this is the root cause which swells up a skin pore and creates acne.
First there’s human beta-defensin (hBD). This peptide is secreted by skin cells to kill many microorganisms, including p.acnes, but can also be a huge factor in inflammation. HBD draws in numerous other inflammatory chemicals like a magnet, such as neutrophils. This study observed that type 1a and 1b p.acnes bacteria increased hBD secretion fivefold after just 3 hours, but type 2 caused no increase whatsoever.
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Another player is interleukin 8, a pro-inflammatory chemical which is linked directly to acne. This time, all four p.acnes subgroups stimulated interleukin 8, but there was variation even among the type 1a strains, from a 5.5 fold to a 3 fold increase.
Interleukin-1a had a similar story. None of the four strains increased this pro-inflammatory chemical significantly, but a group 1a strain (strain 2005) increased it two fold, compared to a miniscule increase from a 1b strain (p.acnes strain 6609). The immune system chemical TNF-a was increased significantly by subgroups 1a and 1b, but only feebly by subgroup 2.
All four are classic chemicals involved with acne, in the beginning stages of a pimple’s life, so this is pretty strong evidence already.
The secrets of p.acnes
Then there’s the theories about WHY some trigger a fiercer inflammatory response than others, including various proteins, enzymes, and metabolites that different strains naturally produce.
NEURAMINIDASE – one is neuraminidase, an enzyme secreted by p.acnes. Neuraminidases have a pretty obscure role, but what’s more important is they’re what’s called an antigen.
That’s a substance which the immune system uses to identify a target; a good example is influenza molecules, which have neuraminidases in their structure that our immune systems have adapted to recognise. A good metaphor would be a formerly peace-loving great white shark scenting blood (AKA the antigen) and suddenly entering Jaws-mode.
What does this mean for acne? P.acnes types 1a and 1b are proven to secrete more neuraminidase. This study even found that 90.0% of p.acnes strains from acne-prone skin secreted neuraminidase, compared to 72.7% in healthy skin. The result is more targets for your immune system to identify and assault, with TNF-a, IL-8 and all the rest.
DERMATAN-SULPHATE-BINDING-PROTEIN – DS-BP is a molecule which binds to dermatan sulphate and prevents it from working. Dermatan sulphate is a glycosaminoglycan, a substance involved with wound repair and skin structure.
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P.acnes secretes DS-binding protein, for mysterious reasons, but possibly because dermatan sulphate contains a nutrient which p.acnes wants to extract and consume. More importantly, DS-BP is strong antigen just like neuraminidase. It makes sense, since the immune system obviously won’t like a compound which makes your skin crumble to dust. Type 1a and 1b p.acnes secrete DS-BPs, but types 2 and 3 do not.
LIPASES – lipases are enzymes which break down fatty acids, which all humans have in their stomachs to digest fats in food. P.acnes bacteria also secretes lipases, in order to digest their main energy source, sebum…
…but type 1a strains such as strain complex 18 significantly overproduce lipases, while type 2 strains produce far less. They overproduce a specific lipase called glycerol-ester hydrolase A (gehA), used to break down sebum triglycerides. This breakdown process produces inflammatory metabolites such as glycerol and free fatty acids.
LIPOGLYCANS – also known lipopolysaccharides, these are one of the main proteins your immune system uses to identify bacteria. Lipoglycans have been proven again and again to induce an inflammatory response; they’re much better researched than the two antigens above. They are the kings of the antigens, produced by countless bacteria.
The most important thing to know – type 1a and 1b p.acnes pump out significantly more lipoglycans than type 2.
It doesn’t end there, as those are only the clearest factors. Type 1a p.acnes lacks 10 genes associated with carbohydrate metabolism; maybe that’s why it produces extra lipase, to obtain more energy from fat instead. Type 2 p.acnes lacks the sugar galactose in its outer cell wall. P.acnes strains also secrete proteins with wildly varying compositions of amino acids.
Are these differences consequential? Not necessarily, because propionibacterium acnes wasn’t created by nature solely to give us acne. It’s just another microorganism trying to survive, and these differences may be completely unrelated. Make no mistake though, that there’s more to this bacteria than what meets the eye.
P.acnes also has benefits!
Just as some strains of p.acnes are worse than others, many have protective powers.
The consumption of sebum is a nice gift, as this normally keeps your skin pores open, even if its reasons are selfish, to obtain energy. Before the dawn of antibiotics, the inevitable p.acnes growth that resulted from this feast would be kept in check by blue light.
More interesting is that p.acnes manufactures its own bacteriocins, or bacteriocin-like compounds, such as acnecin, propionicin PLG-1, bacteriocin RTT108 and jenseniin G. These are active against other skin flora microorganisms without harming our own skin. Targets include various yeasts, moulds, and infectious bacteria.
For example, acnecin is known to act against other members of the p.acnes family (perhaps it protects against the unhealthy strains), while bacteriocin RTT108 impacts a far wider set of bacteria, both gram positive and negative.
While p.acnes might give you acne when in world domination mode, it’s a healthy bacteria for human skin overall.
More obscure facts
Another surprising characteristic of p.acnes bacteria is the lack of diversity around the world. Somehow, the p.acnes strains of a Chinaman in Beijing are hardly any different to a Scandinavian in a cool mountain hut. Subgroups such as 1a and 3 occur in fairly equal quantities around the world. Gut flora, meanwhile, is known to be more regional.
Now surely there’s a clear explanation here: p.acnes lives on the skin’s surface, people touch and rub their face constantly, and it must be easy for p.acnes to spread from human to human in airports.
It has also been observed that p.acnes cross infects visitors to dermatology clinics. Presumably the effect here would be negative, because visitors would inherently be more likely to have acne. Hence, that’s yet another reason to rely on natural methods.
Another interesting phenomenon relates to antibiotic resistance, the ever growing epidemic. In the 2013 study, it was found that ribotypes 4 and 5, the two worst strains for acne, had a gene which confers increased resistance to the widely prescribed antibiotic tetracycline. Even patients who had never taken antibiotics possessed these antibiotic resistant strains. However, it remained strain specific, with 4, 5, and 10 being the most resistant. Interestingly, they were also 3 of the worst strains for acne in the study.
What does this mean for acne?
To date, no studies have taken advantage of this interesting phenomenon. Right now, there are no prospects at all, but in the future, it’s very possible that we can target and wipe out the deadliest strains of p.acnes, and thus target acne like a laser rather than a shotgun.
Such a treatment is possible; with numerous physical differences between the strains, like the absence of carbohydrates in the cell walls, or differing proteins, scientists with all their ingenuity will surely come up something. The only problem is this: when this mysterious treatment does come around, it will probably be a pharmaceutical synthetic to begin with…
…and like benzoyl peroxide or Accutane there will surely be many side effects which emerge over time. So the best prospects are in the natural world of acne treatments. But there’s a problem there too: what plant or herb will happen to have the exact nutrient profile for killing one p.acnes strain over the other? Broad antibacterial powers like those in raw honey or tea tree oil are one thing, this is far more specific.
There are some interesting studies though: the lipases secreted by p.acnes were found to be strongly inhibited by the flavonoid antioxidants catechin and kaempferol (study), while plant saponins glycyrrhicic acid (found in licorice root) and digitonin had little effect.
So for us, the best treatment could be a cream compiled of other natural compounds like this, compounds which inhibit neuraminidase, lipases, DS-BP, and other differentiating factors in malignant p.acnes strains.
The benefits could be substantial, as the studies speak for themselves – acne patients have more of certain malignant strains.
Some would surely benefit more than others – if your acne more is related to wacky hormones or antioxidant deficiencies, then person B would benefit less than person A, and walk away disappointed. Two people with the exact same quantity of acne could still have differing facial flora, and benefit differently from our futuristic anti-strain cream.
Overall though, this won’t just be a niche strategy – a wide swathe of people could feel the benefits.
Conclusion
There’s much more to the p.acnes bacteria story than many people realise. It isn’t one uniform strain, determined to ruin everybody’s skin. P.acnes is just as biodiverse as everything else in nature.
Even if we can’t take advantage of the information here yet, it’s always great to accumulate more and more knowledge. Perhaps this does explain why certain antibacterial remedies fail miserably for some people, while succeeding for others. Perhaps this has happened to you.
Regardless, you are now more of an expert on acne than ever.
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Thanks for reading!