The bacteria that causes eczema

Eczema, known as atopic dermatitis, is the most common form of dermatitis. This skin condition makes the skin itchy, flaky, and dry, plaguing the affected individual with an incredible amount of discomfort. We know that environment and genetics both play a role in who has this condition; however, now eczema is being considered an autoimmune disorder, involving both systemic and cutaneous immunity. What does the cutaneous immune system, and by proxy the skin microbiome, have to do with eczema? What is the bacteria linked to eczema to flares? And does the bacteria in our microbiome actually affect our skin cells?

ARTICLE KEY: eczema = atopic skin = atopic dermatitis

S. aureus and atopic skin

One of the most common markers of an atopic skin microbiome is an overgrowth of a bacteria called S. aureus, or staphylococcus aureus.

: a gram-positive bacteria that causes a wide variety of clinical diseases… it is found in the environment and is also found in normal human flora, located on the skin and mucous membranes (most often the nasal area) of most healthy individuals. S. aureus does not normally cause infection on healthy skin; however, if it is allowed to enter the bloodstream or internal tissues, these bacteria may cause a variety of potentially serious infections. PMID 28722898

Although certain types of S. aureus can be native to the skin microbiome, an abundance of AD positive (AD+) S. aureus is quite problematic. There is a close correlation between the severity of atopic skin and the abundance of AD+ S. aureus habitation. This was discussed in a meta-analysis of various studies measuring S. aureus abundance on the skin microbiome. On non-lesional skin, a 39% abundance was recorded, while a 70% abundance was recorded at lesion sites. The study concluded: “S. aureus density is known to correlate with disease severity, regardless of the site.” PMID 30987008.

Compositional changes in the atopic skin microbiome

Excessive S. aureus has implications on the skin microbiome that go beyond directly causing disease. By nature, S. aureus is (at the very least) opportunistic and in many cases outright pathogenic. This is likely one explanation for the other hallmark of atopic skin, a severe lack of diversity in the skin microbiome. Eczema patients show a low diversity of species. There is a notable lack of Cutibacterium, Streptococcus, Acinetobacter, Corynebacterium, and Prevotella on the skin when someone is experiencing an AD flare.

The lack of certain bacterial species may be significant. Recent sequencing has shown that there may be an inverse relationship between Cutibacterium acnes (C.acnes) and S. aureus. Additionally, there seems to be an inverse relationship between Corynebacterium and S. aureus. C.acnes tend to inhabit sebaceous microenvironments (face, chest, back); corynebacterium tend to inhabit moist microenvironments (armpit, inside of elbows, back side of knees). While the exact mechanism for these observed relationships is not fully understood, it’s speculated that they could be a result of the creation of the antibacterial metabolites that cutibacterium and corynebacterium secrete. Regardless of the mechanism, the absence of these two species in the microbiome of AD patients is significant.

Surrounding bacteria is also a possible explanation for why eczema is more common in children. Children have different microbiomes from adults for a number of reasons, spanning from environment to overall lack of developmental ability. AD is present in almost 30% of children, while only 3% carry the condition into adulthood. A potential reason for this is the fact that the two bacteria that have this inverse relationship to S. aureus, cutibacterium, and corynebacterium are exclusive to the adult skin microbiome.

S. aureus effects on skin barrier in eczema patients

Amazingly, S. aureus not only has a huge impact on the bacteria in our skin microbiome, this bacteria also has impacts on our actual skin cells! (this blew my mind btw). One of the most notorious effects of eczema is a severely compromised skin barrier. This means that the brick and mortar structure that makes up the barrier is often weak and cracked, leading to excessive water loss or increased levels of TEWL (transepidermal water loss). As it turns out, the AD+ S. aureus strain plays a significant role in the degradation of the skin barrier. The mechanism is as follows:

“S.aureus secretes a pore forming a-toxin which penetrates host cell membrane. In the epidermis, the a-toxin forms direct pore forming a-toxin which penetrates host cell membrane. In the epidermis, the a-toxin forms direct pores on keratinocytes, which destroys the skin barrier. S.aureus also produces a number of proteases, which dissolve the stratum corneum.” - PMID 30987008

To summarize, S. aureus secretes a toxin (aptly named a-toxin) that eats away at the skin barrier causing MAJOR disruption. This could be why S.aureus, skin barrier degradation, and eczema are so closely linked.

Bottom line:

The skin microbiome plays no small role in either the state or progression of atopic dermatitis. The main culprit? AD+ S. aureus bacteria! Although we all have it, the AD+ strain of S. aureus has strong ties to atopic skin. The two cornerstones of atopic skin is a lack of diversity in the skin microbiome and a weakened/damaged skin barrier which allows for advanced TEWL, cracking, and bacterial infection. S. aureus seems to have causal roots to both of these cornerstone characteristics for eczema. Therapies related to microbiome modulation are being seriously looked at and considered for eczema reduction therapies. New discoveries are being uncovered at a rapid rate, and while I believe it is likely not as simple and eradicating the AD+ S. aureus strain from the skin microbiome, it’s an exciting time in this field, as we are getting closer to cracking the microbial code.

https://www.ncbi.nlm.nih.gov/books/NBK441868/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6518061/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6518061/