How skin bacteria influence dermatitis

If you’ve been diagnosed with eczema or dermatitis, you might have been told that your skin barrier is weakened or damaged and that it is important to support it by applying creams or ointments. But why is your skin barrier weakened? 

A decade ago, research investigated genetic reasons for why some have a more sensitive barrier than others, and they found the Filaggrin gene, an important step, but one that only told part of the story. 

A decade on and another piece of the puzzle is emerging in the form of a tiny world of bacteria, fungi and other microorganisms living on your skin. Your skin microbiome. 

Just like your gut microbiome, your skin microbiome isn’t just there doing nothing. It works constantly to protect your barrier; it interacts with your immune system and even plays a role in managing inflammation. When your skin microbiome is unbalanced (dysbiosis), it can influence skin conditions such as eczema and dermatitis, making them harder to manage.  

It may be hard to believe that twenty-five years ago, the gut microbiome was barely on the scientific radar, especially as we all know about the importance of digestive health and the role our gut bacteria play in a whole host of conditions. Now it’s the turn for another of our body’s microbiomes to be unravelled. Our skin microbiome.

Diversity matters

Many studies have confirmed that what’s important is the range of different types of bacteria in our gut microbiome, not just small numbers of large populations of one type. Different bacteria play various roles, and it is the harmonious living and working together of these different types that ensures that our microbiome is at its healthiest. The exact same is true of our skin microbiome.   

What’s particularly interesting for those of us with eczema/dermatitis is that research has found that those with eczema/dermatitis have a lower skin microbiome diversity than the average, with the less-than-helpful Staphylococcus aureus being disproportionately present, especially during a flare. (1,2).

Dysbiosis, or the imbalance of bacteria, doesn’t just happen in the gut; it also happens on our skin. A proportionally large population of S. aureus, which is known to produce toxins that can harm the skin barrier and cause inflammation, means that there is less space for other, more beneficial and balanced types, such as Staphylococcus epidermidis, Cutibacterium, and Corynebacterium (3). Without these protective microbes, our whole skin’s ecosystem becomes unstable.

Staph is good at evading targeting 

Some bacteria and fungi know that we don’t really want them there, so they have developed strategies to avoid our attempts to dislodge them. Staphylococcus, for example, has been found to partner with a fungus called Alternaria to create a protective sticky shield or biofilm that they both hide behind. Not only do these biofilms help them avoid the treatments that are targeted at them, but they can also themselves inflame the skin and block healing (4,5). This vicious cycle may be the explanation why some people experience chronic or even treatment-resistant eczema or dermatitis. 

Flares trigger changes in our microbiome

Scientists have also uncovered that our skin microbiome changes as our skin symptoms worsen. It’s been found that during a flare, we have much less general skin microbiome diversity and a larger S. aureus population, but when the flare subsides, the S. aureus population declines, and our skin microbiome diversity increases again (6). 

This raises a chicken-and-egg type question: is the declining skin microbiome population leaving room for S. aureus to move in, or is it the S. aureus that takes up so much space that other species are pushed out? In other words, how can we make our skin less appealing to the more negative species of our microbiome and more supportive to the bacteria we want to nourish? Ongoing support, such as skin care, but also nutrition, can help make sure that our microbiome stays in balance. 

Different types of dermatitis, similar skin microbiome behaviours 

Most of the skin microbiome research to date has been focused on atopic dermatitis; however, similar microbiome changes have been found in both contact and seborrhoeic dermatitis (7). Whilst research is still in its early days, it does appear that skin dysbiosis is involved across all dermatitis types, leading to the irritation, inflammation and itch we sufferers all know too well.

Is the skin microbiome influenced by nutrition and lifestyle? 

We already know that the skin and gut microbiomes communicate with each other, and research shows that nutrition that supports the gut microbiome also supports our skin microbiome. A diet rich in variety and plant fibres can play a really important role. Including plenty of multi-coloured vegetables, fibre, and omega-3 fatty acids may help maintain microbial diversity, and reducing processed foods and sugar has been shown to reduce inflammation (8).

In a nutshell 

Knowing that your skin has its own microbiome is an important part of the dermatitis management picture. Being aware that your body’s different microbiome populations speak to each other is another piece in the puzzle. 

Nourishing your microbiome may help reduce inflammation and improve resilience against eczema flares, something most people suffering from chronic eczema hope for. 

Our skin takes the brunt of a lot of things, especially during these colder months, so here are some practical tips that may help keep your skin microbiome in balance: 

• avoid harsh soaps and antibacterial products
• use gentle, microbiome-friendly skincare such as Aurelia London or Esse
• eat a wide range of multi-coloured plant foods daily
• manage stress and prioritise good-quality sleep

The science of the skin microbiome is still in its infancy, but the evidence so far is promising in relation to the fact that supporting your skin’s natural ecosystem can make a real difference. 

References 

Bay L, Barnes CJ, Fritz B, Ravnborg N, Ruge I, Halling-Sønderby A-S, et al. Unique dermal bacterial signature differentiates atopic dermatitis skin from healthy. mSphere. 2025;10(2):e00156-25.

Byrd AL, Deming C, Cassidy S, Harrison O, Ng W-I, Conlan S, et al. Staphylococcus aureus and Staphylococcus epidermidis strain diversity underlying paediatric atopic dermatitis. Sci Transl Med. 2017;9(397):eaal4651.

Fyhrquist N, Muirhead G, Prast-Nielsen S, Jeanmougin M, Oláh P, Skoog T, et al. Microbe–host interplay in atopic dermatitis and psoriasis. Nat Commun. 2019;10(1):4703.

Hammond M, Gamal A, Mukherjee P, Damiani G, McCormick T, Ghannoum M, et al. Cutaneous dysbiosis may amplify barrier dysfunction in patients with atopic dermatitis. Front Microbiol. 2022;13:944365.

Gościńska A, Będzichowska A, Lipińska-Opałka A. Atopic dermatitis and the human skin microbiota. Pediatr Med Rodz. 2023;19(1):1–12.

Kong HH, Oh J, Deming C, Conlan S, Grice EA, Beatson MA, et al. Temporal shifts in the skin microbiome associated with disease flares and treatment in children with atopic dermatitis. Genome Res. 2012;22(5):850–9.

Edslev SM, Agner T, Andersen PS. Skin microbiome in atopic dermatitis. Acta Derm Venereol. 2020;100(12):adv00242.

Kim H, Alexander H, Um J, Chung B, Park CW, Flohr C, et al. Skin microbiome dynamics in atopic dermatitis: understanding host–microbiome interactions. Allergy Asthma Immunol Res. 2025;17(2):165–77.