The Reverse Gut-Skin Axis: How Your Skin Affects Your Microbiome

The short answer

For years, researchers focused on how the gut microbiome affects the skin. New research is now showing the conversation runs both ways. A 2024 study in Nature Communications found that when the skin is injured, scratched or inflamed, fragments of a sugar molecule called hyaluronan are released. These fragments travel to the gut and change the behaviour of intestinal bacteria, which then affects gut immunity.

In plain English: a flare on your skin can ripple through to your gut and shift the microbes living there. It’s a reverse axis, and it has big implications for anyone living with eczema or other chronic skin conditions.

One important note. This is a fast-moving area of science. The cleanest evidence so far comes from mouse studies. The human picture is more indirect and will need more clinical work to confirm. What follows is my best read of the current peer-reviewed research, not a finished story.

Why I’m writing this

I’ll admit something. After more than 30 years of living with eczema, raising three kids (two of whom flare regularly) and reading every research paper I could find on the microbiome, I thought I had a handle on it. I knew that what was happening inside my gut influenced my skin. That was the story I told myself and the story I’d been telling Salvida customers.

Then I scrolled past a post by @marievollmar on Instagram. She broke down a piece of research I had completely missed. Not only does the gut affect the skin, the skin affects the gut. Skin inflammation, skin wounds, even the scratch-itch-scratch cycle so familiar to anyone with eczema, can change what’s happening in the gut microbiome.

I sat there a little stunned. Three eczema kids, decades of personal flares and I didn’t know it worked in reverse.

That’s the whole reason I made Salvida and the Skin-ED blog. There’s always more to learn, and the moment you stop learning is the moment you stop helping. So this article is me catching up on something I didn’t know, and bringing you along.

Big credit to Marie. If you’re not already following her on Instagram, she’s the kind of educator who turns dense research into something you can actually use. This article wouldn’t have happened without her post.

If you want the other half of the picture, my companion article on how the microbiome affects the skin walks through the more familiar direction of the axis. Read both. They make more sense together.

My quick eczema backstory (so you know where I’m coming from)

I had eczema starting as a baby until my mid-twenties. The classic itchy patches on the inside of my elbows and behind my knees that flared whenever I was stressed, hot or wearing the wrong fabric. It calmed down in my late-twenties but in a gradual way that mostly escaped my attention until one day it was just gone. I thought I had simply outgrown it.

A few years of reprieve and then when I got pregnant for the first time it came back. Thankfully it cleared shortly after, but during my second pregnancy it came back. My GP put me on probiotics, predominantly for the baby. I didn’t really understand why at the time, I just did as I was told because pregnancy is exhausting and I’d take any small win. Same thing happened with my third pregnancy. Probiotics again. So no probiotics with my eldest, who’s 15 now, still has eczema that needs to be actively managed. The two younger ones flare too, but less often and less severely. It is not proof of anything. It is, however, consistent with the published perinatal probiotic trials, and it sits in the back of my mind.

For years I framed this as ‘the gut is upstream, the skin is downstream’. Fix the gut, calm the skin. That framing isn’t wrong, but it’s incomplete. What the latest research is showing is that the relationship runs both ways. When my kids scratch a patch into a raw mess, that physical disruption to the skin sends signals down to their gut. And the gut, already a little reactive in eczema families, then sends signals back. It’s a feedback loop, not a one-way street.

What the new research actually found

The paper that flipped my understanding is Dermal injury drives a skin-to-gut axis that disrupts the intestinal microbiome and intestinal immune homeostasis in mice, published in Nature Communications in April 2024 by researchers in the lab of Richard Gallo at UC San Diego.

Here’s the short version of what they did and what they found:

1. They wounded the skin of mice in controlled ways (scrapes, abrasions). Nothing severe, just enough to mimic what happens in a real-world skin flare.
2. They tracked what happened in the gut. Within days, the microbial composition of the mouse intestines changed. Some bacteria became more abundant, others less, and the behaviour of those microbes shifted too.
3. They identified the messenger. When the dermis is disrupted, it releases fragments of a molecule called hyaluronan (often called hyaluronic acid in skincare circles). These fragments don’t just stay at the site of injury. They circulate.
4. The hyaluronan fragments turned up in the colon, where they triggered the colon cells to ramp up two host defence genes called Reg3 and Muc2. Those genes tell the gut lining to produce more mucus and antimicrobial peptides. The gut, in effect, was responding to a skin injury as if it were under threat.
5. The microbiome shifted to a more inflammatory profile. When the researchers then chemically induced colitis (gut inflammation) in those same mice, the colitis was worse than in mice without skin wounds. Their guts had been ‘primed’ for inflammation by the skin event.
6. Antibiotics and germ-free mice rescued the effect. When the researchers wiped out the gut bacteria with antibiotics, or used mice that had no gut bacteria to begin with, the skin-to-gut effect was much weaker. That tells us the microbiome is the mechanism, not just a bystander.

The headline finding: damage to the skin can disrupt the gut microbiome and prime the gut for inflammation. The skin and the gut are not separate systems. They are talking constantly, in both directions, and the messenger molecules are turning out to be things we already knew (like hyaluronan) but with a job description we didn’t fully appreciate.

This is animal research. Mouse models often translate to humans, but not always cleanly. The pathway needs more human clinical studies before it becomes settled medicine, and those studies are now underway. I’ll update this article as they land.

Why this matters for eczema-prone families

Sit with this for a minute. People with eczema:

• Have a compromised skin barrier (skin is easier to disrupt).
• Often scratch, which physically wounds the skin.
• Tend to flare, which is essentially repeated cycles of inflammation and barrier damage.

If the Nature Communications findings translate to humans (and the early human evidence is consistent, though more research is needed), it means that:

• Every flare may be sending inflammatory signals to the gut.
• A more inflamed gut microbiome can then send more inflammatory signals back up to the skin.
• The feedback loop is part of why chronic eczema can feel so hard to break out of.

This also helps explain something a lot of eczema families notice. Gut issues and skin issues seem to track together. The same kid who has eczema often also has reflux, food sensitivities, tummy aches or constipation. Researchers used to assume the gut symptoms came first. The reverse axis says it’s not that simple. Sometimes the skin flare is feeding the gut symptoms.

How the skin talks to the gut (the four main pathways)

The Nature Communications paper is the cleanest demonstration of skin-to-gut signalling, but it’s not the only mechanism. Here’s what the broader literature describes.

1. Hyaluronan fragments (the messenger I didn’t know about)

Hyaluronan (HA) is a large sugar molecule that sits in the dermis. When the skin is healthy, it’s mostly in large, stable forms. When the skin is wounded or chronically inflamed, enzymes break HA into smaller fragments. These fragments are biologically active. They circulate. They reach the colon. They tell the gut to mount a defence response. They appear to be the molecular link between a skin event and a gut response.

Translation: the same hyaluronic acid that lots of skincare products advertise as ‘hydrating’ is, in its fragmented form, a stress signal that the body sends from skin to gut.

2. Systemic inflammatory signals (cytokines)

When the skin is inflamed, immune cells release signalling proteins called cytokines (IL-4, IL-13, TNF-alpha and others). These don’t stay local. They circulate through the bloodstream and reach the gut, where they can shift the immune environment and change which bacteria thrive.

3. Disrupted skin microbiome → systemic effects

The skin has its own microbiome. When that microbiome shifts (for example when Staphylococcus aureus overgrows on eczema-prone skin), the skin barrier becomes more permeable, more bacterial fragments cross into the bloodstream, and the immune system tilts inflammatory. That tilt then influences the gut.

4. The itch-scratch-flare cycle (behaviour matters too)

Scratching damages skin. Damaged skin releases the inflammatory signals above. There’s also a behavioural and sleep impact (eczema kids and adults often sleep badly, and bad sleep wrecks gut health). It’s all connected.

What this research changes (and what it doesn’t)

I want to be careful here. The reverse axis research hasn’t changed my day-to-day eczema practices. It has validated them. The things I was already doing for skin (protect the barrier, settle small patches before they snowball, cut the fragrance, run the humidifier, keep the nails short) now have a second reason behind them: every flare prevented is one less inflammatory pulse heading to the gut.

Here is how the findings line up with the approaches I already use, and why they feel more important now:

• Treating early flares seriously. A small patch caught early stops the cycle before it ramps up the systemic signals. The reverse axis says those signals reach further than we used to think.
• Breaking the scratch cycle. Cutting nails, wet wraps overnight, distraction techniques, whatever it takes. Every uninterrupted scratching session is a dermis disruption, which means hyaluronan fragments in circulation.
• Treating fragrance, harsh washes and rough fabrics as systemic issues, not just skin issues. Anything that irritates the skin is also, indirectly, irritating the gut.
• Keeping up with the gut work too. Fibre diversity, fermented foods, sleep, stress (see the companion article on the gut-to-skin direction). The reverse axis doesn’t replace the original axis. It joins it.

This is a feedback loop, not a hierarchy. Both ends matter. The reverse axis just adds extra weight to barrier protection.

The honest takeaway

Three things stayed with me after I read this research:

1. Calming a flare from the outside isn’t just about comfort. It’s about reducing the systemic signals that the skin sends to the gut. Settling skin is part of settling the immune system.

2. The skin barrier is the front door of the whole system. A breach there is felt in places you can’t see.

3. There is always more to learn. I’ve had eczema for decades, raised three kids with eczema, read more papers than I can count, and I still missed this entire mechanism until Marie’s post popped up on my feed. Be kind to yourself if you feel like you’re behind. We are all catching up.

And the honest caveat. This is still emerging research, and it requires further studies to validate it and to better understand the complex pathways that exist within our bodies. I am sharing my interpretation of the current peer-reviewed literature. The picture will keep getting sharper. When it does, I will update this article.

How this shaped Salvida

I made Salvida because I wanted products I could trust on my own family. The reverse axis research has made me more confident, not less, in what I built. Here’s why.

Everything in the Salvida range is built around one idea: protect the barrier, calm the surface, reduce the chance of a flare in the first place. The reverse axis research adds a new reason to take that seriously. Every flare prevented is one less inflammatory pulse heading to the gut.

• Barrier NPR+ balm is the heavyweight for stubborn patches. It seals in moisture so the skin can stop losing water and start to settle and repair. Less disruption to the dermis means fewer hyaluronan fragments in circulation. That matters.
• Bodyguard moisturising lotion is the daily layer my whole family uses. Fragrance-free, dye-free, essential-oil-free. The goal is fewer triggers, not more.
• Every Day, Everywhere face and body wash replaces the fragranced washes that strip the barrier. Cleansing should not be a flare trigger.

I am not claiming these products fix the gut microbiome. They can’t, and any brand that says otherwise should be rightfully questioned. What they can do is reduce one major source of barrier damage and inflammation, which on the reverse axis matters more than I previously realised.

A note on the evolving science

The skin-to-gut axis is one of the newest frontiers in immunology and dermatology. The findings discussed here are my interpretation of current peer-reviewed research, primarily a 2024 mouse study with supporting mechanistic work in humans. More clinical research is needed to confirm how directly the findings translate to people. I will update this article as the science updates.

Further reading (the sources I leaned on)

Marie’s post pointed me here, the papers did the rest:

• Dermal injury drives a skin-to-gut axis that disrupts the intestinal microbiome and intestinal immune homeostasis in mice (Nature Communications, 2024)
• The gut-skin axis: a bi-directional, microbiota-driven relationship with therapeutic potential (Gut Microbes, 2026)
• Skin Microbiome in Health and Disease: Mechanisms and Emerging Therapeutic Strategies (PMC, 2024)
• The skin microbiome: impact of modern environments on skin ecology, barrier integrity and systemic immune programming (PMC)
• Eczema Support Australia: understanding flares
• @marievollmar on Instagram (where this all started for me)

What I’d read next

• How your microbiome shapes your skin (the other half of the axis)
• What causes eczema flare-ups: the 10 triggers I wish I’d known about
• Why fragrance-free really matters for sensitive skin

One last thing

If this article has taught me anything, it’s to stay humble. I’ve lived with eczema since I was a kid. I’ve raised three children, two of whom still flare, and I’ve read more research papers than I’d care to admit. And yet I still got blindsided by an Instagram post and a paper I hadn’t seen. That’s a good thing. It means the science is moving, and the way we look after our kids and ourselves can get better.

Thank you Marie for the post that made me sit up. And thank you to every customer who has shared their family’s story with me. Salvida exists because of those conversations. I made it so I had products I could trust to use on my own family, and I keep going because I learn something new from this community every week.

Send me an email or a DM any time. I read every single one.

Jacqui x

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