Could a probiotic help strengthen the gut in ACLD?

24 February 2026

In advanced chronic liver disease (ACLD), the damage isn’t confined to the liver itself. Deep in the gut, a quiet breakdown is often underway.

As disease progresses, the balance of bacteria in the gut shifts. The protective lining of the intestine becomes weaker, inflammation increases, and together, these changes can drive complications that lead to hospital admission and, in the most serious cases, organ failure.

Now, new research led by Dr Maria-Emanuela Maxan at the Roger Williams Institute of Liver Studies suggests targeting the gut microbiome may offer a promising new approach.

Published today in The International Journal of Pharmaceutics, the study explores how a multi-strain probiotic could help influence the gut environment in advanced liver disease.

Strengthening the body's essential filter

The liver and the gut are closely connected. When the gut barrier is strong, it acts as a filter, preventing harmful bacteria and toxins from entering the bloodstream. But in ACLD, that barrier can become ‘leaky’.

At the same time, the mix of bacteria in the gut changes in ways that promote inflammation. This combination of microbial imbalance and immune activation is thought to play a key role in disease progression.

That’s why researchers are increasingly asking the same important question: if we can restore balance in the gut, could we help protect ACLD patients from further harm?

Testing a probiotic in a lifelike gut model

To explore this, Dr Maxan and her team used an advanced lab model that recreates key features of the human gut. They introduced faecal samples from people with alcohol-related ACLD, then treated the system with a live, multi-strain probiotic preparation.

Over 48 hours, they closely monitored what happened and found encouraging results.

The probiotic altered the composition of gut bacteria in a positive way. Markers of gut barrier strength improved, suggesting tighter junctions between cells and better protection against leakage. And the team also observed faster wound healing in intestinal cells exposed to the probiotic.

There were also changes in immune signalling. Anti-inflammatory molecules increased, while several pro-inflammatory mediators fell. Production of beneficial short-chain fatty acids (compounds known to support gut health) also improved.

Taken together, the findings point to a shift towards a healthier, more resilient gut environment.

From lab insight to clinical trials

It’s important to be clear about what this study does and does not show.

The work was carried out in a sophisticated laboratory model rather than in patients themselves, involving samples from a small number of donors. This means the results aren’t ready to be translated directly into clinical practice.

However, the mechanistic data is strong. It gives us a clear scientific rationale for testing this probiotic approach in people with ACLD through carefully-designed clinical trials.

For a condition where treatment options are limited and complications can escalate quickly, that’s a vital piece of progress.

Rethinking treatment beyond the liver

Dr Maxan’s study reflects a broader shift in liver research. Instead of focusing only on the damaged liver itself, scientists are increasingly looking at the whole gut-liver axis and how different organs interact.

By combining expertise in microbiology, immunology and advanced in vitro modelling, the Roger Williams Institute of Liver Studies continues to lead the way in translating complex science into real treatment possibilities.

If future trials confirm the study’s findings, modulating the gut microbiome could one day become an integral part of managing ACLD.

“This study helps us move from theory to evidence. We can now see, in a controlled setting, that modulating the microbiome has measurable biological effects. That’s a really strong foundation to now take into clinical trials.”
– Dr Maria-Emanuela Maxan, The Roger Williams Institute of Liver Studies

Click here to read the paper in full. Abstract below:

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