Dr Naiara Beraza contributed to a new study led by the Technical University of Munich (TUM) and King’s College London that has found strong evidence that bacteria from the mouth migrate to the gut in chronic liver disease and exacerbate the disease.

Each year, more than two million people die from advanced chronic liver disease (ACLD). Previous research has linked gut microbiome disruptions to this condition and suggested that bacteria typically found in the mouth may colonise the gut.

A new study published in the journal Nature Microbiology shows that identical bacterial strains occur in both the mouth and gut of patients with advanced chronic liver disease and also reveals a mechanism by which oral bacteria affect gut health. The researchers also found that this process coincides with worsening liver health.

Researchers analyzed bacterial populations in saliva and stool samples from 86 patients. The team found that both the gut and oral microbiome undergo significant changes as liver disease worsened, where changes of the oral microbiome were detectable already at earlier disease stages.

In healthy individuals, bacterial communities differ substantially between body sites. In patients with liver disease, however, oral and gut microbiomes became increasingly similar as the disease progressed and nearly identical bacterial strains were recovered from the mouth and gut of patients.

“These strains are typically found in the mouth and are rarely present in the healthy gut. However, we observed increases in the absolute abundances of these oral bacteria in patients with advanced chronic liver disease. This strongly suggests that these bacteria translocate from the mouth and colonise the gut,” explains Melanie Schirmer, Professor of Translational Microbiome Data Integration at TUM.

The team identified several oral bacterial species that colonized patients’ guts. They also found evidence that higher levels of these bacteria in stool samples were associated with damage to the intestinal barrier.

“To investigate this link, we performed a gene analysis,” says Shen Jin, one of the study’s first authors. “We discovered that these bacteria carry genes encoding collagen-degradation enzymes.” The team confirmed these enzymes were active by testing isolated bacteria from stool samples and synthesizing the enzyme. “Collagen breakdown can compromise the gut barrier, potentially allowing bacteria and bacterial products to reach other organs, such as the liver. We believe this may worsen the disease,” explains Aurelie Cenier, a doctoral researcher and co-first author.

Experiments in a mouse model for liver disease supported this hypothesis: introducing these bacteria from human patients exacerbated gut barrier damage and worsened liver fibrosis.

“Our findings open potential new therapeutic strategies for people with advanced chronic liver disease. Protecting or restoring the gut barrier could help slow disease progression. Targeting the oral microbiome offers a way to positively influence the course of the disease and prevent clinical complications,” says Dr. Vishal Patel from King’s College London.

The study also suggests a new diagnostic approach. The team examined the bacterial gene involved in collagen degradation in more detail. Its abundance in stool samples could serve as a future disease marker. In the study, this marker reliably distinguished sick individuals from healthy ones.

“Our findings in preclinical models have demonstrated the active contribution of oral microbes in promoting liver disease progression” said Dr Naiara Beraza.

“These studies have also allowed us to better define the mechanisms mediating the detrimental effects of these oral microbes when they translocate to the gut in chronic liver disease patients. This wealth of knowledge is invaluable to inform the development of future therapeutic strategies to treat chronic liver disease targeting the oral microbiome”.

Reference: Microbial collagenase activity is linked to oral–gut translocation in advanced chronic liver disease, Jin, S., Cenier, A., Wetzel, D. et al. Nature Microbiology 11, 211–227 (2026). DOI: 10.1038/s41564-025-02223-0