Changes in the bacteria living in the mouth were consistently linked to inflammation in primary biliary cholangitis (PBC) and other autoimmune liver diseases, according to a study published recently in Clinics and Research in Hepatology and Gastroennterology.
The systematic review found that people with autoimmune hepatitis and PBC have distinct oral microbiome patterns compared with healthy individuals, supporting the idea of an “oral gut liver axis” that may influence liver damage.
“The evidence available so far suggests that the dysbiosis in oral microbiota may constitute a significant factor in immune-inflammatory processes of autoimmune liver diseases,” stated this study’s authors.
Researchers reviewed studies published between 2015 and 2021 that examined oral bacteria in patients with autoimmune liver disease. After screening 85 records from PubMed, Web of Science and Scopus, investigators included six observational studies involving 252 patients with autoimmune hepatitis and 345 healthy controls. One study also included a small subgroup of patients with PBC.
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Across studies, patients with autoimmune liver disease, including PBC, showed clear oral microbiota dysbiosis, meaning an imbalance in normal bacteria. The most consistent finding was an increase in Veillonella and, in the PBC subgroup, Eubacterium. At the same time, beneficial or common bacteria such as Streptococcus and Fusobacterium were reduced. These patterns were identified mainly through saliva testing using 16S rRNA sequencing and other molecular techniques.
Importantly for patients with PBC, these bacterial changes were not just laboratory findings. Higher Veillonella levels were associated with increased inflammatory markers in saliva, including interleukins IL 1β, IL 6, IL 8, IL 12p70, interferon γ, tumor necrosis factor α and IgA. Some studies found that the abundance of Veillonella correlated with measures of liver inflammation such as aspartate aminotransferase levels and overall disease activity. In contrast, Streptococcus appeared to show an opposite, potentially protective pattern.
Several studies also examined stool samples and intestinal tissue, showing reduced gut microbial diversity, increased opportunistic anaerobes and evidence of “leaky gut,” including higher lipopolysaccharide levels and altered tight junction proteins such as ZO 1 and occludin. These findings suggest that oral bacteria or their byproducts may travel to the gut and liver, contributing to immune activation through pathways involving Toll-like receptors and ongoing inflammation in PBC.
For patients living with PBC, this research does not yet change day-to-day treatment. It does not prove that mouth bacteria cause liver disease. However, it raises the possibility that saliva tests could one day help monitor disease activity, and that targeting the oral microbiome through improved dental care, probiotics or other therapies might complement existing medications. The oral gut liver axis may offer a new frontier in understanding and managing PBC.
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