Supragingival Actinomyces naeslundii aggravates metabolic dysfunction-associated fatty liver disease via the oral–gut axis

TL;DR

This study shows that a specific oral bacterium, Actinomyces naeslundii, may worsen fatty liver disease by affecting gut health in mice.

Contribution

The study identifies Actinomyces naeslundii as a novel oral bacterium linked to the progression of MAFLD through the oral–gut axis.

Findings

Patients with MAFLD had reduced oral microbial diversity and altered composition compared to healthy individuals.

Actinomyces naeslundii was enriched in MAFLD patients and correlated with disease severity.

Administering A. naeslundii to mice worsened MAFLD and caused gut dysbiosis on a high-fat diet.

Abstract

Metabolic dysfunction-associated fatty liver disease (MAFLD) is the most prevalent chronic liver disease but lacks effective therapies. Oral microbial dysbiosis is closely associated with metabolic dysfunction.

This study aimed to delineate MAFLD-specific oral microbiota signatures and identify diagnostic biomarkers.

Supragingival plaque samples from 21 patients with MAFLD and 20 healthy individuals were subjected to metagenomic sequencing. Potential oral biomarkers were identified bioinformatically and further validated using a MAFLD mouse model.

Patients with MAFLD exhibited significantly reduced supragingival microbial diversity, altered composition, and enhanced consortial interactions compared to healthy individuals. Seven resident oral species were identified as candidate biomarkers. Among these, Actinomyces naeslundii was notably enriched in the oral cavity of patients with MAFLD and strongly correlated with clinical indices. In vivo experiments further demonstrated that the oral administration of A. naeslundii significantly aggravated MAFLD phenotypes and induced gut dysbiosis in mice fed a high-fat diet.

This study reveals a potential link between the oral microbiota and MAFLD. Specifically, the excessive enrichment of the oral resident bacterium A. naeslundii is associated with the MAFLD progression in mice.

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