Oral–gut bacterial transport drives chronic liver disease – Microbiology Research

Experiments in mice with CCl₄-induced liver and gut fibrosis confirmed that oral administration of patient-derived prtC⁺ Veillonella and Streptococcus inoculates worsens both gut barrier dysfunction (indicated by plasma levels of fatty acid binding protein 2 (FABP2)) and fibrotic disease severity compared with CCl₄ alone. Immunofluorescence studies showed that gut epithelia from prtC-exposed mice exhibited disrupted tight-junction architectures with cytoplasmic relocation of the tight junction proteins E-cadherin and occludin. These findings suggest that oral–gut translocation of collagenase-producing bacterial strains might promote ACLD progression by inducing gut barrier disruption, which could lead to further microbial translocation along the gut–liver axis (the leaky gut hypothesis) that exacerbates liver and intestinal fibrosis. Thus, targeting the oral microbiome might have a role in preventing ACLD progression.