The gastrointestinal (GI) barrier is a highly coordinated, multilayered defence system
that maintains intestinal homeostasis by separating the luminal microbiota from the internal milieu. In liver cirrhosis, this barrier undergoes profound structural and functional disruption, emerging as a central driver of bacterial translocation and infection-related complications. Among these, spontaneous bacterial peritonitis (SBP) represents a major determinant of morbidity, mortality, and disease progression. Barrier failure in cirrhosis is not attributable to a single defect but results from the convergence of multiple interconnected mechanisms. Structural alterations include disruption of epithelial tight junctions and deterioration of the mucus layer, leading to increased intestinal permeability and loss of spatial compartmentalisation. These changes are compounded by microbial dysbiosis,characterised by reduced diversity, depletion of short-chain fatty acid-producing taxa, and expansion of pathobionts. In parallel, cirrhosis-associated immune dysfunction impairs both mucosal and systemic antimicrobial defences, while gut–vascular barrier disruption facilitates systemic dissemination of bacteria and microbial products. The resulting increase
in bacterial translocation plays a pivotal role in the pathogenesis of SBP and contributes to systemic inflammation, circulatory dysfunction, and acute decompensation. Importantly, this process establishes a self-amplifying pathogenic loop in which barrier dysfunction, dysbiosis, and immune dysregulation mutually reinforce each other. Recent advances have identified key molecular pathways involved in barrier regulation, including bile acid–FXR signalling and microbiome-derived metabolites, providing novel targets for therapeutic intervention. While current management relies largely on antibiotics and supportive care, emerging strategies aim to restore barrier integrity and modulate the gut–liver axis.
A deeper understanding of GI barrier dysfunction offers new opportunities to prevent
bacterial translocation and improve clinical outcomes in patients with liver cirrhosis.