Gut microbiota links to infection in liver transplantation

PURPOSE OF REVIEW: Infectious complications remain a major source of morbidity and mortality following liver transplantation, with Enterococcus spp. and Enterobacterales among the most common causative pathogens. Increasing evidence suggests that the intestinal microbiota plays a central role in regulating susceptibility to these infections through maintenance of colonization resistance, epithelial barrier integrity, and host immune signaling. RECENT FINDINGS: Patients with end-stage liver disease frequently develop intestinal dysbiosis characterized by reduced microbial diversity, depletion of obligate anaerobes, and expansion of pathobionts prior to transplantation. Liver transplantation further exacerbates these disruptions through perioperative antibiotics, surgical injury, ischemia-reperfusion injury, altered bile acid metabolism, and immunosuppressive therapy. Recent studies have demonstrated associations between loss of microbial diversity, depletion of beneficial microbial metabolites, including short-chain fatty acids and secondary bile acids, and subsequent postoperative infections in liver transplant recipients. These findings suggest that the microbiome may function both as a mechanistic mediator and biomarker of infection risk. SUMMARY: Mechanisms of colonization resistance, microbiome-mediated maintenance of the intestinal barrier, and the emergence of pathobiont domination, are critical in the development of infection following liver transplant and requires strategies to diagnose and therapeutically restore microbiome function to avoid infection.