Introduction Transarterial chemoembolization (TACE) remains one of the most important treatments for unresectable hepatocellular carcinoma, but its clinical benefit is often limited by post-procedural liver injury. Traditionally, this injury has been attributed mainly to ischemia and chemotherapy-related damage to non-tumoral liver tissue.
Introduction
Transarterial chemoembolization (TACE) remains one of the most important treatments for unresectable hepatocellular carcinoma, but its clinical benefit is often limited by post-procedural liver injury. Traditionally, this injury has been attributed mainly to ischemia and chemotherapy-related damage to non-tumoral liver tissue. However, this explanation does not fully account for the variability in liver injury seen after TACE, suggesting that additional biological mechanisms are involved. This study explores whether disruption of the gut microbiota contributes to TACE-related liver injury.
Problem Statement
TACE-induced liver injury is a common complication that can compromise tolerance to repeated treatment and adversely affect long-term survival. Although direct hepatic injury is well recognized, the role of the gut–liver axis in this setting has remained poorly understood. Identifying modifiable microbial mechanisms could open a new strategy to reduce post-TACE complications and improve outcomes in HCC.
Summary
This study shows that TACE is associated with significant gut microbiota disturbance, and that this disturbance is not merely an epiphenomenon but a contributor to liver injury. In both rats and patients, TACE reduced the abundance of Limosilactobacillus reuteri and lowered levels of its tryptophan-derived metabolite indole-3-lactic acid (ILA). Lower levels of both were associated with more severe liver injury and poorer overall survival. Importantly, administration of live L. reuteri or ILA significantly reduced TACE-induced liver injury. Mechanistically, ILA suppressed macrophage-driven inflammation by inhibiting the HSP90–NLRP3 inflammasome pathway. This work identifies a novel microbiota-mediated mechanism of TACE toxicity and suggests that microbial or metabolite supplementation may become a practical adjunct to improve safety and prognosis in patients undergoing TACE.
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