Targeting the gut-liver axis in liver disease

Abstract

The gut-liver axis is widely implicated in the pathogenesis of liver diseases, where it is increasingly the focus of clinical research. Recent studies trialling an array of therapeutic and preventative strategies have yielded promising results. Considering these strategies, the armamentarium for targeting the gut-liver axis will continue to expand. Further clinical trials, translated from our current knowledge of the gut-liver axis, promise an exciting future in liver treatment.

Diet affects gut microbiota and modulates hospitalization risk differentially in an international cirrhosis cohort

“…However, the detailed impact of diet on the microbiota has not been studied systematically in liver cirrhosis. Cirrhosis is the end result of multiple hepatic insults that culminates in a significant disruption in the gut‐liver axis . As a result of impaired bile secretion and the generalized immunosuppressive state in advancing cirrhosis, gut microbiota proliferate and their products adversely impact the intestinal barrier, systemic inflammatory profile, and ultimately the prognosis .…”

Impact of Rifaximin Therapy on Ischemia/Reperfusion Injury in Liver Transplantation: A Propensity Score–Matched Analysis

“…Numerous studies indicate that inflammatory cells, such as neutrophils and macrophages, respond to bacterial products via nuclear factor kappa B and production of proinflammatory cytokines/chemokines, suggesting that these cells would be responsive to physiologically relevant levels of microbial products that reach the liver . Rifaximin directly affects bacterial growth, leading to a lower proinflammatory response . In a recent study examining patients with nonalcoholic fatty liver disease (NAFLD), 28 days of treatment with rifaximin was shown to exert beneficial effects in early clinical trials, lowering endotoxemia and reducing transaminases .…”

Origins of Portal Hypertension in Nonalcoholic Fatty Liver Disease

“…Intestinal decontamination by rifaximin in mice following bile duct ligation reduces liver fibrosis, angiogenesis, and PHT in association with diminished activation of the LPS/TLR4 pathway and fibronectin production, which is limiting the cross talk between HSCs and LSECs [69]. Thus, modulation of the gut-liver axis may prove to be a helpful strategy for preventing and managing NAFLDassociated PHT [70,71].…”