Compromise of α-Defensin Function in Liver Cirrhosis Facilitates the Toxic Relationship Between Gut Permeability and Endotoxemia

Excerpt

Innate and adaptive immune dysfunction, also referred to as cirrhosis-associated immune dysfunction syndrome (CAIDS), is a major component of liver cirrhosis (LC), substantially contributing to the pathogenesis of the acute and chronic deterioration of liver function [1]. In advanced LC with CAID, small intestinal bacterial overgrowth (SIBO) and increased intestinal permeability (IP) are frequent findings linked to the translocation of bacteria and bacterial components such as endotoxin (lipopolysaccharide; LPS) from gut lumen to the systemic circulation, termed bacterial translocation (BT) [2]. BT is presumed to be the major mechanism leading to the development of spontaneous infections in liver cirrhosis, occurring in up to 30% of patients with decompensated LC, associated with a high mortality [3]. Despite the significant clinical burden, the precise underlying cellular and molecular pathways implicated in the phenomenon of BT in LC have not yet been studied. …