Uncovering the molecular events associated with increased intestinal permeability in liver cirrhosis: The pivotal role of enterocyte tight junctions and future perspectives

摘要

To the Editor: We read with great interest the recently published research study by Dr. Du Plessis and colleagues on the role of intestinal macrophages in intestinal epithelial barrier dysfunction and hyperpermeability in patients with cirrhosis [1]. The authors demonstrated that decompensated liver cirrhosis was associated with the presence of significantly higher numbers of activated intestinal macrophages (CD33~+/CD14~+/Trem-1~+) expressing iNOS and secreting NO and IL-6, in conjunction with increased duodenal paracellular permeability and increased expression of the tight junction (TJ) protein Claudin-2. They speculated that activation of intestinal macrophages might represent an important molecular event implicated in the disruption of the intestinal epithelial barrier in cirrhosis through secretion of TJ-regulating factors such as NO and IL-6.