Endotoxemia and gut barrier dysfunction in alcoholic liver disease.

摘要

A growing body of evidence indicates that endo toxemia is closely associated with alcoholic liver disease (ALD). Endo toxins stimulate different cells in the liver releasing cytokines, chemokines, and reactive oxygen species (ROS) by toll-like receptor-4 (TLR-4)-mediated mechanisms. Intestinal microflora is the source of circulating endotoxins, and the gut barrier dysfunction leading to elevated intestinal permeability is considered the main cause of endotoxemia in ALD. The mechanism of ethanol-induced gut barrier disruption is an active area of investigation. Evidence indicates that intestinal microflora, the metabolism of ethanol, and acetaldehyde-in-duced cell signaling are involved in ethanol-induced intestinal barrier dysfunction. Recent advances in alcoholic endotoxemia, the mechanism of epithelial barrier disruption, and the factors that prevent alcoholic endotoxemia are discussed in this article. The current understanding of these issues is illustrated in Fig. 1.