An important role in the endotoxin immobilization and transport from the intestine into the portal circulation belongs to the granulocytes which are likely able to transfer lipopolysaccharide to Kupffer cells. If the endotoxin diffusion into the mesenterial microvessels increases and (or) the portal circulation speed decreases, the interaction of lipopolysaccharide with granulocytes may become irreversible and facilitate the development of the systemic endotoxemia and the leucocyte-mediated liver damage. Intestinal flora endotoxin takes part in the liver damage pathogenesis in various forms of hepatitis, cirrhosis in various forms of hepatitis, cirrhosis and conditions followed by the circulation deficiency.