[ The intestine-liver-lung axis in septic syndrome]

Abacteremic sepsis is frequent in intensive care units, and is closely associated with the development of adult respiratory distress syndrome (ARDS) and multiple systems organ failure (MSOF). It carries a high mortality. The gut is thought to be the "motor" of such septic states and the first step of a "gut-liver-lung axis". Shock of any type or sepsis can by themselves lead to increased permeability of the intestinal mucosal barrier. This, in turn, may promote bacterial translocation, i.e. the passage of bacteria or bacterial products such as endotoxin from the lumen of the gut into the portal bloodstream. When such products reach the liver, activation of Küpffer cells occurs, resulting in the secretion of pro-inflammatory and hypotensive mediators. The latter are mainly the tumor necrosis factor-alpha and interleukins-1 and -6. These substances trigger many biologic cascades, and may explain the development of abacteremic septic states and MSOF. The mediators cause binding of polymorphonuclear neutrophils to pulmonary endothelial cells, and their degranulation. In addition, they activate local and systemic coagulation mechanisms. This explains the morphological changes observed in early sepsis-induced ARDS, i.e. pulmonary edema, vascular thrombosis and hemorrhages. Studies are currently in progress in an attempt to limit bacterial and endotoxin translocation and the action of the mediators.