[The role of cell adhesion molecules and proinflammatory mediators in the pathogenesis of endotoxin adult respiratory distress syndrome].

The Gram-negative bacterial sepsis that is resistant to therapy results in the development of septic shock and the multiple organ dysfunction syndrome (MODS). It is established that the adult respiratory distress syndrom (ARDS) as a component of MODS is the reason for high mortality in these patients. The basic pathogenetic link between ARDS and the septic shock are the lesions of the alveolo-capillary membrane. They result from the sequestrated neutrophil cells in the lungs. Neutrophil extravasation is manifested by the following steps (stages): 1) weak initial adhesion; 2) rolling; 3) stable adhesion; and 4) extravasation. These processes are mediated by cell adhesion molecules that belong to four classes: selectins, selectin ligands, integrins and immunoglobulin superfamily. Thus cell adhesion molecules mediate the sequestration of neutrophil cells in the lungs and the damage of the pulmonary surfactant system.