Leukocyte antibodies and biologically active mediators in the pathogenesis of transfusion-related acute lung injury

Abstract

Transfusion-related acute lung injury (TRALI) is a clinical constellation of signs and symptoms associated with transfusion. In severe cases, the most prominent feature is acute onset of pulmonary edema. Two mechanisms have been advanced to explain pulmonary injury in this syndrome. One mechanism involves the presence of antibodies to white blood cells, usually in a transfused blood component. Interaction of antibodies, with white blood cells in the transfusion recipient, is hypothesized to cause cellular activation with release of cytokines resulting in pulmonary vascular endothelial damage and exudation of fluid across the pulmonary basement membrane. In the biologically active mediator mechanism, two events are hypothesized to cause TRALI. In the first event, polymorphonuclear cells become primed and pulmonary vascular endothelium becomes activated secondary to the production of biologically active mediators, as a result of physiologic stress. The second event is the infusion of biologically active mediators in a stored cellular blood product. The second event causes release of cellular activators with subsequent endothelial damage and exudation of fluid into the pulmonary alveoli.