Roles of the neutrophil and other mediators in adult respiratory distress syndrome

Abstract

The adult respiratory distress syndrome (ARDS) and transfusion-related acute lung injury (TRALI) are characterized by diffuse, acute lung injury. Most likely, TRALI is a type of ARDS although it is associated with a much lower morbidity and mortality than found with classic ARDS. For years, the pathogenesis of ARDS has been explained by the complement hypothesis in which pulmonary neutrophilic sequestration and degranulation follow complement-mediated neutrophil chemotaxis. A definitive role for the neutrophil in diffuse, acute lung injury, however, has not been established. Although numerous chemoattractants for neutrophils are generated in the lungs and, through degranulation and formation of toxic oxygen free radicals, the neutrophil is fully capable of causing tissue injury, substantial evidence refutes the requirement for neutrophils in diffuse, acute lung injury. Other potential factors in the pathogenesis of ARDS include primary endothelial cell injury, alveolar macrophage activity, and hemostatic disorders.