Pathophysiology of transfusion-related acute lung injuryLooney, Mark Ra,b,c; Gilliss, Brian Ma; Matthay, Michael Aa,bCurrent Opinion in Hematology: September 2010 - Volume 17 - Issue 5 - p 418–423 doi: 10.1097/MOH.0b013e32833c07d3 Hemostasis and thrombosis: Edited by George J. Broze Jr and Charles S. Abrams Buy Abstract Author InformationAuthors Article MetricsMetrics Purpose of review The purpose of this review is to summarize the recent experimental and clinical literature on the pathogenesis of transfusion-related acute lung injury (TRALI). Recent findings In both experimental and clinical TRALI, an immune priming step is generally necessary to produce lung injury. Experimental studies have used mainly lipopolysaccharide (LPS) as the priming step, whereas in clinical TRALI the specific priming events are currently being defined and include recent surgery and active infections. Experimental studies have modeled TRALI by using anti-major histocompatibility complex antibodies, antineutrophil antibodies, and also bioactive lipids isolated from stored human blood. A common theme among the experimental TRALI models is the central importance of neutrophils in mediating the early immune response and lung vascular injury. New work has focused on the interplay between neutrophils and platelets in the lung microcirculation. Finally, plasma mitigation strategies implemented in several countries are showing early promise in decreasing the incidence of TRALI from high plasma volume blood products. Summary TRALI requires an immune priming step followed by transfusion of a blood product with either leukocyte allo-antibodies or biological response modifiers. TRALI invokes an acute immune response dominated by neutrophils interacting with platelets and the lung endothelium. aCardiovascular Research Institute, USA bDepartment of Medicine, USA cDepartment of Laboratory Medicine, University of California, San Francisco, USA Correspondence to Michael A. Matthay, MD, 505 Parnassus Avenue, Room M917, San Francisco, CA 94143-0624, USA Tel: +1 415 353 1210; fax: +1 415 353 1990; e-mail: firstname.lastname@example.org © 2010 Lippincott Williams & Wilkins, Inc.