Pathophysiology of transfusion-related acute lung injury

被引:43
作者
Looney, Mark R. [1 ,2 ,3 ]
Gilliss, Brian M. [1 ]
Matthay, Michael A. [1 ,2 ]
机构
[1] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Dept Med, San Francisco, CA USA
[3] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA
关键词
acute lung injury; neutrophils; platelets; transfusions; RED-BLOOD-CELLS; ANIMAL-MODELS; PLATELETS; PLASMA; ANTIBODIES; LIPIDS; INFLAMMATION; NEUTROPHILS; DONORS;
D O I
10.1097/MOH.0b013e32833c07d3
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:418 / 423
页数:6
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