Abstract

To examine the existing animal models of transfusion-related acute lung injury (TRALI) for insight into disease pathogenesis. The data were taken from published research and from our own experimental results. Animal models have disproved the microaggregate theory of acute lung injury from blood transfusions. The two major hypotheses of TRALI, passively transfused neutrophil and human leukocyte antigen antibodies and biologically active lipids that accumulate in older, cellular blood products, have been replicated in animal models. The proposed two-hit model of TRALI is also supported by animal studies. A new in vivo mouse model of TRALI based on major histocompatibility complex (MHC) I antibodies has replicated several features of human TRALI, focusing prominently on the role of neutrophils. Experimental animal models support both the antibody and lipid theories of TRALI. The essential role of neutrophils to producing lung injury is common to all existing models of TRALI. There is a lack of clinically relevant animal models that explain why transfusion of donor antibodies to cognate antigens in the recipient does not always lead to TRALI.

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