Neutrophils and their Fcγ receptors are essential in a mouse model of transfusion-related acute lung injury

被引:247
作者
Looney, Mark R.
Su, Xiao
Van Ziffle, Jessica A.
Lowell, Clifford A.
Matthay, Michael A.
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 94143 USA
[3] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA
[4] Univ Calif San Francisco, Dept Anesthesia, San Francisco, CA 94143 USA
关键词
D O I
10.1172/JCI27238
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Transfusion-related acute lung injury (TRALI) is the most common cause of transfusion-related mortality. To explore the pathogenesis of TRALI, we developed an in vivo mouse model based on the passive transfusion of an MHC class I (MHC I) mAb (H2K(d)) to mice with the cognate antigen. Transfusion of the MHC I mAb to BALB/c mice produced acute lung injury with increased excess lung water, increased lung vascular and lung epithelial permeability to protein, and decreased alveolar fluid clearance. There was 50% mortality at a 2-hour time point after Ab administration. Pulmonary histology and immunohistochemistry revealed prominent neutrophil sequestration in the lung microvasculature that occurred concomitantly with acute peripheral blood neutropenia, all within 2 hours of administration of the mAb. Depletion of neutrophils by injection of anti-granulocyte mAb Gr-1 protected mice from lung injury following MHC I mAb challenge. FcR gamma(-/-) mice were resistant to MHC I mAb-induced lung injury, while adoptive transfer of wild-type neutrophils into the FcR gamma(-/-) animals restored lung injury following MHC I ntAb challenge. In conclusion, in a clinically relevant in vivo mouse model of TRALI using an MHC I mAb, the mechanism of lung injury was dependent on neutrophils and their Fc gamma receptors.
引用
收藏
页码:1615 / 1623
页数:9
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