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An animal model of transfusion‐related acute lung injury and the role of soluble CD40 ligand
Author(s) -
Hu Ai,
Chen Weiyun,
Wu Shubin,
Pan Boju,
Zhu Afang,
Yu Xuerong,
Huang Yuguang
Publication year - 2020
Publication title -
vox sanguinis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.68
H-Index - 83
eISSN - 1423-0410
pISSN - 0042-9007
DOI - 10.1111/vox.12895
Subject(s) - transfusion related acute lung injury , bronchoalveolar lavage , medicine , proinflammatory cytokine , lung , evans blue , red blood cell , blood transfusion , cytokine , immunology , anesthesia , inflammation , pulmonary edema
Background and objectives Transfusion‐related acute lung injury (TRALI) is a life‐threatening complication of transfusion and is one of leading causes of transfusion‐associated fatalities. However, the pathogenesis of TRALI is still unclear. Soluble CD40 ligand (sCD40L) is a proinflammatory cytokine that accumulates during blood component storage and is involved in transfusion reactions. The objective of this study was to establish a clinically relevant TRALI animal model and to evaluate the role of sCD40L in TRALI. Materials and methods Rats’ red‐blood‐cell (RBC) suspensions were prepared, and the quality of RBC was evaluated. A trauma–haemorrhage–transfusion strategy was applied to build the animal model. Lung oedema was evaluated by histopathology examination, total bronchoalveolar lavage fluid (BALF) protein concentration, Evans blue dye (EBD) leakage and inflammatory cytokines. The sCD40L concentrations were measured. Results Storage lesions of RBCs gradually increased over time. Obvious histological evidence of lung injury of rats transfused with a 35‐day RBC was observed. The total BALF protein concentration, EBD leakage, inflammatory cytokines concentration were increased significantly in the Day 35 group. The sCD40L concentration increased significantly in the storage RBC suspension over time but was slightly elevated in rat plasma. Conclusions These findings indicated successful establishment of a TRALI animal model with trauma–haemorrhage–transfusion, in which sCD40L may play a minor role in the development of TRALI.

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