Background: Transfusion-related acute lung injury (TRALI) is a serious post-transfusion respiratory syndrome. However, the underlying pathophysiology of TRALI remains obscure. Fibrin deposition in lung is not only the pathological feature of lung inflammation but also plays a pathogenic role in destroying the vascular endothelial structure and inhibiting the alveolar surfactant. Nevertheless, the role of the fibrin in TRALI has never been reported.

Aims: To determine whether fibrin deposition in lung participates in the progress of TRALI.

Methods: Eight-to-ten weeks male Balb/c mice were primed with lipopolysaccharide（LPS）18 h prior to challenge with an anti-MHCI mAb or isotype control antibody administrated into the tail vein.The characteristics of TRALI were assessed by the ratio of pulmonary wet to dry (W/D) and lung tissue histology score. Immunofluorescent staining assay and corresponding mean optic density (MOD) were used to evaluate fibrin deposition in lung.

Results: Compared with control mice, TRALI group mice displayed a significant increase in lung W/D ratio(P< 0.05). In addition, increased alveolar septal thickening, exudated indicating edema intra-alveolar polymorphonuclear leucocyte infiltration and high lung tissue histology score（P< 0.05）were observed in TRALI mice. Moreover, we found that upon TRALI induction ,the fibrin deposition in lung was significant and the MOD obviously upregulated in mice（P< 0.01）.

Conclusions: Our results suggest that the presence of fibrin deposition in lung is involved in TRALI pathological responses, possibly resulting from excess activation of the coagulation cascade or decreased fibrinolysis. Further studies are needed to prove the hypothesis.

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ISTH Congress Abstracts - https://abstracts.isth.org/abstract/fibrin-deposition-in-mouse-transfusion-related-acute-lung-injury-via-coagulation-or-fibrinolysis-dysfunction/