Platelet depletion limits the severity but does not prevent the occurrence of experimental transfusion‐related acute lung injury

Transfusion ◽  
2020 ◽  
Vol 60 (4) ◽  
pp. 713-723 ◽  
Author(s):  
Fabrice Cognasse ◽  
Sofiane Tariket ◽  
Hind Hamzeh‐Cognasse ◽  
Charles‐Antoine Arthaud ◽  
Marie‐Ange Eyraud ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Platelet Depletion

Effects of platelet depletion on PMA-induced acute lung injury in awake sheep

1995 ◽  
Vol 101 (2) ◽  
pp. 207-217 ◽  
Author(s):  
Tsuyoshi Nakano ◽  
Kenji Miyamoto ◽  
Akira Aida ◽  
Shunichi Saito ◽  
Masaharu Nishimura ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Platelet Depletion

scholarly journals Platelet depletion and aspirin treatment protect mice in a two-event model of transfusion-related acute lung injury

2009 ◽  
Author(s):  
Mark R. Looney ◽  
John X. Nguyen ◽  
Yongmei Hu ◽  
Jessica A. Van Ziffle ◽  
Clifford A. Lowell ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Event Model ◽  
Platelet Depletion

The Role of Recipient Platelets In the Prevention of Antibody-Mediated Transfusion Related Acute Lung Injury (TRALI)

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3351-3351
Author(s):  
Yuhan Chen ◽  
Michael Kim ◽  
Arata Tabuchi ◽  
Wolfgang M. Kuebler ◽  
Rukhsana Aslam ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Conflicts Of Interest ◽  
Scid Mice ◽  
Lung Damage ◽  
Cell Mediated Immunity ◽  
Shock Lung ◽  
Inflammatory Milieu ◽  
Platelet Depletion

Abstract Abstract 3351 Transfusion related acute lung injury (TRALI) is a serious complication of transfusion. The pathogenesis of TRALI is not fully understood but previous findings have suggested that platelet depletion can protect mice in a two-hit model of TRALI (Looney et al J Clin Invest 119:3450, 2009). To further understand the role of platelets in preventing antibody-mediated TRALI, two mouse models of immune thrombocytopenia (ITP) were utilized. In the passive ITP model, SCID mice were injected with a monoclonal anti-platelet antibody (MWReg30) intraperitoneally (ip, 18 h before TRALI induction) or intravenously (iv, 2 h before TRALI induction). In the active ITP model, SCID mice were transferred with splenocytes from anti-CD61 immune GPIIIa-knockout mice and thrombocytopenia occurred within 2 weeks post transfer (Chow et al Blood 115;1247, 2010). TRALI induction was performed by injecting the various thrombocytopenic SCID mice with a murine monoclonal MHC class I antibody (mAb, 34-1 -2s) iv and several parameters were observed for up to 2 h post antibody injection. In control, non-thrombocytopenic SCID mice, 34-1 -2s injection caused severe systemic shock as noted by reduced rectal temperatures which was associated with significant lung damage and mortality (45%) within 1 hour of 34-1 -2s infusion as previously shown (Fung et al. Blood DOI 10.1182/blood-2010-05-284570). In contrast, while SCID mice depleted of platelets by the passive ip route had systemic shock, lung damage and a 60% mortality rate, those mice made thrombocytopenic by the iv route were completely protected from mortality. On the other hand, in the active ITP model, where the induced thrombocytopenia is associated with a proinflammatory anti-platelet immune response, no mortality was observed in those mice made thrombocytopenic by antibody-mediated immune mechanisms whereas 80% of mice rendered thrombocytopenic by CD8+ T cell-mediated immunity were dead within 1 hr post 34-1 -2s infusion. These results suggest that thrombocytopenia in itself does not protect against antibody-mediated TRALI severity but the nature of the thrombocytopenia induction (e.g. acute passive iv infusion or active ITP immune transfer) is important. In fact, depending on the inflammatory milieu associated with the thrombocytopenia, platelets may actually increase the severity of TRALI. Disclosures: No relevant conflicts of interest to declare.

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