Evaluation of Platelet Responses in Transfusion-Related Acute Lung Injury (TRALI)

Laan, Eveline A. Zeeuw van der; Velden, Saskia van der; Porcelijn, Leendert; Semple, John W.; Schoot, C. Ellen van der; Kapur, Rick

doi:10.1016/j.tmrv.2020.08.002

Cited by 15 publications

(12 citation statements)

References 55 publications

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“…We and others have previously reported that, in WT mice, monocytes/macrophages are essential to induce TRALI with the mouse IgG2a anti-MHC I mAb 34-1-2S 7,12,13,15 , while neutrophils and platelets are dispensable 7,8,11,12 . Controversies have long existed, however, especially regarding the contribution of the recipient platelets to the pathology, notwithstanding the recent consensus that platelets may not be critically required for the onset and development of TRALI in WT mice 36, 37 . Here, similar cell-dependent features were observed in CD32Aanimals when TRALI was induced by the chimera hIgG1-34-1-2S.…”

Section: Discussionmentioning

confidence: 99%

Platelet FcγRIIA-induced serotonin release exacerbates the severity of transfusion-related acute lung injury in mice

et al. 2021

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Transfusion-related acute lung injury (TRALI) remains a major cause of transfusion-related fatalities. The mechanism of human antibody-mediated TRALI, especially the involvement of the Fcγ receptors, is not clearly established. Contrary to mice, human platelets are unique in their expression of the FcγRIIA/CD32A receptor, suggesting that our understanding of the pathogenesis of antibody-mediated TRALI is partial, since the current murine models incompletely recapitulate the human immunology. We evaluated the role of FcγRIIA/CD32A in TRALI using a humanized mouse model expressing the FcγRIIA/CD32A receptor. When challenged with a recombinant chimeric human IgG1/mouse anti-MHC I monoclonal antibody, these mice showed exacerbated alveolar edema and higher mortality compared to WT mice. Unlike in WT mice, monocytes/macrophages were accessory for TRALI initiation in CD32A+ mice pointing to the decisive contribution of another cell type. Platelet activation was dramatically increased in CD32A+ animals resulting in their increased consumption and massive release of their granule contents. Platelet depletion prevented the exacerbation of TRALI in CD32A+ mice but did not affect TRALI in WT animals. By blocking platelet serotonin uptake with fluoxetine, we showed that the severity of TRALI in CD32A+ mice resulted from the serotonin released by activated platelets. Furthermore, inhibition of 5-hydroxytryptamine 2A serotonin receptor with sarpogrelate, before or after the induction of TRALI, abolished the aggravation of lung edema in CD32A+ mice. Our findings demonstrate that platelet FcγRIIA/CD32A activation exacerbates antibody-mediated TRALI and provide a rationale for designing prophylactic and therapeutic strategies targeting the serotonin pathway to attenuate TRALI in patients.

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Section: Discussionmentioning

confidence: 99%

Platelet FcγRIIA-induced serotonin release exacerbates the severity of transfusion-related acute lung injury in mice

et al. 2021

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“…It is commonly believed that antibody-mediated TRALI is the result of pulmonary damage caused by neutrophils. However, the pathogenic role of other cells, including monocytes, macrophages, endothelial cells and platelets have been well studied (1,14,15,(34)(35)(36)(37). Nevertheless, these cellular pathways remain complex and somehow depend on antibody specificities (1).…”

Section: Discussionmentioning

confidence: 99%

“…In the classical antibody-mediated TRALI model, neutrophils have been implicated as important factors (9)(10)(11), while other studies have reported that monocytes and macrophages, rather than neutrophils, play crucial roles in the development of TRALI (12,13). Significant controversy, however, still exists concerning the role of platelets in TRALI (14). Recent studies in murine models have demonstrated that osteopontin, secreted by macrophages, was critically required for TRALI induction via stimulation of neutrophil-recruitment into the lungs (15), and that Fc-mediated complement activation was an important feature of TRALI (16).…”

Section: Introductionmentioning

confidence: 99%

Mechanism and intervention of murine transfusion-related acute lung injury caused by anti-CD36 antibodies

Chen¹,

Tian²,

Xu³

et al. 2023

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Anti-CD36 antibodies have been suggested to induce transfusion-related acute lung injury (TRALI) upon blood transfusion, particularly in Asian populations. However, little is known about the pathological mechanism of anti-CD36-mediated TRALI, and potential therapies haven't yet been identified. Here, we developed a murine model of anti-CD36-mediated TRALI to address these questions. We found that administration of mouse monoclonal antibody against CD36 (mAb GZ1) or human anti-CD36 IgG, but not GZ1 F(ab')2 fragments, induced severe TRALI in Cd36 +/+ male mice. Pre-depletion of recipient monocytes or complement, but not neutrophils or platelets, prevented the development of murine TRALI. Moreover, plasma C5a levels after TRALI induction by anti-CD36 were increased more than 3-fold, implying a critical role of complement C5 activation in the mechanism of Fc-dependent anti-CD36-mediated TRALI.Administration of GZ1 F(ab')2, antioxidant (NAC) or C5-blocker (mAb BB5.1) before TRALI induction completely protected mice from anti-CD36-mediated TRALI. Although no significant amelioration in TRALI was observed when mice were injected with GZ1 F(ab')2 after TRALI induction, significant improvement was achieved when mice were treated post-induction with NAC or anti-C5. Importantly, anti-C5 treatment completely rescued mice from TRALI, suggesting the potential role of existing anti-C5 drugs in the treatment of patients with TRALI caused by anti-CD36.

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“…Por otro lado, estudios sugieren que las plaquetas presentes tanto en el receptor como en el donador pueden tener un papel patogénico en los cuadros de daño pulmonar, incluido TRALI o en SDRA, sin embargo, su participación es limitada (28).…”

Section: Fisiopatologíaunclassified

Aspectos generales de Lesión Pulmonar aguda producida por transfusión sanguínea o TRALI.

Barquero¹

2022

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TRALI o Lesión Pulmonar aguda producida por transfusión sanguínea es un síndrome clínico caracterizado por cursar con hipoxemia aguda y edema pulmonar (no cardiogénico) que ocurre durante o después de la transfusión de algún hemoderivado. Es una de las principales causantes de muerte relacionadas con una transfusión sanguínea. Adicionalmente ha sido clasificada en tipo I y II, donde la principal diferencia radica en que en el tipo II se incluyen pacientes con factores de riesgo para la aparición de SDRA. La investigación del cuadro permite manifestar que cualquier estado inflamatorio, sea cual sea la causa, cursa como el primer evento necesario para que se desarrolle el síndrome en estudio, y que el segundo evento involucrado, es la transfusión sanguínea.

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Evaluation of Platelet Responses in Transfusion-Related Acute Lung Injury (TRALI)

Cited by 15 publications

References 55 publications

Platelet FcγRIIA-induced serotonin release exacerbates the severity of transfusion-related acute lung injury in mice

Platelet FcγRIIA-induced serotonin release exacerbates the severity of transfusion-related acute lung injury in mice

Mechanism and intervention of murine transfusion-related acute lung injury caused by anti-CD36 antibodies

Aspectos generales de Lesión Pulmonar aguda producida por transfusión sanguínea o TRALI.

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