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


Journal

Transfusion
ISSN: 1537-2995
Titre abrégé: Transfusion
Pays: United States
ID NLM: 0417360

Informations de publication

Date de publication:
04 2020
Historique:
received: 24 09 2019
revised: 07 02 2020
accepted: 07 02 2020
pubmed: 29 2 2020
medline: 9 9 2020
entrez: 29 2 2020
Statut: ppublish

Résumé

Transfusion-related acute lung injury (TRALI) is a severe pulmonary reaction due to blood transfusions. The pathophysiology of this complication is still not widely elucidated by the scientific community, especially regarding the direct role of blood platelets within the cellular mechanism responsible for the development of TRALI. In this study, a mouse model was used to induce the development of antibody-mediated acute lung injury through injections of lipopolysaccharide and an anti-major histocompatibility complex Class I antibody. BALB/c mice were pretreated with an anti-GPIbα antibody, which induces platelet depletion, or ML354, a protease receptor 4 pathway inhibitor, 30 minutes before TRALI induction. Depletion of platelets before TRALI induction appeared to reduce the severity of TRALI without completely inhibiting its development. Also, inhibition of platelet activation by ML354 did not prevent the onset of TRALI. Finally, the stimuli used for TRALI induction also triggered specific platelet activation upon ex vivo stimulation. This study suggests that blood platelets are not critically required for TRALI induction, although they are to some extent involved in its pathophysiology.

Sections du résumé

BACKGROUND
Transfusion-related acute lung injury (TRALI) is a severe pulmonary reaction due to blood transfusions. The pathophysiology of this complication is still not widely elucidated by the scientific community, especially regarding the direct role of blood platelets within the cellular mechanism responsible for the development of TRALI.
STUDY DESIGN AND METHODS
In this study, a mouse model was used to induce the development of antibody-mediated acute lung injury through injections of lipopolysaccharide and an anti-major histocompatibility complex Class I antibody. BALB/c mice were pretreated with an anti-GPIbα antibody, which induces platelet depletion, or ML354, a protease receptor 4 pathway inhibitor, 30 minutes before TRALI induction.
RESULTS
Depletion of platelets before TRALI induction appeared to reduce the severity of TRALI without completely inhibiting its development. Also, inhibition of platelet activation by ML354 did not prevent the onset of TRALI. Finally, the stimuli used for TRALI induction also triggered specific platelet activation upon ex vivo stimulation.
CONCLUSIONS
This study suggests that blood platelets are not critically required for TRALI induction, although they are to some extent involved in its pathophysiology.

Identifiants

pubmed: 32108957
doi: 10.1111/trf.15738
doi:

Substances chimiques

Antibodies 0
Indoles 0
Platelet Glycoprotein GPIb-IX Complex 0
VU0099704 0
adhesion receptor 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

713-723

Subventions

Organisme : Association "Les Amis de Rémi" Savigneux, France
ID : Grant
Pays : International
Organisme : French National Blood Service
ID : EFS (Grant APR)
Pays : International

Commentaires et corrections

Type : CommentIn

Informations de copyright

© 2020 AABB.

Références

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Auteurs

Fabrice Cognasse (F)

Université de Lyon, GIMAP-EA3064, Saint-Etienne, France.
Établissement Français du Sang Auvergne-Rhône-Alpes, Saint-Étienne, France.

Sofiane Tariket (S)

Université de Lyon, GIMAP-EA3064, Saint-Etienne, France.
Établissement Français du Sang Auvergne-Rhône-Alpes, Saint-Étienne, France.

Hind Hamzeh-Cognasse (H)

Université de Lyon, GIMAP-EA3064, Saint-Etienne, France.

Charles-Antoine Arthaud (CA)

Université de Lyon, GIMAP-EA3064, Saint-Etienne, France.
Établissement Français du Sang Auvergne-Rhône-Alpes, Saint-Étienne, France.

Marie-Ange Eyraud (MA)

Université de Lyon, GIMAP-EA3064, Saint-Etienne, France.
Établissement Français du Sang Auvergne-Rhône-Alpes, Saint-Étienne, France.

Thomas Bourlet (T)

Université de Lyon, GIMAP-EA3064, Saint-Etienne, France.

Philippe Berthelot (P)

Université de Lyon, GIMAP-EA3064, Saint-Etienne, France.

Sandrine Laradi (S)

Université de Lyon, GIMAP-EA3064, Saint-Etienne, France.
Établissement Français du Sang Auvergne-Rhône-Alpes, Saint-Étienne, France.

Sebastien Fauteux-Daniel (S)

Université de Lyon, GIMAP-EA3064, Saint-Etienne, France.
Établissement Français du Sang Auvergne-Rhône-Alpes, Saint-Étienne, France.

Olivier Garraud (O)

Université de Lyon, GIMAP-EA3064, Saint-Etienne, France.
Institut National de la Transfusion Sanguine, Paris, France.
Palliative Care Unit, The Ruffec General Hospital, Ruffec, France.

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