The Role of Complement in Transfusion-Related Acute Lung Injury.


Journal

Transfusion medicine reviews
ISSN: 1532-9496
Titre abrégé: Transfus Med Rev
Pays: United States
ID NLM: 8709027

Informations de publication

Date de publication:
10 2019
Historique:
received: 04 07 2019
revised: 05 09 2019
accepted: 06 09 2019
pubmed: 5 11 2019
medline: 20 9 2020
entrez: 3 11 2019
Statut: ppublish

Résumé

Transfusion-related acute lung injury (TRALI) is a life-threatening complication of acute respiratory distress occurring within 6 hours of blood transfusion. TRALI is one of the leading causes of transfusion-related fatalities and specific therapies are unavailable. Neutrophils are recognized as the major pathogenic cells, whereas T regulatory cells and dendritic cells appear to be important for protection against TRALI. The pathogenesis, however, is complex and incompletely understood. It is frequently postulated that the complement system plays an important role in the TRALI pathogenesis. In this article, we assess the evidence regarding the involvement of complement in TRALI from both human and animal studies. We hypothesize about the potential connection between the complement system and neutrophils in TRALI. Additionally, we draw parallels between TRALI and other acute pulmonary disorders of acute lung injury and acute respiratory distress syndrome regarding the involvement of complement. We conclude that, even though a role for complement in the TRALI pathogenesis seems plausible, studies investigating the role of complement in TRALI are remarkably limited in number and also present conflicting findings. Different types of TRALI animal models, diverse experimental conditions, and the composition of the gastrointestinal microbiota may perhaps all be factors which contribute to these discrepancies. More systematic studies are warranted to shed light on the contribution of the complement cascade in TRALI. The underlying clinical condition of the patient, which influences the susceptibility to TRALI, as well as the transfusion factor (antibody-mediated vs non-antibody-mediated), will be important to take into consideration when researching the contribution of complement. This should significantly increase our understanding of the role of complement in TRALI and may potentially result in promising new treatment strategies.

Identifiants

pubmed: 31676221
pii: S0887-7963(19)30130-0
doi: 10.1016/j.tmrv.2019.09.002
pmc: PMC7127679
pii:
doi:

Substances chimiques

Complement System Proteins 9007-36-7

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

236-242

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

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Auteurs

Ilse Jongerius (I)

Sanquin Research, Department of Immunopathology, Amsterdam and Landsteiner Laboratory, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands; Emma Children's Hospital, Department of Pediatric Immunology, Rheumatology and Infectious Diseases, Amsterdam UMC, Amsterdam, the Netherlands.

Leendert Porcelijn (L)

Department of Immunohematology Diagnostics, Sanquin Diagnostic Services, Amsterdam, the Netherlands.

Anna E van Beek (AE)

Sanquin Research, Department of Immunopathology, Amsterdam and Landsteiner Laboratory, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands; Emma Children's Hospital, Department of Pediatric Immunology, Rheumatology and Infectious Diseases, Amsterdam UMC, Amsterdam, the Netherlands.

John W Semple (JW)

Division of Hematology and Transfusion Medicine, Department of Laboratory Medicine, Lund University, Lund, Sweden.

C Ellen van der Schoot (CE)

Sanquin Research, Department of Experimental Immunohematology, Amsterdam and Landsteiner Laboratory, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.

Alexander P J Vlaar (APJ)

Department of Intensive Care Medicine, Amsterdam UMC, AMC, Amsterdam, the Netherlands; Laboratory of Experimental Intensive Care and Anesthesiology (L.E.I.C.A.), Amsterdam UMC, AMC, Amsterdam, the Netherlands.

Rick Kapur (R)

Sanquin Research, Department of Experimental Immunohematology, Amsterdam and Landsteiner Laboratory, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands. Electronic address: r.kapur@sanquin.nl.

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