The Role of Complement in Transfusion-Related Acute Lung Injury

Research output: Contribution to journalReview article

Standard

The Role of Complement in Transfusion-Related Acute Lung Injury. / Jongerius, Ilse; Porcelijn, Leendert; van Beek, Anna E.; Semple, John W.; van der Schoot, C. Ellen; Vlaar, Alexander P.J.; Kapur, Rick.

In: Transfusion Medicine Reviews, Vol. 33, No. 4, 2019, p. 236-242.

Research output: Contribution to journalReview article

Harvard

Jongerius, I, Porcelijn, L, van Beek, AE, Semple, JW, van der Schoot, CE, Vlaar, APJ & Kapur, R 2019, 'The Role of Complement in Transfusion-Related Acute Lung Injury', Transfusion Medicine Reviews, vol. 33, no. 4, pp. 236-242. https://doi.org/10.1016/j.tmrv.2019.09.002

APA

Jongerius, I., Porcelijn, L., van Beek, A. E., Semple, J. W., van der Schoot, C. E., Vlaar, A. P. J., & Kapur, R. (2019). The Role of Complement in Transfusion-Related Acute Lung Injury. Transfusion Medicine Reviews, 33(4), 236-242. https://doi.org/10.1016/j.tmrv.2019.09.002

CBE

Jongerius I, Porcelijn L, van Beek AE, Semple JW, van der Schoot CE, Vlaar APJ, Kapur R. 2019. The Role of Complement in Transfusion-Related Acute Lung Injury. Transfusion Medicine Reviews. 33(4):236-242. https://doi.org/10.1016/j.tmrv.2019.09.002

MLA

Vancouver

Jongerius I, Porcelijn L, van Beek AE, Semple JW, van der Schoot CE, Vlaar APJ et al. The Role of Complement in Transfusion-Related Acute Lung Injury. Transfusion Medicine Reviews. 2019;33(4):236-242. https://doi.org/10.1016/j.tmrv.2019.09.002

Author

Jongerius, Ilse ; Porcelijn, Leendert ; van Beek, Anna E. ; Semple, John W. ; van der Schoot, C. Ellen ; Vlaar, Alexander P.J. ; Kapur, Rick. / The Role of Complement in Transfusion-Related Acute Lung Injury. In: Transfusion Medicine Reviews. 2019 ; Vol. 33, No. 4. pp. 236-242.

RIS

TY - JOUR

T1 - The Role of Complement in Transfusion-Related Acute Lung Injury

AU - Jongerius, Ilse

AU - Porcelijn, Leendert

AU - van Beek, Anna E.

AU - Semple, John W.

AU - van der Schoot, C. Ellen

AU - Vlaar, Alexander P.J.

AU - Kapur, Rick

PY - 2019

Y1 - 2019

N2 - 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.

AB - 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.

KW - C5a

KW - C5Ar

KW - Complement

KW - NETs

KW - TRALI

KW - Transfusion-related acute lung injury

U2 - 10.1016/j.tmrv.2019.09.002

DO - 10.1016/j.tmrv.2019.09.002

M3 - Review article

VL - 33

SP - 236

EP - 242

JO - Transfusion Medicine Reviews

JF - Transfusion Medicine Reviews

SN - 0887-7963

IS - 4

ER -