Elevation of C-reactive protein levels in patients with transfusion-related acute lung injury

Rick Kapur, Michael Kim, Matthew T Rondina, Leendert Porcelijn, John W Semple, Rick Kapur, Michael Kim, Matthew T Rondina, Leendert Porcelijn, John W Semple

Abstract

Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related fatalities and is characterized by the onset of acute respiratory distress within six hours following blood transfusion. In most cases, donor antibodies are suggested to be involved, however, the pathogenesis is poorly understood. A two-hit model is generally assumed to underlie TRALI pathogenesis where the first hit consists of a patient predisposing factor such as inflammation and the second hit is due to donor antibodies present in the transfused blood. We recently demonstrated that the acute phase protein C-reactive protein (CRP) could enhance murine anti-major histocompatibility complex (MHC) class I-mediated TRALI. Whether CRP is increased in human TRALI patients which would support its role as a risk factor for human TRALI, is currently unknown. For that purpose, we measured CRP levels in the plasma of human TRALI patients and found CRP levels to be significantly elevated compared to transfused control patients. These data support the notion that CRP may be a novel first hit risk factor in human TRALI and that modulation of CRP levels could be an effective therapeutic strategy for this serious adverse event of transfusion.

Keywords: CRP; TRALI; TRALI first hit; TRALI risk factor; human TRALI.

Conflict of interest statement

CONFLICTS OF INTEREST

There are no potential conflicts of interest.

Figures

Figure 1. CRP levels are increased in…
Figure 1. CRP levels are increased in human TRALI patients
CRP levels were measured in plasma from transfused control patients (who did not undergo any adverse pulmonary transfusion reactions including TRALI, n=10) and from TRALI patients (n=12). A one-sided and unpaired t-test was performed, **: P

References

    1. Peters AL, Van Stein D, Vlaar AP. Antibody-mediated transfusion-related acute lung injury; from discovery to prevention. Br J Haematol. 2015;170:597–614.
    1. Fatalities Reported to FDA Following Blood Collection and Transfusions: Annual Summary for Fiscal Year 2014. Washington, DC: US Department of Health and Human Services, Office of the Assistant Secretary of Health; 2014.
    1. Bux J, Becker F, Seeger W, Kilpatrick D, Chapman J, Waters A. Transfusion-related acute lung injury due to HLA-A2-specific antibodies in recipient and NB1-specific antibodies in donor blood. Br J Haematol. 1996;93:707–713.
    1. Middelburg RA, Van Stein D, Briet E, van der Bom JG. The role of donor antibodies in the pathogenesis of transfusion-related acute lung injury: a systematic review. Transfusion. 2008;48:2167–2176.
    1. Toy P, Gajic O, Bacchetti P, Looney MR, Gropper MA, Hubmayr R, Lowell CA, Norris PJ, Murphy EL, Weiskopf RB, Wilson G, Koenigsberg M, Lee D, et al. Transfusion-related acute lung injury: incidence and risk factors. Blood. 2012;119:1757–1767.
    1. Vlaar AP, Hofstra JJ, Determann RM, Veelo DP, Paulus F, Levi M, Zeerleder S, Vroom MB, Schultz MJ, Juffermans NP. Transfusion-related acute lung injury in cardiac surgery patients is characterized by pulmonary inflammation and coagulopathy: a prospective nested case-control study. Crit Care Med. 2012;40:2813–2820.
    1. Roubinian NH, Looney MR, Kor DJ, Lowell CA, Gajic O, Hubmayr RD, Gropper MA, Koenigsberg M, Wilson GA, Matthay MA, Toy P, Murphy EL. Cytokines and clinical predictors in distinguishing pulmonary transfusion reactions. Transfusion. 2015;55:1838–1846.
    1. Kapur R, Kim M, Shanmugabhavananthan S, Liu J, Li Y, Semple JW. C-reactive protein enhances murine antibody-mediated transfusion-related acute lung injury. Blood. 2015;126:2747–2751.
    1. Pepys MB, Hirschfield GM. C-reactive protein: a critical update. J Clin Invest. 2003;111:1805–1812.
    1. Kapur R, Heitink-Polle KM, Porcelijn L, Bentlage AE, Bruin MC, Visser R, Roos D, Schasfoort RB, de HM, van der Schoot CE, Vidarsson G. C-reactive protein enhances IgG-mediated phagocyte responses and thrombocytopenia. Blood. 2015;125:1793–1802.
    1. Strait RT, Hicks W, Barasa N, Mahler A, Khodoun M, Kohl J, Stringer K, Witte D, Van RN, Susskind BM, Finkelman FD. MHC class I-specific antibody binding to nonhematopoietic cells drives complement activation to induce transfusion-related acute lung injury in mice. J Exp Med. 2011;208:2525–2544.
    1. Bayat B, Tjahjono Y, Sydykov A, Werth S, Hippenstiel S, Weissmann N, Sachs UJ, Santoso S. Anti-human neutrophil antigen-3a induced transfusion-related acute lung injury in mice by direct disturbance of lung endothelial cells. Arterioscler Thromb Vasc Biol. 2013;33:2538–2548.
    1. Silliman CC, Curtis BR, Kopko PM, Khan SY, Kelher MR, Schuller RM, Sannoh B, Ambruso DR. Donor antibodies to HNA-3a implicated in TRALI reactions prime neutrophils and cause PMN-mediated damage to human pulmonary microvascular endothelial cells in a two-event in vitro model. Blood. 2007;109:1752–1755.
    1. Pasceri V, Willerson JT, Yeh ET. Direct proinflammatory effect of C-reactive protein on human endothelial cells. Circulation. 2000;102:2165–2168.
    1. McGrath FD, Brouwer MC, Arlaud GJ, Daha MR, Hack CE, Roos A. Evidence that complement protein C1q interacts with C-reactive protein through its globular head region. J Immunol. 2006;176:2950–2957.
    1. Eisenhardt SU, Habersberger J, Murphy A, Chen YC, Woollard KJ, Bassler N, Qian H, von Zur Muhlen C, Hagemeyer CE, Ahrens I, Chin-Dusting J, Bobik A, Peter K. Dissociation of pentameric to monomeric C-reactive protein on activated platelets localizes inflammation to atherosclerotic plaques. Circ Res. 2009;105:128–137.
    1. Habersberger J, Strang F, Scheichl A, Htun N, Bassler N, Merivirta RM, Diehl P, Krippner G, Meikle P, Eisenhardt SU, Meredith I, Peter K. Circulating microparticles generate and transport monomeric C-reactive protein in patients with myocardial infarction. Cardiovasc Res. 2012;96:64–72.
    1. Thiele JR, Habersberger J, Braig D, Schmidt Y, Goerendt K, Maurer V, Bannasch H, Scheichl A, Woollard KJ, von Dobschütz E, Kolodgie F, Virmani R, Stark GB, et al. Dissociation of pentameric to monomeric C-reactive protein localizes and aggravates inflammation: in vivo proof of a powerful proinflammatory mechanism and a new anti-inflammatory strategy. Circulation. 2014;130:35–50.
    1. Looney MR, Gropper MA, Matthay MA. Transfusion-related acute lung injury: a review. Chest. 2004;126:249–258.
    1. Yomtovian R, Kline W, Press C, Clay M, Engman H, Hammerschmidt D, McCullough J. Severe pulmonary hypersensitivity associated with passive transfusion of a neutrophil-specific antibody. Lancet. 1984;1:244–246.
    1. Ausley MB., Jr Fatal transfusion reactions caused by donor antibodies to recipient leukocytes. Am J Forensic Med Pathol. 1987;8:287–290.
    1. Leger R, Palm S, Wulf H, Vosberg A, Neppert J. Transfusion-related lung injury with leukopenic reaction caused by fresh frozen plasma containing anti-NB1. Anesthesiology. 1999;91:1529–1532.
    1. Looney MR, Nguyen JX, Hu Y, Van Ziffle JA, Lowell CA, Matthay MA. Platelet depletion and aspirin treatment protect mice in a two-event model of transfusion-related acute lung injury. J Clin Invest. 2009;119:3450–3461.
    1. Caudrillier A, Kessenbrock K, Gilliss BM, Nguyen JX, Marques MB, Monestier M, Toy P, Werb Z, Looney MR. Platelets induce neutrophil extracellular traps in transfusion-related acute lung injury. J Clin Invest. 2012;122:2661–2671.
    1. Kapur R, Zufferey A, Boilard E, Semple JW. Nouvelle cuisine: platelets served with inflammation. J Immunol. 2015;194:5579–5587.
    1. Kapur R, Semple JW. The nonhemostatic immune functions of platelets. Semin Hematol. 2016;53:S2–S6.
    1. Boudreau LH, Duchez AC, Cloutier N, Soulet D, Martin N, Bollinger J, Paré A, Rousseau M, Naika GS, Lévesque T, Laflamme C, Marcoux G, Lambeau G, et al. Platelets release mitochondria serving as substrate for bactericidal group IIA-secreted phospholipase A2 to promote inflammation. Blood. 2014;124:2173–2183.

Source: PubMed

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