Flow‐cytometric approach to the prompt laboratory diagnosis of TRALI: a case report

Porretti, Laura; Coluccio, Elena; Prati, Daniele; Colombo, M. B.; Lopa, R.; Tombolini, P; Ambrosone, Antonella; Crespiatico, L.; Scalamogna, M.; Rebulla, Paolo

doi:10.1111/j.1600-0609.2004.00279.x

Cited by 6 publications

(7 citation statements)

References 26 publications

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“…[77][78][79][80] Therefore, if PMNs become primed and adherent, do they then express HLA class II antigens that may be recognized by HLA class II antibodies infused with the transfusion, and, if so, would not ligation of these antigens on primed, adherent PMNs then cause activation of the microbicidal arsenal, endothelial damage, and TRALI? 81,82 Such a mechanism is plausible but would require 2 events: the first would cause adherence of PMNs to the pulmonary microvasculature, and the second would be the passive infusion of specific HLA class II antibodies directed against the class II antigens on the cell surfaces of the primed, sequestered PMNs. 10,81,83 Despite the plausibility of this mechanism, one must remember that in vitro cytokine exposure of 72 hours is required for surface expression of HLA class II antigens on PMNs [77][78][79][80][81] and that there may be significant differences between the effects of cytokines on leukocytes in vitro and in vivo.…”

Section: Trali Secondary To the Infusion Of Class II Hla Antibodiesmentioning

confidence: 99%

“…[95][96][97][98] In addition, many investigators, transfusion medicine professionals, and the American Association of Blood Banks advocate temporary disqualification of donors implicated in TRALI reactions until leukocyte antibody testing can be completed. 9,13,76,82 If these donors have antibodies to highfrequency leukocyte antigens, such as HNA-3a, HLA-A 2 , and HLA-B 12 , they should be disqualified from plasma or platelet donation; otherwise, if these findings are negative, they should be returned to the donor pool. 9,13,76,82 Although these precautions seem reasonable, there are a number of questions with this approach: What is the expense of such testing?…”

Section: Preventionmentioning

confidence: 99%

“…9,13,76,82 If these donors have antibodies to highfrequency leukocyte antigens, such as HNA-3a, HLA-A 2 , and HLA-B 12 , they should be disqualified from plasma or platelet donation; otherwise, if these findings are negative, they should be returned to the donor pool. 9,13,76,82 Although these precautions seem reasonable, there are a number of questions with this approach: What is the expense of such testing? Who will pay?…”

Section: Preventionmentioning

confidence: 99%

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Transfusion-related acute lung injury

Silliman¹,

Ambruso²,

Boshkov³

2005

Blood

395

379

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Transfusion-related acute lung injury (TRALI) is a life-threatening adverse effect of transfusion that is occurring at increasing incidence in the United States and that, in the past 2 reporting years, has been the leading cause of transfusionrelated death. TRALI and acute lung injury (ALI) share a common clinical definition except that TRALI is temporally and mechanistically related to the transfusion of blood/blood components. In prospec

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Section: Trali Secondary To the Infusion Of Class II Hla Antibodiesmentioning

confidence: 99%

Section: Preventionmentioning

confidence: 99%

Section: Preventionmentioning

confidence: 99%

See 1 more Smart Citation

Transfusion-related acute lung injury

Silliman¹,

Ambruso²,

Boshkov³

2005

Blood

395

379

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“…Neutrophils (PMNs) have been implicated as the effector cells in TRALI, although they do not normally express HLA class II antigens on their cell surface . Both in vitro and in vivo cytokine stimulation of PMNs may induce HLA class II antigen surface expression on PMNs . Chronic clinical conditions also induce the surface expression of MHC class II antigens on PMNs .…”

mentioning

confidence: 99%

Antibodies to major histocompatibility complex class II antigens directly prime neutrophils and cause acute lung injury in a two‐event in vivo rat model

et al. 2016

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BACKGROUND Transfusion-related acute lung injury (TRALI) is a significant cause of mortality, especially after transfusions containing antibodies to major histocompatibility complex (MHC) class II antigens. We hypothesize that a first event induces both 1) polymorphonuclear neutrophils (PMNs) to express MHC class II antigens, and 2) activation of the pulmonary endothelium, leading to PMN sequestration, so that the infusion of specific MHC class II antibodies to these antigens causes PMN-mediated acute lung injury (ALI). STUDY DESIGN AND METHODS Rats were treated with saline (NS), endotoxin (lipopolysaccharide [LPS]), or cytokines (interferon-γ [IFNγ], macrophage colony-stimulating factor [MCSF], tumor necrosis factor-α [TNFα]); the PMNs were isolated; and the surface expression of the MHC class II antigen OX6 and priming by OX6 antibodies were measured by flow cytometry or priming assays. RESULTS A two-event model of ALI was completed with NS, LPS, or IFNγ/MCSF/TNFα (first events) and the infusion of OX6 (second event). Compared with NS incubation, rats treated with either LPS or IFNγ/MCSF/TNFα exhibited OX6 PMN surface expression, OX6 antibodies primed the formyl-methionyl-leucyl phenylalanine (fMLF)-activated respiratory burst, and PMN sequestration was increased. OX6 antibody infusion into LPS-incubated or IFNγ/MCSF/TNFα-incubated rats elicited ALI, the OX6 antibody was present on the PMNs, and PMN depletion abrogated ALI. CONCLUSION Proinflammatory first events induce PMN MHC class II surface expression, activation of the pulmonary endothelium, and PMN sequestration such that the infusion of cognate antibodies precipitates TRALI.

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“…Kopko et al 15 were the first to report an association between anti-HLA class II antibodies and TRALI in a small series of patients. A number of case reports were published subsequently, [16][17][18][19] and plasma containing anti-HLA DR was shown to cause TRALI in a healthy male volunteer in an experimental setting. 20 Currently available data from large series and published hemovigilance reports indicate that HLA class II antibodies matching the recipients' antigens are present in ϳ 50% of all TRALI cases and thus represent the most frequently detected matched antibodies in implicated donors.…”

Section: Introductionmentioning

confidence: 99%

Mechanism of transfusion-related acute lung injury induced by HLA class II antibodies

Sachs

Wasel

Bayat

et al. 2011

Blood

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Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-associated mortality in the United States and other countries. In most TRALI cases, human leukocyte antigen (HLA) class II antibodies are detected in implicated donors. However, the corresponding antigens are not present on the cellular key players in TRALI: neutrophils and endothelium. In this study, we identify monocytes as a primary target in HLA class II-induced TRALI. Monocytes become activated when incubated with matched HLA class II antibodies and are capable of activating neutrophils, which, in turn, can induce disturbance of an endothelial barrier. In an ex vivo rodent model, HLA class II antibody-dependent monocyte activation leads to severe pulmonary edema in a relevant period of time, whenever neutrophils are present and the endothelium is preactivated. Our data suggest that in most TRALI cases, monocytes are cellular key players, because HLA class II antibodies induce TRALI by a reaction cascade initiated by monocyte activation. Furthermore, our data support the previous assumption that TRALI pathogenesis follows a threshold model. Having identified the biologic mechanism of HLA class II antibodyinduced TRALI, strategies to avoid plasma from immunized donors, such as women with a history of pregnancy, appear to be justified preventive measures. (Blood. 2011;117(2):669-677) IntroductionTransfusion-related acute lung injury (TRALI) is the leading cause of transfusion-associated death in the United States and other countries. 1 It typically presents within 6 hours after transfusion as a clinical syndrome characterized by acute respiratory distress, hypoxemia, and a bilateral pulmonary edema on chest x-ray. 2 The incidence of TRALI has been estimated as 1/5000 for all blood components, and current mortality rates are in the range of 5%-25%. 3 All blood components have been implicated in TRALI, but those containing large amounts of plasma are mainly responsible. [3][4][5] A recently published literature review states that in 80% of all TRALI cases, white blood cell antibodies can be identified in the implicated blood donor, 6 and most implicated donors have been women with a history of pregnancy. Pregnancy results in alloimmunization against paternal white blood cell antigens in 21%-24% of women, 7,8 with 3 main antibody specificities: human leukocyte antigen (HLA) class I, HLA class II, and human neutrophil antigens (HNAs).The capability of antibodies recognizing either HNA 9-11 or HLA class I 12,13 to precipitate TRALI has been proved in different animal models. It is consensus opinion that neutrophil activation is the key mechanism by which antibodies to HNA and to HLA class I mediate TRALI, 4,14 be it by direct binding to the cognate antigen on the surface of the neutrophil [9][10][11]13 or, in the case of HLA class I antibodies, possibly by binding to HLA class I molecules on pulmonary endothelial cells, which leads to neutrophil trapping by the neutrophils' Fc receptors and subsequent neutrophil activation by receptor...

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Flow‐cytometric approach to the prompt laboratory diagnosis of TRALI: a case report

Cited by 6 publications

References 26 publications

Transfusion-related acute lung injury

Transfusion-related acute lung injury

Antibodies to major histocompatibility complex class II antigens directly prime neutrophils and cause acute lung injury in a two‐event in vivo rat model

Mechanism of transfusion-related acute lung injury induced by HLA class II antibodies

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