Comparative analysis of the pathological events involved in immune and non‐immune TRALI models

Tamarozzi, M. B.; Soares, Sandro G.; Sá-Nunes, Anderson; Paiva, H. H.; Saggioro, Fabiano Pinto; Garcia, Aglair Bergamo; Lucena-Araújo, Antonio R.; Falcão, Roberto Passetto; Bordin, José Orlando; Rego, Eduardo Magalhães

doi:10.1111/j.1423-0410.2012.01613.x

Cited by 6 publications

(5 citation statements)

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“…Human neutrophil antigen 2 (HNA-2) alloantibodies have been linked to the induction of TRALI and various pulmonary reactions [ 3 – 6 ] while anti-HNA-3 alloantibodies are frequently implicated in severe and fatal TRALI [ 7 ]. Animal models have firmly established a pathological role for HNA-2 alloantibodies in TRALI [ 8 , 9 ]. Furthermore, HNA-2 alloantibodies have been implicated in multiple human disorders such as neonatal alloimmune neutropenia, autoimmune neutropenia, drug-induced immune neutropenia, and graft failure following marrow transplantation [ 10 – 13 ].…”

Section: Introductionmentioning

confidence: 99%

Genetic Mechanism of Human Neutrophil Antigen 2 Deficiency and Expression Variations

Mair

Schuller

et al. 2015

PLoS Genet

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Human neutrophil antigen 2 (HNA-2) deficiency is a common phenotype as 3–5% humans do not express HNA-2. HNA-2 is coded by CD177 gene that associates with human myeloproliferative disorders. HNA-2 deficient individuals are prone to produce HNA-2 alloantibodies that cause a number of disorders including transfusion-related acute lung injury and immune neutropenia. In addition, the percentages of HNA-2 positive neutrophils vary significantly among individuals and HNA-2 expression variations play a role in human diseases such as myelodysplastic syndrome, chronic myelogenous leukemia, and gastric cancer. The underlying genetic mechanism of HNA-2 deficiency and expression variations has remained a mystery. In this study, we identified a novel CD177 nonsense single nucleotide polymorphism (SNP 829A>T) that creates a stop codon within the CD177 coding region. We found that all 829TT homozygous individuals were HNA-2 deficient. In addition, the SNP 829A>T genotypes were significantly associated with the percentage of HNA-2 positive neutrophils. Transfection experiments confirmed that HNA-2 expression was absent on cells expressing the CD177 SNP 829T allele. Our data clearly demonstrate that the CD177 SNP 829A>T is the primary genetic determinant for HNA-2 deficiency and expression variations. The mechanistic delineation of HNA-2 genetics will enable the development of genetic tests for diagnosis and prognosis of HNA-2-related human diseases.

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Section: Introductionmentioning

confidence: 99%

Genetic Mechanism of Human Neutrophil Antigen 2 Deficiency and Expression Variations

Mair

Schuller

et al. 2015

PLoS Genet

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“…Prevention of complement activation by C1‐inhibitor also prevented lung injury in a two hit‐animal model (Muller et al , ). Two in vivo animal models showed no effect of immune modulation by corticosteroids (Tamarozzi et al , ; Muller et al , ). Treatment strategies have only been tested in pre‐clinical studies or observational clinical studies, Although some pre‐clinical studies look promising, currently no treatment can be recommended other than supportive measures.…”

Section: Methodsmentioning

confidence: 99%

Antibody‐mediated transfusion‐related acute lung injury; from discovery to prevention

2015

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SummaryTransfusion-related acute lung injury (TRALI), a syndrome of respiratory distress caused by blood transfusion, is the leading cause of transfusion-related mortality. The majority of TRALI cases have been related to passive infusion of human leucocyte antigen (HLA) and human neutrophil antigen (HNA) antibodies in donor blood. In vitro, ex vivo and in vivo animal models have provided insight in TRALI pathogenesis. The various classes of antibodies implicated in TRALI appear to have different pathophysiological mechanisms for the induction of TRALI involving endothelial cells, neutrophils, monocytes and, as very recently has been discovered, lymphocytes. The HLA and HNA-antibodies are found mainly in blood from multiparous women as they have become sensitized during pregnancy. The incidence of TRALI has decreased rapidly following the introduction of a maleonly strategy for plasma donation. This review focuses on pre-clinical and clinical studies investigating the pathophysiology of antibody-mediated TRALI.

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“…In rodent models of experimental transfusion-related acute lung injury, 2 mg/kg dexamethasone decreased pulmonary levels of tumor necrosis factor-α but did not reduce neutrophil recruitment or other markers of inflammation such as interleukin-1β or macrophage inflammatory protein-2. 169 In line with these ambiguous preclinical data, glucocorticoids have often been given to patients with transfusion-related acute lung injury, but their contribution to lessening disease severity or hastening recovery remains unclear.…”

Section: Obtain Expert Consultationmentioning

confidence: 99%

Transfusion-related Acute Lung Injury in the Perioperative Patient

et al. 2019

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Comparative analysis of the pathological events involved in immune and non‐immune TRALI models

Abstract: Regardless of the triggering event(s), KC, MIP-2 and integrins participate in TRALI pathogenesis, whereas PAF is essential for capillary leakage when two events are involved.

Cited by 6 publications

References 56 publications

Genetic Mechanism of Human Neutrophil Antigen 2 Deficiency and Expression Variations

Genetic Mechanism of Human Neutrophil Antigen 2 Deficiency and Expression Variations

Antibody‐mediated transfusion‐related acute lung injury; from discovery to prevention

Transfusion-related Acute Lung Injury in the Perioperative Patient

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