Transfusion-Related Acute Lung Injury (TRALI) Induced by Donor-Derived Anti-HLA Antibodies in Aplastic Anemia: Possible Priming Effect of Granulocyte-Colony Stimulating Factor (G-CSF) on the Recipient Neutrophils

Hishizawa, Masakatsu; Mitsuhashi, Ryuichi; Ohno, Tatsuharu

doi:10.2169/internalmedicine.48.2569

Cited by 4 publications

(3 citation statements)

References 17 publications

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“…Neutrophil extracellular traps (NETs) consist of nuclear chromatin, hyper citrullinated histones, granular antimicrobial proteins and cytoplasmic proteins. In an ALI model of bacterial infection (Narayana Moorthy et al, 2013), LPS challenge (Tadie et al, 2013; Liu et al, 2016), transfusion (Hishizawa et al, 2009; Looney et al, 2009), and ventilation (Yildiz et al, 2015), NETs have been well documented, suggesting pivotal roles for NETs in ALI.…”

Section: Introductionmentioning

confidence: 99%

TLR3 Regulated Poly I:C-Induced Neutrophil Extracellular Traps and Acute Lung Injury Partly Through p38 MAP Kinase

Gan

Yang

et al. 2018

Front. Microbiol.

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Acute lung injury (ALI) is the leading cause of morbidity and mortality in critically ill patients. Neutrophil extracellular traps (NETs) have been well documented in the ALI model of bacterial infection. In the present study, we demonstrated that poly I:C could induce pulmonary NETs. Upon poly I:C intratracheal inoculation, neutrophil infiltration in the bronchoalveolar lavage fluid (BALF) was significantly increased. Furthermore, the inflammatory cytokines IL-1β, IL-6, and TNF-α in the lung were also significantly elevated. Neutrophil depletion abolished NETs and decreased both neutrophil infiltration and IL-1β in the lung. As expected, DNase I, an inhibitor of MPO and NADPH, decreased pulmonary inflammation and NETs. Blocking of the poly I:C receptor TLR3 reduced lung inflammation and NETs. The MAPK kinase inhibitor p38 diminished the formation of NETs and restored the expression of the tight junction protein claudin-5 in the mouse lung when challenged with poly I:C. In summary, poly I:C induced the formation of pulmonary NETs and ALI, which may be associated with the activation of p38 MAPK and the decreased expression of claudin-5.

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Section: Introductionmentioning

confidence: 99%

TLR3 Regulated Poly I:C-Induced Neutrophil Extracellular Traps and Acute Lung Injury Partly Through p38 MAP Kinase

Gan

Yang

et al. 2018

Front. Microbiol.

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“…Consensus definitions of TRALI have been developed but remain controversial. Similarly, in light of reports that granulocyte-colony-stimulating factor (G-CSF) might act as a neutrophil priming factor in predisposing patients for ALI (and possibly TRALI) [72][73][74][75], further research on the possible role of G-CSF in TRALI would be interesting. In addition, we need to better understand the pathophysiologic mechanisms that account for the overall worse outcomes of transfused critically ill patients, not necessarily attributable to ALI and respiratory compromise alone (e.g., immunomodulation and increased infection rates).…”

Section: Expert Commentary and Five-year Viewmentioning

confidence: 99%

Transfusion therapy and acute lung injury

Sokolovic

Pastores²

2010

Expert Review of Respiratory Medicine

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Transfusion-related acute lung injury (TRALI) remains the deadliest complication of transfusion. Consensus definitions of TRALI have been developed but remain controversial. Recent evidence supports a strong relationship between blood transfusion and the development of acute lung injury in the critically ill and trauma population. Plasma and platelet transfusions have been the most commonly implicated blood products. The 'two hit' model may best explain the immune and nonimmune pathogenesis of TRALI. Current treatment remains largely supportive; effective measures for decreasing the incidence of TRALI include the use of predominantly male plasma and apheresis platelets. Greater understanding of the blood component and patient risk factors for TRALI will hopefully lead to novel treatment and preventive strategies for reducing the risk of this life-threatening syndrome.

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“…Implicating factors for TRALI include white blood cell antibodies such as anti‐human leukocyte antigen (HLA) Class I and Class II, anti‐neutrophil antibodies, and soluble biologic molecules such as soluble CD40 ligand, lipids, or cytokines . In addition, we have previously reported that heme‐related molecules derived from hemolysis might also serve as an inducer of TRALI because hemin could activate neutrophils and produce ROS 17‐19.…”

mentioning

confidence: 99%

Heme‐related molecules induce rapid production of neutrophil extracellular traps

et al. 2014

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Transfusion-Related Acute Lung Injury (TRALI) Induced by Donor-Derived Anti-HLA Antibodies in Aplastic Anemia: Possible Priming Effect of Granulocyte-Colony Stimulating Factor (G-CSF) on the Recipient Neutrophils

Abstract: Abstract

Cited by 4 publications

References 17 publications

TLR3 Regulated Poly I:C-Induced Neutrophil Extracellular Traps and Acute Lung Injury Partly Through p38 MAP Kinase

TLR3 Regulated Poly I:C-Induced Neutrophil Extracellular Traps and Acute Lung Injury Partly Through p38 MAP Kinase

Transfusion therapy and acute lung injury

Heme‐related molecules induce rapid production of neutrophil extracellular traps

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