Possible involvement of heparin-binding protein in transfusion-related acute lung injury

Yasui, Kazuta; Furuta, Rie; Matsuyama, Nobuki; Fukumori, Yasuo; Kimura, Takafumi; Tani, Yoshihiko; Shibata, Hirotoshi; Hirayama, Fumiya

doi:10.1111/j.1537-2995.2007.01632.x

Cited by 13 publications

(19 citation statements)

References 43 publications

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“…At this point, no data from patient samples are available that would strengthen the perception of a role of azurocidin in ALI. However, antibodies which are found in TRALI have been shown to trigger discharge of azurocidin from neutrophils (192). In addition, in circumstances that may lead to ALI such as severe burns or sepsis, circulating azurocidin levels are increased significantly, allowing speculation on their potential role in lung damage (193)(194)(195).…”

Section: Neutrophil-derived Cationic Polypeptidesmentioning

confidence: 99%

Contribution of Neutrophils to Acute Lung Injury

Grommes

Soehnlein

2010

Mol Med

1,115

897

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Treatment of acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), remain unsolved problems of intensive care medicine. ALI/ARDS are characterized by lung edema due to increased permeability of the alveolar-capillary barrier and subsequent impairment of arterial oxygenation. Lung edema, endothelial and epithelial injury are accompanied by an influx of neutrophils into the interstitium and broncheoalveolar space. Hence, activation and recruitment of neutrophils are regarded to play a key role in progression of ALI/ARDS. Neutrophils are the first cells to be recruited to the site of inflammation and have a potent antimicrobial armour that includes oxidants, proteinases and cationic peptides. Under pathological circumstances, however, unregulated release of these microbicidal compounds into the extracellular space paradoxically can damage host tissues. This review focuses on the mechanisms of neutrophil recruitment into the lung and on the contribution of neutrophils to tissue damage in ALI.

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Section: Neutrophil-derived Cationic Polypeptidesmentioning

confidence: 99%

Contribution of Neutrophils to Acute Lung Injury

Grommes

Soehnlein

2010

Mol Med

1,115

897

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“…In addition, studies have indicated that HBP may play an important role in regulating monocyte accumulation in the lung during acute inflammation [9]. HBP appears to be one of the primary effector molecules of transfusion-related acute lung injury [10]. Considering the effect of HBP on the capillary permeability and its release by activated neutrophils, we investigated the plasma levels of HBP and analyzed its value in patients with ALI/ARDS.…”

Section: Introductionmentioning

confidence: 99%

Increased plasma levels of heparin-binding protein in patients with acute respiratory distress syndrome

Lin

Shen

et al. 2013

Crit Care

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IntroductionHeparin-binding protein (HBP) is an antimicrobial protein stored in neutrophil granules and plays a role in endothelial permeability regulation. The aim was to assess the diagnostic and prognostic value of measuring HBP in patients with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS).MethodsPlasma HBP was collected from 78 patients with ALI/ARDS, 28 patients with cardiogenic pulmonary edema (CPE) and 20 healthy volunteers at enrollment. Levels of HBP were measured by ELISA.ResultsPatients with ALI/ARDS had significantly higher median levels of HBP compared with patients with CPE (17.15 (11.95 to 24.07) ng/ml vs. 9.50 (7.98 to 12.18) ng/ml, P <0.001) at enrollment. There was no significant difference between CPE patients and healthy subjects in terms of HBP value (P = 0.372). The HBP levels of nonsurvivors was significantly higher than that of survivors (23.90 (14.81 to 32.45) ng/ml vs. 16.01 (10.97 to 21.06) ng/ml, P = 0.012) and multivariate logistic regression showed HBP (odds ratio =1.52, P = 0.034) was the independent predictor for 30-day mortality in patients with ALI/ARDS.ConclusionsPlasma HBP levels of ALI/ARDS patients were significantly higher than that of CPE patients. HBP was a strong prognostic marker for short-term mortality in ALI/ARDS.

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“…anti‐HNA‐3a or anti‐HLA‐A2) stiffen neutrophils or even agglutinate them so that they cannot pass through the narrow lung capillaries and are trapped in the lung where the neutrophils become pro‐adhesive (increased CD11b expression) (42), secrete proinflammatory mediators [interleukin‐8 (IL‐8)], produce cytotoxic ROS, and release enzymes by degranulation (e.g. elastase, myeloperoxidase, azurocidin, and heparin‐binding protein) which can injure the endothelium (40, 42, 43). In a mouse TRALI model using a monoclonal HLA class I antibody, the occurrence of TRALI was dependent on neutrophils and their Fcγ receptors as well as on platelets and on housing of the mice in a non‐pathogen‐free barrier room (39, 44).…”

Section: Pathophysiology Of Immune Tralimentioning

confidence: 99%

TRALI – new challenges for histocompatibility and immunogenetics in transfusion medicine

2011

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Antibodies against human leukocyte antigens (HLAs) have long been associated with transfusion-related acute lung injury (TRALI). In contrast to febrile transfusion reactions and refractoriness to platelet transfusions in immunized patients, the causative antibodies in TRALI are present in the transfused blood component, i.e. they are formed by the blood donor and not by the recipient. Consequently, blood components with high plasma volume are particularly associated with TRALI. In addition to antibodies against HLAs, antibodies directed against human neutrophil antigens (HNAs) present in the plasma of predominantly multiparous female blood donors can induce severe TRALI reactions. Especially, antibodies to HLA class II and HNA-3a antigens can induce severe or even fatal ALI in critically ill patients. Over the last decade, the clinical importance of TRALI as major cause for severe transfusion-related morbidities has led to the establishment of new guidelines aimed at preventing this condition, including routine testing for HLA and -HNA antibodies for plasma donors with a history of allogeneic sensitization. This, in turn, poses new challenges for close collaboration between blood transfusion centers and histocompatibility and immunogenetics laboratories, for sensitive and specific detection of the relevant antibodies.

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Possible involvement of heparin-binding protein in transfusion-related acute lung injury

Abstract: HBP appears to be one of the primary effector molecules of antibody-mediated nonhemolytic transfusion reactions including TRALI.

Cited by 13 publications

References 43 publications

Contribution of Neutrophils to Acute Lung Injury

Contribution of Neutrophils to Acute Lung Injury

Increased plasma levels of heparin-binding protein in patients with acute respiratory distress syndrome

TRALI – new challenges for histocompatibility and immunogenetics in transfusion medicine

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