Search citation statements
Paper Sections
Citation Types
Year Published
Publication Types
Relationship
Authors
Journals
Respiratory transfusion reactions represent some of the most severe adverse reactions related to receiving blood products. Of those, transfusion-related acute lung injury (TRALI) is associated with elevated morbidity and mortality. TRALI is characterized by severe lung injury associated with inflammation, pulmonary neutrophil infiltration, lung barrier leak, and increased interstitial and airspace edema which cause respiratory failure. Presently, there are few means of detecting TRALI beyond clinical definitions based on physical examination and vital signs or preventing/treating TRALI beyond supportive care with oxygen and positive pressure ventilation. Mechanistically, TRALI is thought to be mediated by the culmination of two successive pro-inflammatory hits, which typically comprise a recipient factor (1st hit - e.g. systemic inflammatory conditions) and a donor factor (2nd hit - e.g. blood products containing pathogenic antibodies or bioactive lipids). An emerging concept in TRALI research is the contribution of extracellular vesicles (EVs) in mediating the 1st and/or 2nd hit in TRALI. EVs are small, sub-cellular, membrane-bound vesicles which circulate in donor and recipient blood. Injurious EVs may be released by immune or vascular cells during inflammation, by infectious bacteria, or in blood products during storage, and can target the lung upon systemic dissemination. This review assesses emerging concepts such as how EVs: i) mediate TRALI, ii) represent targets for therapeutic intervention to prevent or treat TRALI, and iii) serve as biochemical biomarkers facilitating TRALI diagnosis and detection in at-risk patients.
Respiratory transfusion reactions represent some of the most severe adverse reactions related to receiving blood products. Of those, transfusion-related acute lung injury (TRALI) is associated with elevated morbidity and mortality. TRALI is characterized by severe lung injury associated with inflammation, pulmonary neutrophil infiltration, lung barrier leak, and increased interstitial and airspace edema which cause respiratory failure. Presently, there are few means of detecting TRALI beyond clinical definitions based on physical examination and vital signs or preventing/treating TRALI beyond supportive care with oxygen and positive pressure ventilation. Mechanistically, TRALI is thought to be mediated by the culmination of two successive pro-inflammatory hits, which typically comprise a recipient factor (1st hit - e.g. systemic inflammatory conditions) and a donor factor (2nd hit - e.g. blood products containing pathogenic antibodies or bioactive lipids). An emerging concept in TRALI research is the contribution of extracellular vesicles (EVs) in mediating the 1st and/or 2nd hit in TRALI. EVs are small, sub-cellular, membrane-bound vesicles which circulate in donor and recipient blood. Injurious EVs may be released by immune or vascular cells during inflammation, by infectious bacteria, or in blood products during storage, and can target the lung upon systemic dissemination. This review assesses emerging concepts such as how EVs: i) mediate TRALI, ii) represent targets for therapeutic intervention to prevent or treat TRALI, and iii) serve as biochemical biomarkers facilitating TRALI diagnosis and detection in at-risk patients.
Cold stored platelets (CS) are once again being reintroduced for clinical use. Transfused CS offer benefits over room temperature stored platelets (RTS) such as increased hemostatic effects and prolongation of shelf-life. Despite these advantages little is known about their association with transfusion-related acute lung injury (TRALI). TRALI is associated with prolonged storage RTS and has a mortality of > 15%. Determining the safety of CS is important considering their proposed use in TRALI-vulnerable populations with systemic inflammation such as surgical or trauma patients. Donor platelet-derived ceramide causes TRALI whereas donor platelet sphingosine-1-phosphate (S1P) is barrier protective. Females have higher plasma levels of S1P than males. Cold temperatures increase S1P levels in cells. Therefore, we hypothesized that female (donors or recipients) and/or CS would decrease TRALI. To test this, we compared how male and female donor and recipient allogeneic platelet transfusions of CS (40 C) versus RTS (230 C) stored for five days influence murine TRALI. Transfusion of CS significantly reduced recipient lung tissue wet-to-dry ratios, bronchoalveolar lavage total protein, lung tissue myeloperoxidase enzyme activity, histological lung injury scores and increased plasma sphingosine-1-phosphate (S1P) levels compared with RTS transfusions. Female as opposed to male recipients had less TRALI and higher plasma S1P levels. Female donor mouse platelets had higher S1P levels compared to males. Mouse and human CS platelets had increased S1P levels compared with RTS platelets. Higher recipient plasma S1P levels appears protective considering females, and males receiving platelets from females or male CS platelets had less TRALI.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.