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    Contrasting effects of stored allogeneic red blood cells and their supernatants on permeability and inflammatory responses in human pulmonary endothelial cells

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    Author
    Kim, J.
    Nguyen, T.T.T.
    Li, Y.
    Zhang, C.-O.
    Cha, B.
    Ke, Y.
    Mazzeffi, M.A.
    Tanaka, K.A.
    Birukova, A.A.
    Birukov, K.G.
    Date
    2020
    Journal
    American journal of physiology. Lung cellular and molecular physiology
    Publisher
    American Physiological Society
    Type
    Article
    
    Metadata
    Show full item record
    See at
    https://doi.org/10.1152/ajplung.00025.2019
    Abstract
    Transfusion of red blood cells (RBCs) is a common life-saving clinical practice in severely anemic or hemorrhagic patients; however, it may result in serious pathological complications such as transfusion-related acute lung injury. The factors mediating the deleterious effects of RBC transfusion remain unclear. In this study, we tested the effects of washed long-term (RBC-O; >28 days) versus short-term (RBC-F; <14 days) stored RBCs and their supernatants on lung endothelial (EC) permeability under control and inflammatory conditions. RBCs enhanced basal EC barrier function as evidenced by an increase in transendothelial electrical resistance and decrease in permeability for macromolecules. RBCs also attenuated EC hyperpermeability and suppressed secretion of EC adhesion molecule ICAM-1 and proinflammatory cytokine IL-8 in response to LPS or TNF-α. In both settings, RBC-F had slightly higher barrier protective effects as compared with RBC-O. In contrast, supernatants from both RBC-F and RBC-O disrupted the EC barrier. The early phase of EC permeability response caused by RBC supernatants was partially suppressed by antioxidant N-acetyl cysteine and inhibitor of Src kinase family PP2, while addition of heme blocker and inhibition of NOD-like receptor family pyrin domain containing protein 3 (NLRP3), stress MAP kinases, receptor for advanced glycation end-products (RAGE), or Toll-like receptor-4 (TLR4) signaling were without effect. Morphological analysis revealed that RBC supernatants increased LPS- and TNF-α-induced breakdown of intercellular junctions and formation of paracellular gaps. RBC supernatants augmented LPS- and TNF-α-induced EC inflammation reflected by increased production of IL-6, IL-8, and soluble ICAM-1. These findings demonstrate the deleterious effects of RBC supernatants on EC function, which may have a major impact in pathological consequences associated with RBC transfusion.
    Keyword
    endothelial cells
    inflammation
    red blood cells
    transfusion
    transfusion-related acute lung injury
    vascular permeability
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85081168508&doi=10.1152%2fajplung.00025.2019&partnerID=40&md5=13baff718f1b0bd567e471dd526e1501; http://hdl.handle.net/10713/12310
    ae974a485f413a2113503eed53cd6c53
    10.1152/ajplung.00025.2019
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