Abstract
As an initiator of respiratory distress, transfusion-related acute lung injury (TRALI) is regarded as one of the rare complications associated with transfusion medicine. However, to date, the pathogenesis of TRALI is still unclear, and specific therapies are unavailable. Understanding the mechanisms of TRALI may promote the design of preventive and therapeutic strategies. The immune system plays vital roles in reproduction, development and homeostasis. Sterile tissue damage, such as physical trauma, ischemia, or reperfusion injury, induces an inflammatory reaction that results in wound healing and regenerative mechanisms. In other words, in addition to protecting against pathogens, the immune response may be strongly associated with TRALI prevention and treatment through a variety of immunomodulatory strategies to inhibit excessive immune system activation. Immunotherapy based on immune cells or immunological targets may eradicate complications. For example, IL-10 therapy is a promising therapeutic strategy to explore further. This review will focus on ultramodern advances in our understanding of the potential role of the immune system in TRALI prevention and treatment.
Highlights
Transfusion-related acute lung injury (TRALI) is the onset of respiratory distress and acute lung injury due to blood product transfusion (Semple et al, 2019), and it is a life-threatening complication characterized by the sudden onset of hypoxemic respiratory failure with noncardiogenic pulmonary edema and bilateral lung infiltration that developed within 6 h of blood transfusion (Toy et al, 2005; Gokhale and Hendrickson, 2019)
Low plasma IL-10 levels were associated with transfusion-related acute lung injury (TRALI) susceptibility in a mouse model, and IL-10-knockout mice were hypersensitive to TRALI induction (Kapur et al, 2017a). These results suggested that low IL-10 levels were a risk factor for TRALI in humans (Kapur et al, 2017b)
In H-2Kd/H-2Dd antibody-based severe combined immunodeficient TRALI models, it was demonstrated that the binding of H-2Kd/H-2Dd antibodies to monocytes increased the levels of macrophage inflammatory protein 2 (MIP-2), causing increased pulmonary neutrophil infiltration and subsequently inducing TRALI (McKenzie et al, 2014)
Summary
Transfusion-related acute lung injury (TRALI) is the onset of respiratory distress and acute lung injury due to blood product transfusion (Semple et al, 2019), and it is a life-threatening complication characterized by the sudden onset of hypoxemic respiratory failure with noncardiogenic pulmonary edema and bilateral lung infiltration that developed within 6 h of blood transfusion (Toy et al, 2005; Gokhale and Hendrickson, 2019). The clinical condition of the patient induces the release of a large number of cytokines, which cause neutrophil activation, accumulation and adhesion to pulmonary microvascular endothelial cells. An increasing number of studies have shown that antibody-dependent TRALI is mediated by the activation of neutrophils, which results in the release of oxygen free radicals and proteases, causes endothelial damage, and increases capillary permeability, causing pulmonary edema, and inducing TRALI (Silliman, 2006).
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