<scp>rIL</scp>‐35 prevents murine transfusion‐related acute lung injury by inhibiting the activation of endothelial cells

Qiao, Jiajia; He, Rui; Yin, Yilong; Tian, Lu; Li, Ling; Lian, Zhengqiu; Peng, Fang; Liu, Zhong

doi:10.1111/trf.15805

Cited by 4 publications

(3 citation statements)

References 44 publications

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“…MPO activity was measured to assess inflammation in the lung. Consistent with previous studies ( 24 , 25 ), pulmonary neutrophil infiltration, as evidenced by increased MPO activity, was typically observed in TRALI mice ( Fig. 2A ).…”

Section: Resultssupporting

confidence: 92%

Pulmonary coagulation and fibrinolysis abnormalities that favor fibrin deposition in the lungs of mouse antibody-mediated transfusion-related acute lung injury

Yu¹,

Jiang²,

Sun³

et al. 2021

Mol Med Rep

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Transfusion-related acute lung injury (TRALI) is a life-threatening disease caused by blood transfusion. However, its pathogenesis is poorly understood and specific therapies are not available. Experimental and clinical studies have indicated that alveolar fibrin deposition serves a pathological role in acute lung injuries. The present study investigated whether pulmonary fibrin deposition occurs in a TRALI mouse model and the possible mechanisms underlying this deposition. The TRALI model was established by priming male Balb/c mice with lipopolysaccharide (LPS) 18 h prior to injection of an anti-major histocompatibility complex class I (MHC-I) antibody. Untreated mice and mice administered LPS plus isotype antibody served as controls. At 2 h after TRALI induction, blood and lung tissue were collected. Disease characteristics were assessed based on lung tissue histology, inflammatory responses and alterations in the alveolar-capillary barrier. Immunofluorescence staining was used to detect pulmonary fibrin deposition, platelets and fibrin-platelet interactions. Levels of plasminogen activator inhibitor-1 (PAI-1), thrombin-antithrombin complex (TATc), tissue factor pathway inhibitor (TFPI), coagulation factor activity and fibrin degradation product (FDP) in lung tissue homogenates were measured. Severe lung injury, increased inflammatory responses and a damaged alveolar-capillary barrier in the LPS-primed, anti-MHC-I antibody-administered mice indicated that the TRALI model was successfully established. Fibrin deposition, fibrin-platelet interactions and platelets accumulation in the lungs of mouse models were clearly promoted. Additionally, levels of TATc, coagulation factor V (FV), TFPI and PAI-1 were elevated, whereas FDP level was decreased in TRALI mice. In conclusion, both impaired fibrinolysis and enhanced coagulation, which might be induced by boosted FV activity, increased pulmonary platelets accumulation and enhanced fibrin-platelet interactions and contributed to pulmonary fibrin deposition in TRALI mice. The results provided a therapeutic rationale to target abnormalities in either coagulation or fibrinolysis pathways for antibody-mediated TRALI. acute respiratory syndrome coronavirus 2 infection-induced ALI (7), idiopathic pulmonary fibrosis (8), alcohol-induced ALI ( 9) and trauma-induced ALI (10). Fibrin deposition can

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Section: Resultssupporting

confidence: 92%

Pulmonary coagulation and fibrinolysis abnormalities that favor fibrin deposition in the lungs of mouse antibody-mediated transfusion-related acute lung injury

Yu¹,

Jiang²,

Sun³

et al. 2021

Mol Med Rep

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“…Therefore, other than IL-10 and IL-8, other cytokines may be also potential research targets for TRALI prevention and treatment. For example, Qiao et al (2020) preliminarily confirmed that IL-35 could prevent murine TRALI by inhibiting the activation of endothelial cells. The study of additional immunological factors in combination with previous research findings could shape the field of TRALI research.…”

Section: Other Factorsmentioning

confidence: 87%

The Immune System in Transfusion-Related Acute Lung Injury Prevention and Therapy: Update and Perspective

Guo

S.K.

2021

Front. Mol. Biosci.

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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.

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“…IL-35, which belongs to the IL-12 cytokine family, is regarded as a novel immune-suppressive cytokine (149). IL-35 may alleviate disease states by inhibiting pulmonary endothelial proliferation, apoptosis, and activation (133,150). IL-35 treatment has been proven to prevent murine TRALI via inhibition of endothelial activation (133), which could provide new insights into therapeutic targets.…”

Section: Targeting Endothelial Activationmentioning

confidence: 99%

Update on transfusion-related acute lung injury: an overview of its pathogenesis and management

Lian

2023

Front. Immunol.

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Transfusion-related acute lung injury (TRALI) is a severe adverse event and a leading cause of transfusion-associated death. Its poor associated prognosis is due, in large part, to the current dearth of effective therapeutic strategies. Hence, an urgent need exists for effective management strategies for the prevention and treatment of associated lung edema. Recently, various preclinical and clinical studies have advanced the current knowledge regarding TRALI pathogenesis. In fact, the application of this knowledge to patient management has successfully decreased TRALI-associated morbidity. This article reviews the most relevant data and recent progress related to TRALI pathogenesis. Based on the existing two-hit theory, a novel three-step pathogenesis model composed of a priming step, pulmonary reaction, and effector phase is postulated to explain the process of TRALI. TRALI pathogenesis stage-specific management strategies based on clinical studies and preclinical models are summarized with an explication of their models of prevention and experimental drugs. The primary aim of this review is to provide useful insights regarding the underlying pathogenesis of TRALI to inform the development of preventive or therapeutic alternatives.

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rIL‐35 prevents murine transfusion‐related acute lung injury by inhibiting the activation of endothelial cells

Cited by 4 publications

References 44 publications

Pulmonary coagulation and fibrinolysis abnormalities that favor fibrin deposition in the lungs of mouse antibody-mediated transfusion-related acute lung injury

Pulmonary coagulation and fibrinolysis abnormalities that favor fibrin deposition in the lungs of mouse antibody-mediated transfusion-related acute lung injury

The Immune System in Transfusion-Related Acute Lung Injury Prevention and Therapy: Update and Perspective

Update on transfusion-related acute lung injury: an overview of its pathogenesis and management

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