Platelet‐derived microparticles induce polymorphonuclear leukocyte‐mediated damage of human pulmonary microvascular endothelial cells

Xie, R. F.; Hu, Ping; Zc, Wang; Yang, Jie; Yang, Yi; Gao, Li; Fan, Hua; Zhu, Yimin

doi:10.1111/trf.12952

Cited by 43 publications

(36 citation statements)

References 18 publications

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“…Whether EVs are causal of the adverse effects associated with RBC transfusion in patients is not known, but evidence is emerging that EVs may have an effect on key players during a transfusion-related acute lung injury, including white blood cells and the endothelium. It was recently found that neutrophil-induced activation of pulmonary endothelial cells depended on the presence of platelet-derived EVs [16]. Also, in experimental murine models, injection of RBC-derived EVs from stored RBC units was shown to exacerbate lung injury [17,18].…”

Section: Discussionmentioning

confidence: 99%

Extracellular Vesicles from Red Blood Cell Products Induce a Strong Pro-Inflammatory Host Response<b>, </b> Dependent on Both Numbers and Storage Duration

Straat

Böing²,

Boer

et al. 2015

Transfus Med Hemother

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Background: Transfusion of red blood cells (RBCs) is associated with adverse outcome, but the causative factor is unknown. Extracellular vesicles (EVs) have pro-inflammatory properties. We hypothesized that EVs released from both fresh and stored RBC products can induce a host inflammatory response in a dose-dependent manner. Methods: Whole blood was incubated with supernatant from RBC units stored for different time periods, either containing (different numbers of) EVs or depleted from EVs. Results: Incubation with both fresh and stored supernatant containing EVs induced a strong host response with production of TNF, IL-6 and IL-8. In supernatant depleted from EVs, this host response was completely abrogated. IL-10 levels were not affected. EV-induced host response was both dependent on the number of EVs as well as on storage time. Conclusions: EVs from both fresh and stored RBC units illicit a strong inflammatory host response in recipients and may therefore contribute to adverse outcome of RBC transfusion.

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Section: Discussionmentioning

confidence: 99%

Extracellular Vesicles from Red Blood Cell Products Induce a Strong Pro-Inflammatory Host Response<b>, </b> Dependent on Both Numbers and Storage Duration

Straat

Böing²,

Boer

et al. 2015

Transfus Med Hemother

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“…T lymphocytes are recruited in the atherosclerotic lesion and an immunomodulatory role of pMVs on T cells has been recently described (Sadallah et al, 2014). pMVs carry a concentrated CD40L signal, induce polymorphonuclear leukocyte-damage of human pulmonary microvascular ECs and may affect the development of transfusion-related acute lung injury (Xie et al, 2015). Since MVs from platelets contain active executive caspase-3, they have also been involved in apoptosis (Boing et al, 2008).…”

Section: Molecular and Cellular Mechanisms Relating Pmvs With Atherosmentioning

confidence: 99%

Role of Platelet-Derived Microvesicles As Crosstalk Mediators in Atherothrombosis and Future Pharmacology Targets: A Link between Inflammation, Atherosclerosis, and Thrombosis

Suades²,

et al. 2016

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Reports in the last decade have suggested that the role of platelets in atherosclerosis and its thrombotic complications may be mediated, in part, by local secretion of platelet-derived microvesicles (pMVs), small cell blebs released during the platelet activation process. MVs are the most abundant cell-derived microvesicle subtype in the circulation. High concentrations of circulating MVs have been reported in patients with atherosclerosis, acute vascular syndromes, and/or diabetes mellitus, suggesting a potential correlation between the quantity of microvesicles and the clinical severity of the atherosclerotic disease. pMVs are considered to be biomarkers of disease but new information indicates that pMVs are also involved in signaling functions. pMVs evoke or promote haemostatic and inflammatory responses, neovascularization, cell survival, and apoptosis, processes involved in the pathophysiology of cardiovascular disease. This review is focused on the complex cross-talk between platelet-derived microvesicles, inflammatory cells and vascular elements and their relevance in the development of the atherosclerotic disease and its clinical outcomes, providing an updated state-of-the art of pMV involvement in atherothrombosis and pMV potential use as therapeutic agent influencing cardiovascular biomedicine in the future.

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“…This PMN-dependent endothelial cell damage also occurred when adding sCD40L instead of lysoPC [64]. Also other studies found PMN-mediated endothelial cell damage using an in vitro TRALI model in a setting of both non-antibody mediated TRALI [65] and antibody-mediated TRALI [61,66,67]. Furthermore, PMNs were found to interact with von Willebrand factor via choline transporter-like protein-2 (CTL-2), which allowed anti-HNA-3a antibody to induce signal transduction via CD11b/CD18, leading to PMN activation and agglutination [54].…”

Section: Neutrophil Involvement In Tralimentioning

confidence: 99%

The Pathogenic Involvement of Neutrophils in Acute Respiratory Distress Syndrome and Transfusion-Related Acute Lung Injury

Rebetz

Semple

Kapur

2018

Transfus Med Hemother

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The acute respiratory distress syndrome (ARDS) is a serious and common complication of multiple medical and surgical interventions, with sepsis, pneumonia, and aspiration of gastric contents being common risk factors. ARDS develops within 1 week of a known clinical insult or presents with new/worsening respiratory symptoms if the clinical insult is unknown. Approximately 40% of the ARDS cases have a fatal outcome. Transfusion-related acute lung injury (TRALI), on the other hand, is characterized by the occurrence of respiratory distress and acute lung injury, which presents within 6 h after administration of a blood transfusion. In contrast to ARDS, acute lung injury in TRALI is not attributable to another risk factor for acute lung injury. ‘Possible TRALI', however, may have a clear temporal relationship to an alternative risk factor for acute lung injury. Risk factors for TRALI include chronic alcohol abuse and systemic inflammation. TRALI is the leading cause of transfusion-related fatalities. There are no specific therapies available for ARDS or TRALI as both have a complex and incompletely understood pathogenesis. Neutrophils (polymorphonuclear leukocytes; PMNs) have been suggested to be key effector cells in the pathogenesis of both syndromes. In the present paper, we summarize the literature with regard to PMN involvement in the pathogenesis of both ARDS and TRALI based on both human data as well as on animal models. The evidence generally supports a strong role for PMNs in both ARDS and TRALI. More research is required to shed light on the pathogenesis of these respiratory syndromes and to more thoroughly establish the nature of the PMN involvement, especially considering the heterogeneous etiologies of ARDS.

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Platelet‐derived microparticles induce polymorphonuclear leukocyte‐mediated damage of human pulmonary microvascular endothelial cells

Abstract: PMPs carry a concentrated CD40L signal, promote PMN-mediated HMVEC damage, and may affect the development of transfusion-related acute lung injury.

Cited by 43 publications

References 18 publications

Extracellular Vesicles from Red Blood Cell Products Induce a Strong Pro-Inflammatory Host Response<b>, </b> Dependent on Both Numbers and Storage Duration

Extracellular Vesicles from Red Blood Cell Products Induce a Strong Pro-Inflammatory Host Response<b>, </b> Dependent on Both Numbers and Storage Duration

Role of Platelet-Derived Microvesicles As Crosstalk Mediators in Atherothrombosis and Future Pharmacology Targets: A Link between Inflammation, Atherosclerosis, and Thrombosis

The Pathogenic Involvement of Neutrophils in Acute Respiratory Distress Syndrome and Transfusion-Related Acute Lung Injury

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