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      Influence of hemoadsorption during cardiopulmonary bypass on blood vesicle count and function

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          Abstract

          Background

          Extracorporeal circulation during major cardiac surgery triggers a systemic inflammatory response affecting the clinical course and outcome. Recently, extracellular vesicle (EV) research has shed light onto a novel cellular communication network during inflammation. Hemoadsorption (HA) systems have shown divergent results in modulating the systemic inflammatory response during cardiopulmonary bypass (CPB) surgery. To date, the effect of HA on circulating microvesicles (MVs) in patients undergoing CPB surgery is unknown.

          Methods

          Count and function of MVs, as part of the extracellular vesicle fraction, were assessed in a subcohort of a single-center, blinded, controlled study investigating the effect of the CytoSorb device during CPB. A total of 18 patients undergoing elective CPB surgery with (n = 9) and without (n = 9) HA device were included in the study. MV phenotyping and counting was conducted via flow cytometry and procoagulatory potential was measured by tissue factor-dependent MV assays.

          Results

          Both study groups exhibited comparable counts and post-operative kinetics in MV subsets. Tissue factor-dependent procoagulatory potential was not detectable in plasma at any timepoint. Post-operative course and laboratory parameters showed no correlation with MV counts in patients undergoing CPB surgery.

          Conclusion

          Additional artificial surfaces to the CPB-circuit introduced by the use of the HA device showed no effect on circulating MV count and function in these patients. Larger studies are needed to assess and clarify the effect of HA on circulating vesicle counts and function.

          Trial registration ClinicalTrials.Gov Identifier: NCT01879176; registration date: June 17, 2013; https://clinicaltrials.gov/ct2/show/NCT01879176

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          Most cited references23

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          HMGB1 loves company.

          HMGB1, outside of a cell, is a trigger of inflammation and a stimulus for tissue reconstruction; the balance may depend on the complexes it forms with other molecules. HMGB1 is the prime example of a danger signal that originates from the damaged self rather than from invading pathogens. HMGB1 is released by cells that die traumatically and is secreted by cells destined to die and by activated cells of the innate immunity system. As a danger signal, HMGB1 is expected to trigger inflammation, but recent reports indicate that pure recombinant HMGB1 has no proinflammatory activity and only acts as a chemoattractant and a mitogen. However, HMGB1 forms highly inflammatory complexes with ssDNA, LPS, IL-1beta, and nucleosomes, which interact with TLR9, TLR4, IL-1R, and TLR2 receptors, respectively. Thus, HMGB1 has dual activities, solo or in company; I speculate that this may serve our body's necessity to sacrifice or reconstruct tissues as required by the presence or absence of pathogens.
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            Inflammatory response to cardiopulmonary bypass.

            Inflammation in cardiac surgical patients is produced by complex humoral and cellular interactions with numerous pathways including activation, generation, or expression of thrombin, complement, cytokines, neutrophils, adhesion molecules, mast cells, and multiple inflammatory mediators. Because of the redundancy of the inflammatory cascades, profound amplification occurs to produce multiorgan system dysfunction that can manifest as coagulopathy, respiratory failure, myocardial dysfunction, renal insufficiency, and neurocognitive defects. Coagulation and inflammation are also closely linked through networks of both humoral and cellular components including proteases of the clotting and fibrinolytic cascades, including tissue factor. Vascular endothelial cells also mediate inflammation and the cross talk between coagulation and inflammation. Novel antiinflammatory agents inhibit these processes by several mechanisms such as preventing proteolysis of the protease-activated receptor (aprotinin), inhibiting complement-mediated injury (pexelizumab), or inhibiting contact activation (kallikrein inhibitors). Surgery alone also activates specific hemostatic responses, activation of immune mechanisms, and inflammatory response mediated by the release of various cytokines and chemokines. Novel agents are under investigation to further improve outcomes in cardiac surgical patients.
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              The alarmin HMGB1 acts in synergy with endogenous and exogenous danger signals to promote inflammation.

              The nuclear protein HMGB1 has previously been demonstrated to act as an alarmin and to promote inflammation upon extracellular release, yet its mode of action is still not well defined. Access to highly purified HMGB1 preparations from prokaryotic and eukaryotic sources enabled studies of activation of human PBMC or synovial fibroblast cultures in response to HMGB1 alone or after binding to cofactors. HMGB1 on its own could not induce detectable IL-6 production. However, strong enhancing effects on induction of proinflammatory cytokine production occurred when the protein associated with each of the separate proinflammatory molecules, rhIL-1beta, the TLR4 ligand LPS, the TLR9 ligand CpG-ODN, or the TLR1-TLR2 ligand Pam3CSK4. The bioactivities were recorded in cocultures with preformed HMGB1 complexes but not after sequential or simultaneous addition of HMGB1 and the individual ligands. Individual A-box and B-box domains of HMGB1 had the ability to bind LPS and enhance IL-6 production. Heat denaturation of HMGB1 eliminated this enhancement. Cocultures with HMGB1 and other proinflammatory molecules such as TNF, RANKL, or IL-18 did not induce enhancement. HMGB1 thus acts broadly with many but not all immunostimulatory molecules to amplify their activity in a synergistic manner.
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                Author and article information

                Contributors
                martin.bernardi@meduniwien.ac.at
                Journal
                J Transl Med
                J Transl Med
                Journal of Translational Medicine
                BioMed Central (London )
                1479-5876
                15 May 2020
                15 May 2020
                2020
                : 18
                : 202
                Affiliations
                [1 ]GRID grid.22937.3d, ISNI 0000 0000 9259 8492, Comprehensive Center for Pediatrics, Department of Paediatrics and Adolescent Medicine, Division of Neonatology, Paediatric Intensive Care & Neuropaediatrics, , Medical University of Vienna, ; Vienna, Austria
                [2 ]GRID grid.22937.3d, ISNI 0000 0000 9259 8492, Department of Surgery, Research Labs, , Medical University of Vienna, ; Vienna, Austria
                [3 ]GRID grid.22937.3d, ISNI 0000 0000 9259 8492, Clinical Division of Haematology and Haemostaseology, Department of Medicine I, , Medical University of Vienna, ; Vienna, Austria
                [4 ]GRID grid.15462.34, ISNI 0000 0001 2108 5830, Christian Doppler Laboratory for Innovative Therapy Approaches in Sepsis, Department for Biomedical Research, , Danube University Krems, ; Krems, Austria
                [5 ]GRID grid.413250.1, ISNI 0000 0000 9585 4754, Department of Anesthesia and Intensive Care Medicine, , Landeskrankenhaus Feldkirch, ; Feldkirch, Austria
                [6 ]GRID grid.22937.3d, ISNI 0000 0000 9259 8492, Division of Cardiac Thoracic Vascular Anaesthesia and Intensive Care Medicine, , Medical University of Vienna, ; Waehringer Guertel 18-20, 1090 Vienna, Austria
                [7 ]GRID grid.22937.3d, ISNI 0000 0000 9259 8492, Core Facility Flow Cytometry, , Medical University of Vienna, ; Vienna, Austria
                Author information
                http://orcid.org/0000-0002-8297-898X
                Article
                2369
                10.1186/s12967-020-02369-x
                7229608
                32414386
                3049c7b0-c69e-403e-abff-494588cb74de
                © The Author(s) 2020

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 24 August 2019
                : 7 May 2020
                Categories
                Research
                Custom metadata
                © The Author(s) 2020

                Medicine
                blood vesicle,cardiopulmonary bypass,extracellular vesicles,hemoadsorption,microvesicles
                Medicine
                blood vesicle, cardiopulmonary bypass, extracellular vesicles, hemoadsorption, microvesicles

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