Academic literature on the topic 'Immunothrombose'
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Journal articles on the topic "Immunothrombose"
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Lou, Jianbo, Jianning Zhang, Quanjun Deng, and Xin Chen. "Neutrophil extracellular traps mediate neuro-immunothrombosis." Neural Regeneration Research 19, no. 8 (December 11, 2023): 1734–40. http://dx.doi.org/10.4103/1673-5374.389625.
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Neutrophil extracellular traps are primarily composed of DNA and histones and are released by neutrophils to promote inflammation and thrombosis when stimulated by various inflammatory reactions. Neutrophil extracellular trap formation occurs through lytic and non-lytic pathways that can be further classified by formation mechanisms. Histones, von Willebrand factor, fibrin, and many other factors participate in the interplay between inflammation and thrombosis. Neuro-immunothrombosis summarizes the intricate interplay between inflammation and thrombosis during neural development and the pathogenesis of neurological diseases, providing cutting-edge insights into post-neurotrauma thrombotic events. The blood-brain barrier defends the brain and spinal cord against external assaults, and neutrophil extracellular trap involvement in blood-brain barrier disruption and immunothrombosis contributes substantially to secondary injuries in neurological diseases. Further research is needed to understand how neutrophil extracellular traps promote blood-brain barrier disruption and immunothrombosis, but recent studies have demonstrated that neutrophil extracellular traps play a crucial role in immunothrombosis, and identified modulators of neuro-immunothrombosis. However, these neurological diseases occur in blood vessels, and the mechanisms are unclear by which neutrophil extracellular traps penetrate the blood-brain barrier to participate in immunothrombosis in traumatic brain injury. This review discusses the role of neutrophil extracellular traps in neuro-immunothrombosis and explores potential therapeutic interventions to modulate neutrophil extracellular traps that may reduce immunothrombosis and improve traumatic brain injury outcomes.
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Hou, Mengyu, Jingxuan Wu, Jiangshuo Li, Meijuan Zhang, Hang Yin, Jingcheng Chen, Zhili Jin, and Ruihua Dong. "Immunothrombosis: A bibliometric analysis from 2003 to 2023." Medicine 103, no. 37 (September 13, 2024): e39566. http://dx.doi.org/10.1097/md.0000000000039566.
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Background: Immunothrombosis is a physiological process that constitutes an intravascular innate immune response. Abnormal immunothrombosis can lead to thrombotic disorders. With the outbreak of COVID-19, there is increasing attention to the mechanisms of immunothrombosis and its critical role in thrombotic events, and a growing number of relevant research papers are emerging. This article employs bibliometrics to discuss the current status, hotspots, and trends in research of this field. Methods: Research papers relevant to immunothrombosis published from January 1, 2003, to May 29, 2023, were collected from the Web of Science Core Collection database. VOSviewer and the R package “Bibliometrix” were employed to analyze publication metrics, including the number of publications, authors, countries, institutions, journals, and keywords. The analysis generated visual results, and trends in research topics and hotspots were examined. Results: A total of 495 target papers were identified, originating from 58 countries and involving 3287 authors from 1011 research institutions. Eighty high-frequency keywords were classified into 5 clusters. The current key research topics in the field of immunothrombosis include platelets, inflammation, neutrophil extracellular traps, Von Willebrand factor, and the complement system. Research hotspots focus on the mechanisms and manifestations of immunothrombosis in COVID-19, as well as the discovery of novel treatment strategies targeting immunothrombosis in cardiovascular and cerebrovascular diseases. Conclusion: Bibliometric analysis summarizes the main achievements and development trends in research on immunothrombosis, offering readers a comprehensive understanding of the field and guiding future research directions.
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Grover, Steven P., and Nigel Mackman. "Neutrophils, NETs, and immunothrombosis." Blood 132, no. 13 (September 27, 2018): 1360–61. http://dx.doi.org/10.1182/blood-2018-08-868067.
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In this issue of Blood, Yago et al1 describe the mechanism by which neutrophils adhere to activated endothelium and enhance murine venous thrombosis through formation of neutrophil extracellular traps (NETs).
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Thakur, Manovriti, Carolina Victoria Cruz Junho, Sarah Maike Bernhard, Marc Schindewolf, Heidi Noels, and Yvonne Döring. "NETs-Induced Thrombosis Impacts on Cardiovascular and Chronic Kidney Disease." Circulation Research 132, no. 8 (April 14, 2023): 933–49. http://dx.doi.org/10.1161/circresaha.123.321750.
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Arterial and venous thrombosis constitute a major source of morbidity and mortality worldwide. Association between thrombotic complications and cardiovascular and other chronic inflammatory diseases are well described. Inflammation and subsequent initiation of thrombotic events, termed immunothrombosis, also receive growing attention but are still incompletely understood. Nevertheless, the clinical relevance of aberrant immunothrombosis, referred to as thromboinflammation, is evident by an increased risk of thrombosis and cardiovascular events in patients with inflammatory or infectious diseases. Proinflammatory mediators released from platelets, complement activation, and the formation of NETs (neutrophil extracellular traps) initiate and foster immunothrombosis. In this review, we highlight and discuss prominent and emerging interrelationships and functions between NETs and other mediators in immunothrombosis in cardiovascular disease. Also, with patients with chronic kidney disease suffering from increased cardiovascular and thrombotic risk, we summarize current knowledge on neutrophil phenotype, function, and NET formation in chronic kidney disease. In addition, we elaborate on therapeutic targeting of NETs-induced immunothrombosis. A better understanding of the functional relevance of antithrombotic mediators which do not increase bleeding risk may provide opportunities for successful therapeutic interventions to reduce thrombotic risk beyond current treatment options.
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Chooklin, S., and S. Chuklin. "IMMUNOTHROMBOSIS AS A COMPONENT OF HOST DEFENCE." Fiziolohichnyĭ zhurnal 69, no. 5 (October 5, 2023): 89–99. http://dx.doi.org/10.15407/fz69.05.089.
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Immunothrombosis is a normal physiological phenomenon against harmful pathogens that can limit their further spread. It is an important element of the intravascular innate immune system and performs at least four different physiological functions: it helps to capture and localize pathogens; it prevents the invasion of pathogens into tissues by microthrombosis; it contributes to the destruction of pathogens; it helps to recruit additional immune cells to the site of tissue infection and/or damage. The main driving forces of immunothrombosis are platelets, neutrophils and the complement system. This review examines the role of immunothrombosis in protecting the host and its main mechanisms.
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Goshua, George, Ayesha Butt, and Alfred I. Lee. "Immunothrombosis: a COVID‐19 concerto." British Journal of Haematology 194, no. 3 (July 7, 2021): 491–93. http://dx.doi.org/10.1111/bjh.17666.
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Palankar, Raghavendra, and Andreas Greinacher. "Challenging the concept of immunothrombosis." Blood 133, no. 6 (February 7, 2019): 508–9. http://dx.doi.org/10.1182/blood-2018-11-886267.
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Nakazawa, Daigo, and Akihiro Ishizu. "Immunothrombosis in severe COVID-19." EBioMedicine 59 (September 2020): 102942. http://dx.doi.org/10.1016/j.ebiom.2020.102942.
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Ebeyer-Masotta, Marie, Tanja Eichhorn, René Weiss, Vladislav Semak, Lucia Lauková, Michael B. Fischer, and Viktoria Weber. "Heparin-Functionalized Adsorbents Eliminate Central Effectors of Immunothrombosis, including Platelet Factor 4, High-Mobility Group Box 1 Protein and Histones." International Journal of Molecular Sciences 23, no. 3 (February 5, 2022): 1823. http://dx.doi.org/10.3390/ijms23031823.
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Inflammation and thrombosis are closely intertwined in numerous disorders, including ischemic events and sepsis, as well as coronavirus disease 2019 (COVID-19). Thrombotic complications are markers of disease severity in both sepsis and COVID-19 and are associated with multiorgan failure and increased mortality. Immunothrombosis is driven by the complement/tissue factor/neutrophil axis, as well as by activated platelets, which can trigger the release of neutrophil extracellular traps (NETs) and release further effectors of immunothrombosis, including platelet factor 4 (PF4/CXCL4) and high-mobility box 1 protein (HMGB1). Many of the central effectors of deregulated immunothrombosis, including activated platelets and platelet-derived extracellular vesicles (pEVs) expressing PF4, soluble PF4, HMGB1, histones, as well as histone-decorated NETs, are positively charged and thus bind to heparin. Here, we provide evidence that adsorbents functionalized with endpoint-attached heparin efficiently deplete activated platelets, pEVs, PF4, HMGB1 and histones/nucleosomes. We propose that this elimination of central effectors of immunothrombosis, rather than direct binding of pathogens, could be of clinical relevance for mitigating thrombotic complications in sepsis or COVID-19 using heparin-functionalized adsorbents.
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Ryan, Tristram A. J., Roger J. S. Preston, and Luke A. J. O'Neill. "Immunothrombosis and the molecular control of tissue factor by pyroptosis: prospects for new anticoagulants." Biochemical Journal 479, no. 6 (March 28, 2022): 731–50. http://dx.doi.org/10.1042/bcj20210522.
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The interplay between innate immunity and coagulation after infection or injury, termed immunothrombosis, is the primary cause of disseminated intravascular coagulation (DIC), a condition that occurs in sepsis. Thrombosis associated with DIC is the leading cause of death worldwide. Interest in immunothrombosis has grown because of COVID-19, the respiratory disease caused by SARS-CoV-2, which has been termed a syndrome of dysregulated immunothrombosis. As the relatively new field of immunothrombosis expands at a rapid pace, the focus of academic and pharmacological research has shifted from generating treatments targeted at the traditional ‘waterfall’ model of coagulation to therapies better directed towards immune components that drive coagulopathies. Immunothrombosis can be initiated in macrophages by cleavage of the non-canonical inflammasome which contains caspase-11. This leads to release of tissue factor (TF), a membrane glycoprotein receptor that forms a high-affinity complex with coagulation factor VII/VIIa to proteolytically activate factors IX to IXa and X to Xa, generating thrombin and leading to fibrin formation and platelet activation. The mechanism involves the post-translational activation of TF, termed decryption, and release of decrypted TF via caspase-11-mediated pyroptosis. During aberrant immunothrombosis, decryption of TF leads to thromboinflammation, sepsis, and DIC. Therefore, developing therapies to target pyroptosis have emerged as an attractive concept to counteract dysregulated immunothrombosis. In this review, we detail the three mechanisms of TF control: concurrent induction of TF, caspase-11, and NLRP3 (signal 1); TF decryption, which increases its procoagulant activity (signal 2); and accelerated release of TF into the intravascular space via pyroptosis (signal 3). In this way, decryption of TF is analogous to the two signals of NLRP3 inflammasome activation, whereby induction of pro-IL-1β and NLRP3 (signal 1) is followed by activation of NLRP3 (signal 2). We describe in detail TF decryption, which involves pathogen-induced alterations in the composition of the plasma membrane and modification of key cysteines on TF, particularly at the location of the critical, allosterically regulated disulfide bond of TF in its 219-residue extracellular domain. In addition, we speculate towards the importance of identifying new therapeutics to block immunothrombotic triggering of TF, which can involve inhibition of pyroptosis to limit TF release, or the direct targeting of TF decryption using cysteine-modifying therapeutics.
Dissertations / Theses on the topic "Immunothrombose"
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Garcia, Geoffrey. "Les NETs (Neutrophils Extracellular Traps) et les DNases au cours de la COVID-19." Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0175.
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Au cours des infections, les polynucléaires neutrophiles libèrent des Neutrophil Extracellular Traps (NETs) pour capturer les agents pathogènes et les détruire. Les NETs; en coordination avec les plaquettes et les cellules immunitaires, activent la coagulation et participent à l’immunothrombose pour piéger les agents pathogènes et éviter leur dissémination. Ils sont dégradés physiologiquement par les DNases et les macrophages. Exacerbée, les NETs sont responsables de dommages cellulaires et tissulaires. Ils sont décrits comme des acteurs centraux de nombreuses pathologies, notamment comme participant à la thrombose (artérielle et veineuse), et aux formes sévères de la COVID-19. Cependant, les techniques de dosages de NETs et des DNases ne sont à ce jour pas standardisés et les mécanismes sous-jacent à l’exacerbation de la NETose au cours de la COVID-19 peu décrits.Nous émettons l’hypothèse que l’aggravation clinique des patients au cours de la COVID-19 est liée à un déséquilibre entre les NETS et les DNases.Pour réponde à cette hypothèse, nous avons pour objectifs : (1) définir les conditions pré-analytiques optimales pour doser les marqueurs de NETs; (2) mettre au point et valider une méthode de dosage de l’activité des DNases plasmatiques ; (3) Évaluer la balance entre marqueurs de NETs et activité des DNases en fonction de la sévérité de la COVID-19 ; (4) Étudier les mécanismes responsables de ce déséquilibre NETs/DNases.Identifier déficit en DNase comme facteur aggravant chez les patents permettrait d’imaginer de nouvelles thérapeutiques innovantes pour prévenir cette aggravation clinique comme l’administration de DNaseNeutrophil Extracellular Traps and DNases involvement during During infection, neutrophils release Neutrophil Extracellular Traps (NETs) to capture,prevent the dissemination of, and kill pathogens. NETs contribute to immunothrombosis byinteracting with platelets and immune cells, thus activating coagulation. However, excessiveproduction of NETs can cause thromboinflammation, leading to cellular and tissue damage. NETsare implicated in the pathophysiology of both arterial and venous thrombosis and in severe formsof COVID-19. They are physiologically degraded by DNases and macrophages. Currently, DNasetechniques are not standardized, and the mechanisms underlying the exacerbation of NETosis inCOVID-19 are not well understood. We first aimed to develop a functional assay to evaluate theability of DNases in human samples to degrade DNA or NETs. We established a robust,repeatable, and reproducible method that can be applied to both serum and plasma.Subsequently, we assessed the balance between NET markers and DNase activity according toCOVID-19 severity, and studied the mechanisms responsible for the NETs/DNases imbalance. Weconfirmed that NET markers increase with disease severity and demonstrated a decrease inDNase activity in hospitalized patients, resulting in an imbalance between NET markers andDNase activity in this group. The most severe patients exhibited decreased levels of DNase 1,with some harboring polymorphisms in the DNase 1 gene correlating with low protein levels.Additionally, we observed that critically ill patients had lower levels of plasmacytoid dendriticcells compared to those with severe disease. Reanalysis of public single cell RNA sequencing datashowed that plasmacytoid dendritic cells express less DNase 1L3 RNA as the disease severityincreases. This study demonstrates that COVID-19 severity is associated with an imbalance inNETs and DNases. Identifying this DNase deficit as an aggravating factor in patients could lead tonew therapeutic strategies, such as DNase administration, to prevent clinical deterioration
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Jörg, Paul [Verfasser], and Christian [Akademischer Betreuer] Schulz. "Merkmale der Immunothrombose in arteriellen Thromben von Patienten mit akutem Myokardinfarkt und ischämischem Apoplex : eine explorative Studie zum Vergleich der Histologie und zur Korrelation klinischer Parameter / Paul Jörg ; Betreuer: Christian Schulz." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2020. http://d-nb.info/1223849805/34.
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Frydman, Galit Hocsman. "The role of megakaryocytes and platelets in infection and immunothrombosis." Thesis, Massachusetts Institute of Technology, 2017. http://hdl.handle.net/1721.1/115756.
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Thesis: Sc. D., Massachusetts Institute of Technology, Department of Biological Engineering, 2018.Cataloged from PDF version of thesis. Includes CD-ROM with 9 videos in the .avi format and 2 video in the .mp4 format.
Includes bibliographical references.
Megakaryocytes (MKs), one of the largest and rarest hematopoietic stem cells in the bone marrow, have traditionally played a primary role in hemostasis as precursors to platelets, which are importantly, one of the most abundant cell types in the peripheral circulation. While platelets are studied for their various roles in inflammation, the role of MKs within the innate immune system has not been explored. In a series of comprehensive in vitro experiments, we have demonstrated that both cord blood-derived MKs and MKs from a megakaryoblastic lineage have innate immune cell functions, including: phagocytosis, formation of extracellular traps, and chemotaxis towards pathogenic stimuli. MKs were also observed to directionally release platelets towards pathogenic stimuli. In addition to their primary role as immune cells, MKs were also shown to contain extranuclear histones, which the MKs release along with budding platelets into the circulation. These small packages of histones can play a major role in inflammation and immunothrombosis by promoting inflammation and coagulation. By evaluating blood and tissue samples from patients diagnosed with sepsis, we demonstrated that there is an increased MK concentration both in the peripheral circulation, as well as in the lungs and kidneys. Platelets from patients with sepsis also appeared to have a specific phenotype, including increased DNA and histone staining. MK number in the circulation and end-organs, as well as platelet histone expression appeared to be correlated with both prognosis and type of infection. This newly recognized role of MKs as functional innate immune cells may have significant implications for the role of MKs in conditions such as sepsis and, pending a more profound mechanistic understanding, may further lead to the development of novel targets for the treatment of sepsis.
by Galit Hocsman Frydman.
Sc. D.
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Nordling, Sofia. "Vascular Interactions in Innate Immunity and Immunothrombosis: : Models of Endothelial Protection." Doctoral thesis, Uppsala universitet, Institutionen för immunologi, genetik och patologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-283548.
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The phenomenon known as immunothrombosis has garnered increased attention over the last few years. Much work has been done to characterize the cross talk between hemostasis and the innate immune system. This thesis outlines the role of the vascular endothelial cells during immunothrombotic events as regulators of coagulation, platelet-, and leukocyte recruitment. A newly developed method for investigating the interaction between endothelial cells and the blood compartment illustrated the procoagulant and proinflammatory effects elicited by tumor necrosis factor α activated endothelial cells upon exposure to whole blood. The method was utilized in evaluating treatment of endothelial dysfunction and disruption with a heparin conjugate. Damaged or hypoxic endothelial cells, in addition to basement membrane collagen, that were pretreated with the heparin conjugate prior to contact with blood were found to have reduced activation of coagulation, platelet-, and leukocyte recruitment; in contrast to unfractionated heparin, which had no effect on the aforementioned parameters. The treatment was then investigated in the setting of ischemia reperfusion injury during kidney transplantation and the heparin conjugate was found to bind cultured endothelial cells with high avidity under cold storage conditions. Furthermore, it was found to bind to the renal vasculature during static cold storage and was subsequently found to be beneficial with regard to early graft function in an experimental mouse model of syngeneic kidney transplantation. Recipients of kidneys treated with the heparin conjugate had reduced serum creatinine compared to controls 24 hours after transplantation. Lastly, the anticoagulant properties of the heparin conjugate were investigated in comparison to unfractionated heparin. While the conjugate exerted reduced capacity with regard to thrombin inhibition, it rapidly inhibited the binding of platelets to exposed collagen. The conjugate was furthermore found to preferentially locate to sites of endothelial cell activation at early stage during endotoxic shock in mice. In conclusion, this thesis demonstrates that disrupted functioning of the vascular endothelial cells actively contributes to immunothrombosis, and that it is possible to model endothelial cell function using whole blood assays. Furthermore, this thesis presents a treatment that enhances the hemocompatibility of damaged endothelial cells and subsequently improves the early renal function after kidney transplantation.
Book chapters on the topic "Immunothrombose"
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Nair, Arjun. "Imaging Critically Ill Patients." In Oxford Textbook of Respiratory Critical Care, 165–82. Oxford University PressOxford, 2023. http://dx.doi.org/10.1093/med/9780198766438.003.0018.
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Abstract Summary As with any patient, the need for, and type of, imaging in the critically ill patient must be guided by the clinical question to be answered and an understanding of the advantages and limitations of each type of imaging. Imaging can be used to guide ventilation strategy, assess underlying causative pathology, assess complications, and aid prognostication. Notwithstanding its technical limitations, portable chest radiography overwhelmingly remains the cornerstone of serial critical care imaging. Computed tomographic (CT) protocols can be tailored to the clinical question, with paired low- and high-ventilatory pressure CT a crucial method of assessing alveolar recruitment. Ultrasound has gained an invaluable role in the bedside assessment of both pleural and pulmonary pathology in critically ill patients. In certain units, the COVID-19 pandemic has expanded the role of ultrasound in serial monitoring, given the portable nature of, and simple disinfection procedures for, ultrasound equipment. Newer techniques such as electrical impedance tomography, as well as well-developed but less utilized techniques of positron emission tomography and magnetic resonance imaging, provide valuable pathophysiologic insights but are currently mainly confined to research applications. A potential role for dual-energy CT pulmonary angiography in quantifying reduced pulmonary blood volume, as a marker of pulmonary vascular immunothrombosis, has been proposed.
Conference papers on the topic "Immunothrombose"
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Hayden, Oliver, Klaus Diepold, Christian Klenk, Johanna Erber, David Fresacher, Stefan Röhrl, Manuel Lengl, et al. "Immunothrombosis of acute care patients quantified with phase imaging flow cytometry." In Quantitative Phase Imaging X, edited by YongKeun Park and Yang Liu. SPIE, 2024. http://dx.doi.org/10.1117/12.3022776.
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Mueller, T., S. Meister, M. Thakur, M. Wohlrab, S. Bortoluzzi, N. Jensen, M. Rossner, M. Schmidt-Supprian, S. Massberg, and B. Engelmann. "Microvascular immune cell recruitment regulating development of immunothrombosis in systemic bacterial infection." In 65th Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1728141.
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