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Journal articles on the topic 'Immunothrombose'

Author: Grafiati

Published: 16 November 2024

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1

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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.

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11

Marcos-Jubilar, María, Ramón Lecumberri, and José A. Páramo. "Immunothrombosis: Molecular Aspects and New Therapeutic Perspectives." Journal of Clinical Medicine 12, no. 4 (February 9, 2023): 1399. http://dx.doi.org/10.3390/jcm12041399.

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Thromboinflammation or immunothrombosis is a concept that explains the existing link between coagulation and inflammatory response present in many situations, such as sepsis, venous thromboembolism, or COVID-19 associated coagulopathy. The purpose of this review is to provide an overview of the current data regarding the mechanisms involved in immunothrombosis in order to understand the new therapeutic strategies focused in reducing thrombotic risk by controlling the inflammation.

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12

Xu, Pengxiang, Liuyan Xin, Xiaoping Xiao, Yong Huang, Chuanming Lin, Xiaofang Liu, Haiyan Wei, Rong Xu, and Yijian Chen. "Neutrophils: As a Key Bridge between Inflammation and Thrombosis." Evidence-Based Complementary and Alternative Medicine 2022 (November 9, 2022): 1–7. http://dx.doi.org/10.1155/2022/1151910.

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Immunothrombosis is a mechanism of defense of the organism against pathogenic microorganisms that increases their recognition, limitation, and clearance and is part of the innate immune defense. Physiological immunothrombosis is beneficial to the body against the invasion of pathogenic microorganisms, but when immunothrombosis is out of control, it is easy to cause thrombotic diseases, thus, causing unpredictable consequences to the body. Neutrophils play a pivotal role in this process. Understanding the mechanism of neutrophils in immune thrombosis and out-of-control is particularly important for the treatment of related thrombotic diseases. In this review, we studied the role of neutrophils in immune thrombosis and each link out of control (including endothelial cell dysfunction; activation of platelets; activation of coagulation factor; inhibition of the anticoagulation system; and inhibition of the fibrinolysis system).

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13

Yost, Christian C. "Pediatric immunothrombosis—Understudied… but what potential!" Pediatric Research 86, no. 1 (April 9, 2019): 17–18. http://dx.doi.org/10.1038/s41390-019-0389-5.

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14

Páramo, José Antonio, and Ramón Lecumberri. "New mechanisms in venous thrombosis: Immunothrombosis." Medicina Clínica (English Edition) 153, no. 2 (July 2019): 78–81. http://dx.doi.org/10.1016/j.medcle.2019.05.003.

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15

Hernández-Huerta, María Teresa, Alma Dolores Pérez-Santiago, Laura Pérez-Campos Mayoral, Luis Manuel Sánchez Navarro, Francisco Javier Rodal Canales, Abraham Majluf-Cruz, Carlos Alberto Matias-Cervantes, et al. "Mechanisms of Immunothrombosis by SARS-CoV-2." Biomolecules 11, no. 11 (October 20, 2021): 1550. http://dx.doi.org/10.3390/biom11111550.

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SARS-CoV-2 contains certain molecules that are related to the presence of immunothrombosis. Here, we review the pathogen and damage-associated molecular patterns. We also study the imbalance of different molecules participating in immunothrombosis, such as tissue factor, factors of the contact system, histones, and the role of cells, such as endothelial cells, platelets, and neutrophil extracellular traps. Regarding the pathogenetic mechanism, we discuss clinical trials, case-control studies, comparative and translational studies, and observational studies of regulatory or inhibitory molecules, more specifically, extracellular DNA and RNA, histones, sensors for RNA and DNA, as well as heparin and heparinoids. Overall, it appears that a network of cells and molecules identified in this axis is simultaneously but differentially affecting patients at different stages of COVID-19, and this is characterized by endothelial damage, microthrombosis, and inflammation.

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16

Norris, Brandon, Abraham Chorbajian, John Dawi, Aishvaryaa Shree Mohan, Ira Glassman, Jacob Ochsner, Yura Misakyan, et al. "Evaluation of Glutathione in Spike Protein of SARS-CoV-2 Induced Immunothrombosis and Cytokine Dysregulation." Antioxidants 13, no. 3 (February 22, 2024): 271. http://dx.doi.org/10.3390/antiox13030271.

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Thrombotic microangiopathy has been identified as a dominant mechanism for increased mortality and morbidity in coronavirus disease 2019 (COVID-19). In the context of severe COVID-19, patients may develop immunothrombosis within the microvasculature of the lungs, which contributes to the development of acute respiratory distress syndrome (ARDS), a leading cause of death in the disease. Immunothrombosis is thought to be mediated in part by increased levels of cytokines, fibrin clot formation, and oxidative stress. Glutathione (GSH), a well-known antioxidant molecule, may have therapeutic effects in countering this pathway of immunothrombosis as decreased levels of (GSH) have been associated with increased viral replication, cytokine levels, and thrombosis, suggesting that glutathione supplementation may be therapeutic for COVID-19. GSH supplementation has never been explored as a means of treating COVID-19. This study investigated the effectiveness of liposomal glutathione (GSH) as an adjunctive therapy for peripheral blood mononuclear cells (PBMC) treated with SARS CoV-2 spike protein. Upon the addition of GSH to cell cultures, cytokine levels, fibrin clot formation, oxidative stress, and intracellular GSH levels were measured. The addition of liposomal-GSH to PBMCs caused a statistically significant decrease in cytokine levels, fibrin clot formation, and oxidative stress. The addition of L-GSH to spike protein and untreated PBMCs increased total intracellular GSH, decreased IL-6, TGF-beta, and TNF-alpha levels, decreased oxidative stress, as demonstrated through MDA, and decreased fibrin clot formation, as detected by fluorescence microscopy. These findings demonstrate that L-GSH supplementation within a spike protein-treated PBMC cell culture model reduces these factors, suggesting that GSH supplementation should be explored as a means of reducing mediators of immunothrombosis in COVID-19.

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17

Engelmann, Bernd, and Steffen Massberg. "Innate Immunity, Coagulation, and Thrombosis." Blood 124, no. 21 (December 6, 2014): SCI—28—SCI—28. http://dx.doi.org/10.1182/blood.v124.21.sci-28.sci-28.

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Abstract In evolutionarily ancient animals such as insects and crustaceans, the host responses to physical injury and to invading pathogens can be mediated by the same mechanism of coagulum formation of the hemolymph. During vertebrate evolution hemostasis has emerged as an independent process primarily involved in the rapid repair of blood vessel injuries. The core processes of hemostasis are blood coagulation (resulting in fibrin formation) and platelet activation. Both processes can independently interact with inflammatory responses as apparent in a pathological context such as during development of disseminated intravascular coagulation (DIC). Moreover, extravascular fibrin formation can promote the trapping of pathogens and thereby help to contain infections. Nonetheless, the connections between fibrin formation, platelet activation and innate immunity are incompletely understood. We have recently shown that during early systemic infection with E. coli microvascular thrombi are formed which capture bacteria together with innate leukocytes. These thrombi are fibrin-rich and are in general observed in less than 10% of vessels with diameters < 25 µm. Their formation is not accompanied by marked activation of inflammation since the levels of pro-inflammatory markers are unchanged. Microvascular thrombosis is almost completely suppressed in mice deficient for the neutrophil serine proteases elastase and cathepsin G (NE/CG-/-) which are major microbicidal effectors of neutrophils. In the microcirculation of NE/CG-/- mice, microbes are mostly tissue-associated. In contrast, they are mostly present inside blood vessels in wild type mice. The results of experimental changes in microvascular fibrin formation show that intravascular blood coagulation is causally involved in the capturing of bacteria and of myeloid cells and, additionally, promotes the bacterial killing. Overall this suggests that microvascular thrombosis supports recognition, containment and elimination of bacteria without inducing noticeable damage to the host. It thus fulfills the criteria for a comprehensive intravascular process of innate immunity. This mechanism of intravascular immunity, which was termed "immunothrombosis," is supported by tissue factor (TF), the overall initiator of blood coagulation, and by factor XII, the starter protein of the contact pathway. In particular, extracellular nucleosomes (eNUC)/neutrophil extracellular traps (NETs) are indispensable for immunothrombosis. eNUC/NETs promote thrombosis by critically enhancing degradation of TFPI, the major antagonist of the coagulation start, via neutrophil elastase and by factor XII activation. Release of eNUC/NETs by neutrophils and induction of intravascular coagulation essentially require interaction of activated platelets with neutrophils. Interestingly, intravascular TF, factor XII, eNUC/NETs and innate leukocytes are almost completely dispensable for hemostasis. Furthermore, immunothrombosis in contrast to hemostasis develops in largely intact blood vessels. Together this indicates that thrombosis can be a physiological mechanism of innate immunity that is distinct from hemostasis. We have recently developed a new model for deep vein thrombosis (DVT) which closely reproduces the pathological changes in the vessel wall observed in most patients with DVT. Using this model, we show that intravascular TF, factor XII, eNUC/NETs, innate leukocytes and their interactions with platelets all critically promote DVT. Thus, DVT shares similar triggers (especially pathogens) and identical molecular and cellular mediators with immunothrombosis. In case of DIC, the connections to immunothrombosis are most likely similarly strong or even stronger. Finally, our results also show that mediators of immunothrombosis such as eNUC/NETs and neutrophil serine proteases are main triggers of arterial thrombosis. Hence, together with hemostasis, immunothrombosis likely constitutes the major biological template process for both (pathological) microvascular thrombosis and large vessel thrombosis. Disclosures No relevant conflicts of interest to declare.

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Patel, Pravin, James V. Michael, Ulhas P. Naik, and Steven E. McKenzie. "Platelet FcγRIIA in immunity and thrombosis: Adaptive immunothrombosis." Journal of Thrombosis and Haemostasis 19, no. 5 (March 14, 2021): 1149–60. http://dx.doi.org/10.1111/jth.15265.

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19

Anitua, Eduardo, Roberto Prado, and Sabino Padilla. "Evolutionary Insight into Immunothrombosis as a Healing Mechanism." International Journal of Molecular Sciences 23, no. 15 (July 28, 2022): 8346. http://dx.doi.org/10.3390/ijms23158346.

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Both invertebrates and vertebrates possess a cluster of immediate and local wound-sealing, pathogen-killing, and tissue healing responses known as immunoclotting and immunothrombosis, respectively, to cope with two life-threatening emergencies, namely, bleeding and microbial invasion. Despite their convergence in function, immunoclotting and immunothrombosis are deployed by different blood cells and intravascular multidomain proteins. In vertebrates, these proteins share some domains with intrinsic chemical affinities useful in generating cooperative networks such as pathogen and damage pattern recognition molecules. Moreover, many of the proteins involved in coagulation and fibrinolysis in humans are multifunctional molecules playing roles in other processes from inflammation to healing and beyond. In our modern society, however, the interaction of activated intravascular allosteric proteins with one another and with blood cells entails vulnerabilities posing a biological paradox: intravascular proteins that locally operate as tissue repair enhancers can nevertheless generate pathogenic processes by acting systemically. In this manuscript, we contextualize and frame the coagulation system and hemostasis through an evolutionary time scale, illustrating their role as dual players in the defense against exsanguination and pathogens while significantly influencing wound healing.

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20

Globisch, Maria Ascencion, Favour Chinyere Onyeogaziri, Ross Osborne Smith, Maximiliano Arce, and Peetra Ulrica Magnusson. "Dysregulated Hemostasis and Immunothrombosis in Cerebral Cavernous Malformations." International Journal of Molecular Sciences 23, no. 20 (October 20, 2022): 12575. http://dx.doi.org/10.3390/ijms232012575.

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Cerebral cavernous malformation (CCM) is a neurovascular disease that affects 0.5% of the general population. For a long time, CCM research focused on genetic mutations, endothelial junctions and proliferation, but recently, transcriptome and proteome studies have revealed that the hemostatic system and neuroinflammation play a crucial role in the development and severity of cavernomas, with some of these publications coming from our group. The aim of this review is to give an overview of the latest molecular insights into the interaction between CCM-deficient endothelial cells with blood components and the neurovascular unit. Specifically, we underscore how endothelial dysfunction can result in dysregulated hemostasis, bleeding, hypoxia and neurological symptoms. We conducted a thorough review of the literature and found a field that is increasingly poised to regard CCM as a hemostatic disease, which may have implications for therapy.

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21

Lim, Ming Sheng, and Simon Mcrae. "COVID-19 and immunothrombosis: Pathophysiology and therapeutic implications." Critical Reviews in Oncology/Hematology 168 (December 2021): 103529. http://dx.doi.org/10.1016/j.critrevonc.2021.103529.

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22

Franchi, Thomas, Simon Eaton, Paolo De Coppi, and Stefano Giuliani. "The emerging role of immunothrombosis in paediatric conditions." Pediatric Research 86, no. 1 (February 26, 2019): 19–27. http://dx.doi.org/10.1038/s41390-019-0343-6.

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23

Jayarangaiah, Apoorva, Pramod Theetha Kariyanna, Xiaoyi Chen, Amog Jayarangaiah, and Abhishek Kumar. "COVID-19-Associated Coagulopathy: An Exacerbated Immunothrombosis Response." Clinical and Applied Thrombosis/Hemostasis 26 (January 1, 2020): 107602962094329. http://dx.doi.org/10.1177/1076029620943293.

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Since the onset of the global pandemic in early 2020, coronavirus disease 2019 (COVID-19) has posed a multitude of challenges to health care systems worldwide. In order to combat these challenges and devise appropriate therapeutic strategies, it becomes of paramount importance to elucidate the pathophysiology of this illness. Coronavirus disease 2019, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), is characterized by a dysregulated immune system and hypercoagulability. COVID-associated coagulopathy (CAC) was recognized based on profound d-dimer elevations and evidence of microthrombi and macrothrombi, both in venous and arterial systems. The underlying mechanisms associated with CAC have been suggested, but not clearly defined. The model of immunothrombosis illustrates the elaborate crosstalk between the innate immune system and coagulation. The rendering of a procoagulant state in COVID-19 involves the interplay of many innate immune pathways. The SARS-CoV2 virus can directly infect immune and endothelial cells, leading to endothelial injury and dysregulation of the immune system. Activated leukocytes potentiate a procoagulant state via release of intravascular tissue factor, platelet activation, NETosis, and inhibition of anticoagulant mechanisms. Additional pathways of specific relevance in CAC include cytokine release and complement activation. All these mechanisms have recently been reported in COVID-19. Immunothrombosis provides a comprehensive perspective of the several synergistic pathways pertinent to the pathogenesis of CAC.

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Vazquez-Garza, Eduardo, Carlos Jerjes-Sanchez, Aline Navarrete, Jorge Joya-Harrison, and David Rodriguez. "Venous thromboembolism: thrombosis, inflammation, and immunothrombosis for clinicians." Journal of Thrombosis and Thrombolysis 44, no. 3 (July 20, 2017): 377–85. http://dx.doi.org/10.1007/s11239-017-1528-7.

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Eichhorn, Tanja, Silke Huber, René Weiss, Marie Ebeyer-Masotta, Lucia Lauková, Robert Emprechtinger, Rosa Bellmann-Weiler, et al. "Infection with SARS-CoV-2 Is Associated with Elevated Levels of IP-10, MCP-1, and IL-13 in Sepsis Patients." Diagnostics 13, no. 6 (March 11, 2023): 1069. http://dx.doi.org/10.3390/diagnostics13061069.

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Immunothrombosis, an excessive inflammatory response with simultaneous overactivation of the coagulation system, is a central pathomechanism in sepsis and COVID-19. It is associated with cellular activation, vascular damage, and microvascular thrombosis, which can lead to multiple organ failure and death. Here, we characterized factors related to immunothrombosis in plasma samples from 78 sepsis patients. In the course of routine clinical testing, SARS-CoV-2 was detected in 14 of these patients. Viral infection was associated with a higher mortality. Both, COVID-19 negative and COVID-19 positive sepsis patients showed increased levels of effectors of immunothrombosis, including platelet factor 4, D-dimer, nucleosomes, citrullinated histone H3, high mobility group box-1 protein, as well as phosphatidylserine-expressing platelet-derived extracellular vesicles, compared to healthy controls (n = 25). Using a 27-plex cytokine bead array, we found that Interleukin (IL)-1ra, IL-6, IL-8, IL-13, tumor necrosis factor (TNF)-α, interferon inducible protein (IP)-10, monocyte chemotactic protein (MCP)-1, macrophage inflammatory protein (MIP)-1α, and granulocyte-colony stimulating factor (G-CSF) were elevated in both, COVID-19 negative and COVID-19 positive sepsis patients, as compared to healthy controls. SARS-CoV-2 infection was associated with elevated levels of IP-10, MCP-1, and IL-13, while all other mediators widely overlapped between COVID-19 negative and COVID-19 positive patients.

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26

Slukhanchuk, E. V., V. O. Bitsadze, A. G. Solopova, J. Kh Khizroeva, D. V. Shcherbakov, F. E. Yagubova F.E.Yagubova, J. Ch Gris J.-Ch.Gris, et al. "Immunothrombosis, tumor progression and metastasis. Role of interleukin-8 and neutrophil extracellular traps." Voprosy ginekologii, akušerstva i perinatologii 22, no. 4 (2023): 48–56. http://dx.doi.org/10.20953/1726-1678-2023-4-48-56.

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Immunothrombosis, tumor progression and metastasis are inextricably linked. These close interactions are carried out by several actors. Neutrophils are considered as players in the antimicrobial host defense. Activated neutrophils release extracellular traps (NETs) involved in antimicrobial immune response and pathogenesis of various conditions including tumor growth. Neutrophils and interleukin-8 (IL-8) play a key role in the formation of NETs. Objective. To evaluate the interaction between NETs and IL-8, their contribution to the development of immunothrombosis and tumor progression in patients with reproductive system cancers and breast cancer of different stages. Patients and methods. This study included 77 patients with malignant tumors of the endometrium, ovaries, cervix, and breast, and 33 healthy controls. Concentrations of citrullinated histone H3 (citH3), human myeloperoxidase antigen (MPO:Ag), D-dimer, thrombin-antithrombin complexes (TAT), and IL-8 were assessed in all patients before surgical treatment or chemotherapy upon admission to the hospital. Results. It was shown that the concentration of NETosis markers was significantly higher in cancer patients compared to healthy controls, with an increase in indicators against the background of disease progression in stages. Naturally, markers of hemostatic activation were elevated in gynecologic cancer patients, also with increasing indicators against disease progression. The concentration of IL-8 was used as a marker of inflammation in this study, which was significantly elevated in cancer patients. The correlation analysis showed that IL-8 concentrations increased with increasing levels of NETosis markers, demonstrating maximum values at late stages of the disease, which indicates an important role of immunothrombosis in cancer progression and metastasis. Conclusion. The study showed that the concentrations of NETosis markers and IL-8 are elevated in cancer patients, and the degree of this elevation correlates with the stage of the disease. A possible mechanism is capturing of tumor cells by networks, their shielding from immune system, subsequent expression of IL-8 by tumor cells with further involvement of neutrophils and initiation of NETosis. Key words: neutrophil extracellular traps, interleukin-8, immunothrombosis, metastasis, tumor progression, neutrophils

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Bautista-Becerril, Brandon, Rebeca Campi-Caballero, Samuel Sevilla-Fuentes, Laura M. Hernández-Regino, Alejandro Hanono, Al Flores-Bustamante, Julieta González-Flores, et al. "Immunothrombosis in COVID-19: Implications of Neutrophil Extracellular Traps." Biomolecules 11, no. 5 (May 6, 2021): 694. http://dx.doi.org/10.3390/biom11050694.

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SARS-CoV-2 is a member of the family of coronaviruses associated with severe outbreaks of respiratory diseases in recent decades and is the causative agent of the COVID-19 pandemic. The recognition by and activation of the innate immune response recruits neutrophils, which, through their different mechanisms of action, form extracellular neutrophil traps, playing a role in infection control and trapping viral, bacterial, and fungal etiological agents. However, in patients with COVID-19, activation at the vascular level, combined with other cells and inflammatory mediators, leads to thrombotic events and disseminated intravascular coagulation, thus leading to a series of clinical manifestations in cerebrovascular, cardiac, pulmonary, and kidney disease while promoting severe disease and mortality. Previous studies of hospitalized patients with COVID-19 have shown that elevated levels of markers specific for NETs, such as free DNA, MPO, and H3Cit, are strongly associated with the total neutrophil count; with acute phase reactants that include CRP, D-dimer, lactate dehydrogenase, and interleukin secretion; and with an increased risk of severe COVID-19. This study analyzed the interactions between NETs and the activation pathways involved in immunothrombotic processes in patients with COVID-19.

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Shaw, Rebecca J., Charlotte Bradbury, Simon T. Abrams, Guozheng Wang, and Cheng‐Hock Toh. "COVID‐19 and immunothrombosis: emerging understanding and clinical management." British Journal of Haematology 194, no. 3 (July 7, 2021): 518–29. http://dx.doi.org/10.1111/bjh.17664.

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Gould, T. J., Z. Lysov, and P. C. Liaw. "Extracellular DNA and histones: double-edged swords in immunothrombosis." Journal of Thrombosis and Haemostasis 13 (June 2015): S82—S91. http://dx.doi.org/10.1111/jth.12977.

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Fakhoury, Hana M. A., Peter R. Kvietys, Ismail Shakir, Hashim Shams, William B. Grant, and Khaled Alkattan. "Lung-Centric Inflammation of COVID-19: Potential Modulation by Vitamin D." Nutrients 13, no. 7 (June 28, 2021): 2216. http://dx.doi.org/10.3390/nu13072216.

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SARS-CoV-2 infects the respiratory tract and leads to the disease entity, COVID-19. Accordingly, the lungs bear the greatest pathologic burden with the major cause of death being respiratory failure. However, organs remote from the initial site of infection (e.g., kidney, heart) are not spared, particularly in severe and fatal cases. Emerging evidence indicates that an excessive inflammatory response coupled with a diminished antiviral defense is pivotal in the initiation and development of COVID-19. A common finding in autopsy specimens is the presence of thrombi in the lungs as well as remote organs, indicative of immunothrombosis. Herein, the role of SARS-CoV-2 in lung inflammation and associated sequelae are reviewed with an emphasis on immunothrombosis. In as much as vitamin D is touted as a supplement to conventional therapies of COVID-19, the impact of this vitamin at various junctures of COVID-19 pathogenesis is also addressed.

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Heestermans, Marco, Géraldine Poenou, Anne-Claire Duchez, Hind Hamzeh-Cognasse, Laurent Bertoletti, and Fabrice Cognasse. "Immunothrombosis and the Role of Platelets in Venous Thromboembolic Diseases." International Journal of Molecular Sciences 23, no. 21 (October 29, 2022): 13176. http://dx.doi.org/10.3390/ijms232113176.

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Venous thromboembolism (VTE) is the third leading cardiovascular cause of death and is conventionally treated with anticoagulants that directly antagonize coagulation. However, recent data have demonstrated that also platelets play a crucial role in VTE pathophysiology. In the current review, we outline how platelets are involved during all stages of experimental venous thrombosis. Platelets mediate initiation of the disease by attaching to the vessel wall upon which they mediate leukocyte recruitment. This process is referred to as immunothrombosis, and within this novel concept inflammatory cells such as leukocytes and platelets directly drive the progression of VTE. In addition to their involvement in immunothrombosis, activated platelets can directly drive venous thrombosis by supporting coagulation and secreting procoagulant factors. Furthermore, fibrinolysis and vessel resolution are (partly) mediated by platelets. Finally, we summarize how conventional antiplatelet therapy can prevent experimental venous thrombosis and impacts (recurrent) VTE in humans.

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Leppkes, M., A. Lindemann, S. Gößwein, S. Paulus, D. Roth, A. Hartung, E. Liebing, et al. "P075 Neutrophils prevent rectal bleeding in Ulcerative Colitis by peptidyl-arginine deiminase-4-dependent immunothrombosis." Journal of Crohn's and Colitis 16, Supplement_1 (January 1, 2022): i178—i179. http://dx.doi.org/10.1093/ecco-jcc/jjab232.204.

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Abstract Background Bleeding ulcers and erosions are hallmarks of active ulcerative colitis (UC). However, the mechanisms controlling bleeding and mucosal haemostasis remain elusive. Methods We used high resolution endoscopy and colon tissue samples of active UC (n = 36) as well as experimental models of physical and chemical mucosal damage in mice deficient for peptidyl-arginine deiminase-4 (PAD4), gnotobiotic mice and controls. We employed endoscopy, histochemistry, live-cell microscopy and flow cytometry to study eroded mucosal surfaces during mucosal haemostasis. Results Erosions and ulcerations in UC were covered by fresh blood, haematin or fibrin visible by endoscopy. Fibrin layers rather than fresh blood or haematin on erosions were inversely correlated with rectal bleeding in UC. Fibrin layers contained ample amounts of neutrophils co-aggregated with neutrophil extracellular traps (NETs) with detectable activity of peptidyl-arginine deiminases (PAD). Transcriptome analyses showed significantly elevated PAD4 expression in active UC. In experimentally inflicted wounds, we found that neutrophils underwent NET formation in a PAD4-dependent manner hours after formation of primary blood clots, and remodelled clots to immunothrombi containing citrullinated histones, even in the absence of microbiota. PAD4-deficient mice experienced an exacerbated course of DSS-induced colitis with markedly increased rectal bleeding (96 % vs 10 %) as compared to controls. PAD4-deficient mice failed to remodel blood clots on mucosal wounds eliciting impaired healing. Thus, NET-associated immunothrombi are protective in acute colitis, while insufficient immunothrombosis is associated with rectal bleeding. Conclusion Our findings uncover that neutrophils induce secondary immunothrombosis by PAD4-dependent mechanisms. Insufficient immunothrombosis may favor rectal bleeding in UC.

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Nicolai, Leo, Alexander Leunig, Sophia Brambs, Rainer Kaiser, Tobias Weinberger, Michael Weigand, Maximilian Muenchhoff, et al. "Immunothrombotic Dysregulation in COVID-19 Pneumonia Is Associated With Respiratory Failure and Coagulopathy." Circulation 142, no. 12 (September 22, 2020): 1176–89. http://dx.doi.org/10.1161/circulationaha.120.048488.

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Background: Severe acute respiratory syndrome corona virus 2 infection causes severe pneumonia (coronavirus disease 2019 [COVID-19]), but the mechanisms of subsequent respiratory failure and complicating renal and myocardial involvement are poorly understood. In addition, a systemic prothrombotic phenotype has been reported in patients with COVID-19. Methods: A total of 62 subjects were included in our study (n=38 patients with reverse transcriptase polymerase chain reaction–confirmed COVID-19 and n=24 non–COVID-19 controls). We performed histopathologic assessment of autopsy cases, surface marker–based phenotyping of neutrophils and platelets, and functional assays for platelet, neutrophil functions, and coagulation tests, as well. Results: We provide evidence that organ involvement and prothrombotic features in COVID-19 are linked by immunothrombosis. We show that, in COVID-19, inflammatory microvascular thrombi are present in the lung, kidney, and heart, containing neutrophil extracellular traps associated with platelets and fibrin. Patients with COVID-19 also present with neutrophil-platelet aggregates and a distinct neutrophil and platelet activation pattern in blood, which changes with disease severity. Whereas cases of intermediate severity show an exhausted platelet and hyporeactive neutrophil phenotype, patients severely affected with COVID-19 are characterized by excessive platelet and neutrophil activation in comparison with healthy controls and non–COVID-19 pneumonia. Dysregulated immunothrombosis in severe acute respiratory syndrome corona virus 2 pneumonia is linked to both acute respiratory distress syndrome and systemic hypercoagulability. Conclusions: Taken together, our data point to immunothrombotic dysregulation as a key marker of disease severity in COVID-19. Further work is necessary to determine the role of immunothrombosis in COVID-19.

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Bokarev, I. N. "Bloodcoagulation. Modern state." Clinical Medicine (Russian Journal) 102, no. 4 (July 23, 2024): 285–90. http://dx.doi.org/10.30629/0023-2149-2024-102-4-285-290.

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The article provides information on historical issues — the discovery of blood clotting factors, anticoagulant and thrombolytic therapy, on modern understanding, diagnosis and treatment of arterial and venous thrombosis, atherothrombosis, venous thromboembolism, intravascular microthrombosis syndrome, hemophilias and immunothrombosis. Assumptions about the development of atherosclerosis are presented.

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Morris, Gerwyn, Chiara C. Bortolasci, Basant K. Puri, Lisa Olive, Wolfgang Marx, Adrienne O'Neil, Eugene Athan, et al. "Preventing the development of severe COVID-19 by modifying immunothrombosis." Life Sciences 264 (January 2021): 118617. http://dx.doi.org/10.1016/j.lfs.2020.118617.

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Gaertner, Florian, and Steffen Massberg. "Blood coagulation in immunothrombosis—At the frontline of intravascular immunity." Seminars in Immunology 28, no. 6 (December 2016): 561–69. http://dx.doi.org/10.1016/j.smim.2016.10.010.

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Aarskog, Nikolai Ravn, Ronja Hallem, Jakob Strand Godhavn, and Morten Rostrup. "Time-Dependent Changes in Pulmonary Turnover of Thrombocytes During Critical COVID-19." Critical Care Explorations 6, no. 7 (July 2024): e1128. http://dx.doi.org/10.1097/cce.0000000000001128.

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OBJECTIVES (BACKGROUND): Under normal conditions, pulmonary megakaryocytes are an important source of circulating thrombocytes, causing thrombocyte counts to be higher in arterial than venous blood. In critical COVID-19, thrombocytes may be removed from the circulation by the lungs because of immunothrombosis, possibly causing venous thrombocyte counts to be higher than arterial thrombocyte counts. In the present study, we investigated time-dependent changes in pulmonary turnover of thrombocytes during critical COVID-19 by measuring arteriovenous thrombocyte differences. We hypothesized that the early stages of the disease would be characterized by a net pulmonary removal of circulating thrombocytes because of immunothrombosis and that later stages would be characterized by a net pulmonary release of thrombocytes as normal pulmonary function is restored. DESIGN: Cohort study with repeated measurements of arterial and central venous thrombocyte counts. SETTING: ICU in a large university hospital. PATIENTS: Thirty-one patients with critical COVID-19 that were admitted to the ICU and received invasive or noninvasive mechanical ventilation. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We found a significant positive association between the arteriovenous thrombocyte difference and time since symptom debut. This finding indicates a negative arteriovenous thrombocyte difference and hence pulmonary removal of thrombocytes in the early stages of the disease and a positive arteriovenous thrombocyte difference and hence pulmonary release of thrombocytes in later stages. Most individual arteriovenous thrombocyte differences were smaller than the variance coefficient of the analysis. CONCLUSIONS: The results of this study support our hypothesis that early stages of critical COVID-19 are characterized by pulmonary removal of circulating thrombocytes because of immunothrombosis and that later stages are characterized by the return of normal pulmonary release of thrombocytes. However, in most cases, the arteriovenous thrombocyte difference was too small to say anything about pulmonary thrombocyte removal and release on an individual level.

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Bonaventura, Aldo, Alessandra Vecchié, Lorenzo Dagna, Kimberly Martinod, Dave L. Dixon, Benjamin W. Van Tassell, Francesco Dentali, et al. "Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19." Nature Reviews Immunology 21, no. 5 (April 6, 2021): 319–29. http://dx.doi.org/10.1038/s41577-021-00536-9.

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Elliott, Willie, Maheedhara R. Guda, Swapna Asuthkar, Narasaraju Teluguakula, Durbaka V. R. Prasad, Andrew J. Tsung, and Kiran K. Velpula. "PAD Inhibitors as a Potential Treatment for SARS-CoV-2 Immunothrombosis." Biomedicines 9, no. 12 (December 9, 2021): 1867. http://dx.doi.org/10.3390/biomedicines9121867.

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Since the discovery of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in December 2019, the virus’s dynamicity has resulted in the evolution of various variants, including the delta variant and the more novel mu variant. With a multitude of mutant strains posing as challenges to vaccine efficacy, it is critical that researchers embrace the development of pharmacotherapeutics specific to SARS-CoV-2 pathophysiology. Neutrophil extracellular traps and their constituents, including citrullinated histones, display a linear connection with thrombotic manifestations in COVID-19 patients. Peptidylarginine deiminases (PADs) are a group of enzymes involved in the modification of histone arginine residues by citrullination, allowing for the formation of NETs. PAD inhibitors, specifically PAD-4 inhibitors, offer extensive pharmacotherapeutic potential across a broad range of inflammatory diseases such as COVID-19, through mediating NETs formation. Although numerous PAD-4 inhibitors exist, current literature has not explored the depth of utilizing these inhibitors clinically to treat thrombotic complications in COVID-19 patients. This review article offers the clinical significance of PAD-4 inhibitors in reducing thrombotic complications across various inflammatory disorders like COVID-19 and suggests that these inhibitors may be valuable in treating the origin of SARS-CoV-2 immunothrombosis.

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Oliveira, JD, BMM Fonseca, CO Vaz, KHO Soares, JCS Mariolano, GA Locachevic, GV Damiani, EV Paula, and FA Orsi. "TIME COURSE OF THE DEVELOPMENT OF IMMUNOTHROMBOSIS DURING COVID-19 HOSPITALIZATION." Hematology, Transfusion and Cell Therapy 43 (October 2021): S516—S517. http://dx.doi.org/10.1016/j.htct.2021.10.892.

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PAEZ VARGAS, JUAN, ÁNXELA VIDAL GONZáLEZ, DENIS ROBAGLIA, MIGUEL PIRIS, JOSé FORTES ALéN, MIGUEL GORGOLAS, PILAR LLAMAS, CESAR PEREZ CALVO, JAVIER FLANDES, and LAURA PRIETO-PéREZ. "ANTICOAGULATION, BLEEDING, AND IMMUNOTHROMBOSIS IN CRITICALLY ILL PATIENTS WITH COVID-19." Chest 160, no. 4 (October 2021): A994—A995. http://dx.doi.org/10.1016/j.chest.2021.07.926.

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Beristain-Covarrubias, Nonantzin, Marisol Perez-Toledo, Adriana Flores-Langarica, Malou Zuidscherwoude, Jessica R. Hitchcock, Will M. Channell, Lloyd D. W. King, et al. "Salmonella-induced thrombi in mice develop asynchronously in the spleen and liver and are not effective bacterial traps." Blood 133, no. 6 (February 7, 2019): 600–604. http://dx.doi.org/10.1182/blood-2018-08-867267.

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Abstract Thrombosis is a frequent, life-threatening complication of systemic infection associated with multiple organ damage. We have previously described a novel mechanism of inflammation-driven thrombosis induced by Salmonella Typhimurium infection of mice. Thrombosis in the liver develops 7 days after infection, persisting after the infection resolves, and is monocytic cell dependent. Unexpectedly, thrombosis was not prominent in the spleen at this time, despite carrying a similar bacterial burden as the liver. In this study, we show that thrombosis does occur in the spleen but with strikingly accelerated kinetics compared with the liver, being evident by 24 hours and resolving rapidly thereafter. The distinct kinetics of thrombosis and bacterial burden provides a test of the hypothesis that thrombi form in healthy vessels to trap or remove bacteria from the circulation, often termed immunothrombosis. Remarkably, despite bacteria being detected throughout infected spleens and livers in the early days of infection, immunohistological analysis of tissue sections show that thrombi contain very low numbers of bacteria. In contrast, bacteria are present throughout platelet aggregates induced by Salmonella in vitro. Therefore, we show that thrombosis develops with organ-specific kinetics and challenge the universality of immunothrombosis as a mechanism to capture bacteria in vivo.

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Niculae, Cristian-Mihail, Adriana Hristea, and Ruxandra Moroti. "Mechanisms of COVID-19 Associated Pulmonary Thrombosis: A Narrative Review." Biomedicines 11, no. 3 (March 16, 2023): 929. http://dx.doi.org/10.3390/biomedicines11030929.

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COVID-19, the infectious disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), is frequently associated with pulmonary thrombotic events, especially in hospitalized patients. Severe SARS-CoV-2 infection is characterized by a proinflammatory state and an associated disbalance in hemostasis. Immune pathology analysis supports the inflammatory nature of pulmonary arterial thrombi composed of white blood cells, especially neutrophils, CD3+ and CD20+ lymphocytes, fibrin, red blood cells, and platelets. Immune cells, cytokines, chemokines, and the complement system are key drivers of immunothrombosis, as they induce the damage of endothelial cells and initiate proinflammatory and procoagulant positive feedback loops. Neutrophil extracellular traps induced by COVID-19-associated “cytokine storm”, platelets, red blood cells, and coagulation pathways close the inflammation–endotheliopathy–thrombosis axis, contributing to SARS-CoV-2-associated pulmonary thrombotic events. The hypothesis of immunothrombosis is also supported by the minor role of venous thromboembolism with chest CT imaging data showing peripheral blood clots associated with inflammatory lesions and the high incidence of thrombotic events despite routine thromboprophylaxis. Understanding the complex mechanisms behind COVID-19-induced pulmonary thrombosis will lead to future combination therapies for hospitalized patients with severe disease that would target the crossroads of inflammatory and coagulation pathways.

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Lloyd-Jones, Graham, and Matthijs Oudkerk. "COVID-19: angiotensin II in development of lung immunothrombosis and vasculitis mimics." Lancet Rheumatology 3, no. 5 (May 2021): e325-e326. http://dx.doi.org/10.1016/s2665-9913(21)00068-0.

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Doevelaar, Adrian A. N., Martin Bachmann, Bodo Hölzer, Felix S. Seibert, Benjamin J. Rohn, Frederic Bauer, Oliver Witzke, et al. "von Willebrand Factor Multimer Formation Contributes to Immunothrombosis in Coronavirus Disease 2019." Critical Care Medicine 49, no. 5 (February 15, 2021): e512-e520. http://dx.doi.org/10.1097/ccm.0000000000004918.

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46

Frantzeskaki, Frantzeska, Apostolos Armaganidis, and Stylianos E. Orfanos. "Immunothrombosis in Acute Respiratory Distress Syndrome: Cross Talks between Inflammation and Coagulation." Respiration 93, no. 3 (December 21, 2016): 212–25. http://dx.doi.org/10.1159/000453002.

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47

Wake, Hidenori, Shuji Mori, Kiyoshi Teshigawara, Keyue Liu, Dengli Wang, Yuan Gao, Hideo K. Takahashi, and Masahiro Nishibori. "The role of histidine-rich glycoprotein on immunothrombosis in septic organ failure." Proceedings for Annual Meeting of The Japanese Pharmacological Society WCP2018 (2018): PO3–9–3. http://dx.doi.org/10.1254/jpssuppl.wcp2018.0_po3-9-3.

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48

Wake, Hidenori, Shuji Mori, Keyue Liu, Yuta Morioka, Kiyoshi Teshigawara, Masakiyo Sakaguchi, Kosuke Kuroda, et al. "Histidine-Rich Glycoprotein Prevents Septic Lethality through Regulation of Immunothrombosis and Inflammation." EBioMedicine 9 (July 2016): 180–94. http://dx.doi.org/10.1016/j.ebiom.2016.06.003.

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Glassman, Ira, Nghia Le, Mercedeh Mirhosseini, Cheldon Alcantara, Aamna Asif, Anabel Goulding, Shafi Muneer, et al. "The Role of Glutathione in Prevention of COVID-19 Immunothrombosis: A Review." Frontiers in Bioscience-Landmark 28, no. 3 (March 20, 2023): 59. http://dx.doi.org/10.31083/j.fbl2803059.

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Goggs, Robert, Unity Jeffery, Dana N. LeVine, and Ronald H. L. Li. "Neutrophil-Extracellular Traps, Cell-Free DNA, and Immunothrombosis in Companion Animals: A Review." Veterinary Pathology 57, no. 1 (July 25, 2019): 6–23. http://dx.doi.org/10.1177/0300985819861721.

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Immunothrombosis is a potentially beneficial physiological process that aids innate immunity and host defense against pathogen invasion. However, this process can also be damaging when it occurs to excess or in critical blood vessels. Formation of extracellular traps by leukocytes, particularly neutrophils, is central to our understanding of immunothrombosis. In addition to degranulation and phagocytosis, extracellular traps are the third mechanism by which neutrophils combat potential pathogens. These traps consist of extracellular DNA decorated with bactericidal cellular proteins, including elastase, myeloperoxidase, and cathepsins. Neutrophils can release these structures as part of a controlled cell-death process or via a process termed vital NETosis that enables the cells to extrude DNA but remain viable. There is accumulating evidence that NETosis occurs in companion animals, including dogs, horses, and cats, and that it actively contributes to pathogenesis. Numerous studies have been published detailing various methods for identification and quantification of extracellular trap formation, including cell-free DNA, measurements of histones and proteins such as high-mobility group box–1, and techniques involving microscopy and flow cytometry. Here, we outline the present understanding of these phenomena and the mechanisms of extracellular trap formation. We critically review the data regarding measurement of NETosis in companion animals, summarize the existing literature on NETosis in veterinary species, and speculate on what therapeutic options these insights might present to clinicians in the future.

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