Inflammation and Hemostasis

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 9964

Special Issue Editor

Division of Clinical Laboratory Science and Specialist Clinical Hemostasis Laboratory, Department of Laboratory Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary
Interests: hemostasis; thrombosis; fibrinolysis; factor XIII; stroke; cardiovascular diseases; clinical studies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammation and hemostasis are interrelated processes with extensive crosstalk affecting the balance of both systems. Although it was revealed more than 100 years ago that inflammation leads to excessive coagulation activation, most recently, the COVID-19 pandemic has again focused our attention on the importance of the link between these two systems. An excessive immune response may lead to a dysregulation of the hemostasis balance in numerous ways, which may result in thrombotic events, tissue damage, multiorgan failure, and death. Accumulating evidence suggests that the dysregulation of hemostasis, microvascular thrombosis, and hypercoagulability may not only occur during acute inflammatory events but may also play a significant role in the pathogenesis of a number of chronic inflammatory and autoimmune disorders. Although many aspects of the cellular and molecular interactions between hemostasis and inflammation have already been uncovered, today there is renewed interest in clarifying regulatory elements and undiscovered connections of the underlying pathways. Identifying molecular targets and triggers that are key players of the extensive crosstalk between coagulation and inflammation may provide promising therapeutic targets for both inflammatory and thrombotic disorders.

This Special Issue aims to focus on the complex interactions between inflammation and hemostasis with special attention on the unique biological functions and molecular and cellular interactions between these pathways. Submission of original research articles and reviews is encouraged. Research areas may include (but are not limited to) the following:

  • Basic research studies exploring novel molecular or cellular interactions in the fields of inflammation and hemostasis (including animal models);
  • Clinical studies related to acute or chronic inflammatory states in patients and their effect on the hemostasis system (including studies on COVID-19);
  • Studies addressing novel therapeutic targets in inflammatory and/or hemostasis pathways;
  • Studies on novel methods, models, or biomarkers of related fields.

We look forward to receiving your contributions.

Dr. Zsuzsa Bagoly
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • inflammation
  • hemostasis
  • thrombosis
  • COVID-19
  • infection
  • coagulation

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Published Papers (4 papers)

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Research

13 pages, 4055 KiB  
Article
Molecular Detection of Venous Thrombosis in Mouse Models Using SPECT/CT
by Annemiek Dickhout, Pieter Van de Vijver, Nicole Bitsch, Stefan J. van Hoof, Stella L. G. D. Thomassen, Steffen Massberg, Peter Timmerman, Frank Verhaegen, Rory R. Koenen, Ingrid Dijkgraaf and Tilman M. Hackeng
Biomolecules 2022, 12(6), 829; https://doi.org/10.3390/biom12060829 - 13 Jun 2022
Cited by 1 | Viewed by 2214
Abstract
The efficacy of thrombolysis is inversely correlated with thrombus age. During early thrombogenesis, activated factor XIII (FXIIIa) cross-links α2-AP to fibrin to protect it from early lysis. This was exploited to develop an α2-AP-based imaging agent to detect early clot formation [...] Read more.
The efficacy of thrombolysis is inversely correlated with thrombus age. During early thrombogenesis, activated factor XIII (FXIIIa) cross-links α2-AP to fibrin to protect it from early lysis. This was exploited to develop an α2-AP-based imaging agent to detect early clot formation likely susceptible to thrombolysis treatment. In this study, this imaging probe was improved and validated using 111In SPECT/CT in a mouse thrombosis model. In vitro fluorescent- and 111In-labelled imaging probe-to-fibrin cross-linking assays were performed. Thrombus formation was induced in C57Bl/6 mice by endothelial damage (FeCl3) or by ligation (stenosis) of the infrarenal vena cava (IVC). Two or six hours post-surgery, mice were injected with 111In-DTPA-A16 and ExiTron Nano 12000, and binding of the imaging tracer to thrombi was assessed by SPECT/CT. Subsequently, ex vivo IVCs were subjected to autoradiography and histochemical analysis for platelets and fibrin. Efficient in vitro cross-linking of A16 imaging probe to fibrin was obtained. In vivo IVC thrombosis models yielded stable platelet-rich thrombi with FeCl3 and fibrin and red cell-rich thrombi with stenosis. In the stenosis model, clot formation in the vena cava corresponded with a SPECT hotspot using an A16 imaging probe as a molecular tracer. The fibrin-targeting A16 probe showed specific binding to mouse thrombi in in vitro assays and the in vivo DVT model. The use of specific and covalent fibrin-binding probes might enable the clinical non-invasive imaging of early and active thrombosis. Full article
(This article belongs to the Special Issue Inflammation and Hemostasis)
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9 pages, 661 KiB  
Article
Co-Occurrence of Interleukin-6 Receptor Asp358Ala Variant and High Plasma Levels of IL-6: An Evidence of IL-6 Trans-Signaling Activation in Deep Vein Thrombosis (DVT) Patients
by Rossella Salemi, Giuseppe Gattuso, Barbara Tomasello, Alessandro Lavoro, Agostino Gaudio, Massimo Libra, Salvatore Santo Signorelli and Saverio Candido
Biomolecules 2022, 12(5), 681; https://doi.org/10.3390/biom12050681 - 10 May 2022
Cited by 5 | Viewed by 2130
Abstract
Interleukin-6 (IL-6) is a pleiotropic cytokine involved in several mechanisms, and the alteration of IL-6 signaling leads to the overactivation of various processes including immunity, inflammation, and hemostasis. Although IL-6 increase has been documented in venous thromboembolic diseases, the exact involvement of IL-6 [...] Read more.
Interleukin-6 (IL-6) is a pleiotropic cytokine involved in several mechanisms, and the alteration of IL-6 signaling leads to the overactivation of various processes including immunity, inflammation, and hemostasis. Although IL-6 increase has been documented in venous thromboembolic diseases, the exact involvement of IL-6 signaling in deep vein thrombosis (DVT) has not been fully understood. Consequently, we investigated the involvement of IL-6 trans-signaling in inflammatory events occurring in DVT, focusing on the role of the interleukin-6 receptor (IL6-R) Asp358Ala variant. The circulating levels of IL-6, soluble IL6-R (sIL6-R), and soluble glycoprotein 130, as well as the Asp358Ala genotyping, were assessed in a consecutive cohort of DVT patients and healthy controls. The results indicated that IL-6 was higher in DVT compared to controls. Moreover, sIL6-R levels were strongly correlated to Asp358Ala variant in both groups, showing a high frequency of this mutation across all samples. Interestingly, our results showed a high frequency of both Asp358Ala mutation and raised IL-6 levels in DVT patients (OR = 21.32; p ≤ 0.01), highlighting that this mutation could explain the association between IL-6 overactivation and DVT outcome. Overall, this study represents a proof of concept for the targeting of IL-6 trans-signaling as a new strategy for the DVT adjuvant therapy. Full article
(This article belongs to the Special Issue Inflammation and Hemostasis)
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11 pages, 303 KiB  
Article
The rs8176740 T/A and rs512770 T/C Genetic Variants of the ABO Gene Increased the Risk of COVID-19, as well as the Plasma Concentration Platelets
by Gilberto Vargas-Alarcón, Julian Ramírez-Bello, Rosalinda Posadas-Sánchez, Gustavo Rojas-Velasco, Alberto López-Reyes, Laura Martínez-Gómez, Silvestre Ortega-Peña, Isela Montúfar-Robles, Rosa Elda Barbosa-Cobos, Marva Arellano-González and José Manuel Fragoso
Biomolecules 2022, 12(4), 486; https://doi.org/10.3390/biom12040486 - 23 Mar 2022
Cited by 3 | Viewed by 1998
Abstract
We conducted a case-control study in order to evaluate whether ABO gene polymorphisms were associated with a high risk of developing COVID-19 in a cohort of patients. Six ABO gene polymorphisms (rs651007 T/C, rs579459 T/C, rs495828 T/G [...] Read more.
We conducted a case-control study in order to evaluate whether ABO gene polymorphisms were associated with a high risk of developing COVID-19 in a cohort of patients. Six ABO gene polymorphisms (rs651007 T/C, rs579459 T/C, rs495828 T/G, rs8176746 A/C, rs8176740 T/A, and rs512770 T/C) were determined using TaqMan genotyping assays in a group of 415 COVID-19 patients and 288 healthy controls. The distribution of rs651007 T/C, rs579459 T/C, rs495828 T/G, and rs8176746 A/C polymorphisms was similar in patients and healthy controls. Nonetheless, under co-dominant (OR = 1.89, pCCo-dominant = 6 × 10−6), recessive (OR = 1.98, pCRecessive = 1 × 10−4), and additive (OR = 1.36, pCAdditive = 3 × 10−3) models, the TT genotype of the rs8176740 T/A polymorphism increased the risk of developing COVID-19. In the same way, under co-dominant, recessive, and additive models, the TT genotype of the rs512770 T/C polymorphism was associated with a high risk of developing COVID-19 (OR = 1.87, pCCo-dominant = 2 × 10−3; OR = 1.87, pCRecessive = 5 × 10−4; and OR = 1.35, pCAdditive = 4 × 10−3, respectively). On the other hand, the GTC and GAT haplotypes were associated with a high risk of COVID-19 (OR = 5.45, pC = 1 × 10−6 and OR = 6.33, pC = 1 × 10−6, respectively). In addition, the rs8176740 TT genotype was associated with high-platelet plasma concentrations in patients with COVID-19. Our data suggested that the ABO rs512770 T/C and rs8176740 T/A polymorphisms increased the risk of developing COVID-19 and the plasma concentration of platelets. Full article
(This article belongs to the Special Issue Inflammation and Hemostasis)
12 pages, 1563 KiB  
Article
Circulating Levels of PD-L1, TIM-3 and MMP-7 Are Promising Biomarkers to Differentiate COVID-19 Patients That Require Invasive Mechanical Ventilation
by Leslie Chavez-Galan, Andy Ruiz, Karen Martinez-Espinosa, Hiram Aguilar-Duran, Martha Torres, Ramces Falfan-Valencia, Gloria Pérez-Rubio, Moises Selman and Ivette Buendia-Roldan
Biomolecules 2022, 12(3), 445; https://doi.org/10.3390/biom12030445 - 14 Mar 2022
Cited by 18 | Viewed by 2974
Abstract
Background: COVID-19 is an infectious disease caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Many COVID-19 patients require invasive mechanical ventilation (IMV) while others, even with acute respiratory failure, do not (NIMV). Therefore, we aimed to evaluate serum levels of MMP-7 and [...] Read more.
Background: COVID-19 is an infectious disease caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Many COVID-19 patients require invasive mechanical ventilation (IMV) while others, even with acute respiratory failure, do not (NIMV). Therefore, we aimed to evaluate serum levels of MMP-7 and molecules related to exhausted T-cells as potential biomarkers to differentiate between IMV and NIMV patients. Methods: 105 patients diagnosed with COVID-19 and confirmed by RT-PCR for SARS-CoV-2 were divided into two groups according to the requirement for IMV. Serum levels of sPD-L1, sPD-L2, sTIM-3, sGal-9 and sMMP-7 were quantified by ELISA and correlated with clinical data. Twelve patients were followed up after eight months to compare the levels of the biomarkers between acute disease and post-COVID-19. Results: IMV patients experienced a lower PaO2/FiO2 (p < 0.0001) and a longer hospital stay (p < 0.0001), and exhibited higher levels of sPD-L1 (p < 0.05), sTIM-3 (p < 0.01) and sMMP-7 (p < 0.0001) when compared with NIMV patients. According to a ROC analysis, sMMP-7 had the highest sensitivity (78%) and specificity (76%) with a cut point of 4.5 ng/mL, followed by sTIM-3 and sPD-L1. Eight months post-COVID-19, IMV patients displayed a significant decrease in the initially high levels of sPD-L1, sTIM-3 and sGal-9, while sPD-L2 was increased, and sMMP-7 was unchanged. Conclusion: Circulating levels of sPD-L1, sTIM-3 and sMMP-7 are potential biomarkers of disease severity to distinguish patients requiring IMV. MMP-7 could also be a marker for the persistence of lung lesions post-COVID-19. Full article
(This article belongs to the Special Issue Inflammation and Hemostasis)
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