Altered plasma levels of cytokines, soluble adhesion molecules and matrix metalloproteases in venous thrombosis

Mosevoll, Knut Anders; Lindås, Roald; Tvedt, Tor Henrik Anderson; Bruserud, Øystein; Reikvam, Håkon

doi:10.1016/j.thromres.2015.04.002

Cited by 38 publications

(27 citation statements)

References 36 publications

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“…In the same cohort of patients, sP-selectin levels were significantly higher at DVT onset than in controls and then decreased rapidly within the first month. Elevated plasma sP-selectin and CRP levels upon diagnosis of DVT were also observed by Mosevoll et al [51] and for sP-selectin by Vandy et al [52]. A similar pattern (with elevated CRP, IL6 and sICAM1 upon diagnosis) was reported in a prospective study of over 600 patients [53].…”

Section: Cytokines and Soluble Adhesion Moleculessupporting

confidence: 72%

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Inflammation in deep vein thrombosis: a therapeutic target?

et al. 2019

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Deep vein thrombosis is a common disease associated with a variety of complications including post-thrombotic syndrome as a late complication. It is now clear that in addition to classical deep vein thrombosis triggers such as blood flow disturbance, hypercoagulability, and vessel wall changes, inflammation has a key role in the pathophysiology of deep vein thrombosis, and there is a close relationship between inflammation and coagulation. As attested by changes in several plasma biomarkers, inflammation may have a significant role in the development of post-thrombotic syndrome. Here, we review the link between inflammation and deep vein thrombosis and thus the potential value of anti-inflammatory and/or anticoagulant drugs in the treatment of deep vein thrombosis and the prevention of postthrombotic syndrome.

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Section: Cytokines and Soluble Adhesion Moleculessupporting

confidence: 72%

“…One of the main difference between the above-described studies relates to the nature of the control group, i.e. healthy controls vs. patients initially suspected to have DVT; these two approaches have clear differences [51].…”

Section: Cytokines and Soluble Adhesion Moleculesmentioning

confidence: 99%

Inflammation in deep vein thrombosis: a therapeutic target?

et al. 2019

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“…All these processes might be regulated by cytokines and chemokines either rapidly secreted from endothelial pool and from platelet α‐granules or newly synthetized by activated endothelial and immune cells . We will review basic research focusing on the cytokines and some chemokines involved in VTE and discuss potential role in clinical research …”

Section: Introductionmentioning

confidence: 99%

Cytokine and chemokine regulation of venous thromboembolism

Najem

Couturaud

Lemarié

2020

Journal of Thrombosis and Haemostasis

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Morbidity and mortality from venous thromboembolism (VTE), which refers to deep vein thrombosis and pulmonary embolism, have a substantial effect on the global burden of disease. The field of venous thrombosis research has been dramatically changed over the past 10 years with the improvement of animal models that shed some light on the interaction between inflammation and thrombosis. Important recent advances provided evidence of the implication of the innate immune system in venous thrombosis. In this review, we highlighted the cytokines and chemokines that regulate mechanisms of thrombus formation and resolution. Cytokines are pleiotropic, redundant, and multifunctional endogenous mediators orchestrating the inflammatory responses leading to thrombus formation or resolution. The use of experimental models has revealed the pro‐thrombotic activity of some cytokines including interferon‐γ, interleukin (IL)‐6, chemokine ligand 2, IL‐17A, IL‐9, IL‐1β, and transforming growth factor‐β. Other cytokines such as IL‐10, tumor necrosis factor‐α, and IL‐8 appear to promote thrombus resolution in late phase of venous thromboembolism. The purpose of this review is to bring together the current knowledge regarding the cytokines and chemokines that have been involved in thrombosis formation and resolution. We postulate that an imbalance between pro‐thrombotic and anti‐thrombotic cytokines/chemokines may be involved in the pathophysiology of VTE. However, in‐depth basic and clinical research in venous thrombosis is still require to fully understand the precise mechanism of action of these cytokines.

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“…Neutrophil elastase and MMP2 appear ineffective toward Type III collagen [219,220], while MMP9 can digest both Types I and III [221]. Within human DVT patients, most of the MMP enzymes appear elevated (with the exception of MMP3) [222]. Mouse models recapitulate this elevation, and further suggest that while MMP9 which is elevated throughout DVT remodeling, MMP2 and Membrane-Type-1 MMP are further elevated at later stages [217].…”

Section: Collagenolysismentioning

confidence: 99%

Resolution of Deep Venous Thrombosis: Proposed Immune Paradigms

Nicklas

Gordon

Henke

2020

IJMS

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Venous thromboembolism (VTE) is a pathology encompassing deep vein thrombosis (DVT) and pulmonary embolism (PE) associated with high morbidity and mortality. Because patients often present after a thrombus has already formed, the mechanisms that drive DVT resolution are being investigated in search of treatment. Herein, we review the current literature, including the molecular mechanisms of fibrinolysis and collagenolysis, as well as the critical cellular roles of macrophages, neutrophils, and endothelial cells. We propose two general models for the operation of the immune system in the context of venous thrombosis. In early thrombus resolution, neutrophil influx stabilizes the tissue through NETosis. Meanwhile, macrophages and intact neutrophils recognize the extracellular DNA by the TLR9 receptor and induce fibrosis, a complimentary stabilization method. At later stages of resolution, pro-inflammatory macrophages police the thrombus for pathogens, a role supported by both T-cells and mast cells. Once they verify sterility, these macrophages transform into their pro-resolving phenotype. Endothelial cells both coat the stabilized thrombus, a necessary early step, and can undergo an endothelial-mesenchymal transition, which impedes DVT resolution. Several of these interactions hold promise for future therapy. already progressed past the point of anticoagulant efficacy [12,13]. Thus, there is potential clinical utility in investigating and controlling the process by which DVTs resolve in order to provide better care to these later-stage patients, with less bleeding risk. Overview of Venous Thrombus Development in HumansThe time sequence of DVT development and resolution was correctly suggested as early as 1962, based on empirical stains that detected changes in the nanoscopic roughness of clotted material [14]. As Lendrum et. al. remarked, "we consider that the intracytoplasmic granules, which we think are engulfed fibrin, seen in pulmonary phagocytes and in the endothelium of arteries and veins containing thrombus, are better shown by this (methyl-scarlet-blue) method than by any of the others." In fresh clot (whether in deep veins or in diabetic kidneys), platelets and erythrocytes are initially linked in a fine mesh yielding a relatively smooth surface (stage 1). A mat of the medium-textured fibrin replaces the initial thrombus (stage 2), which is gradually replaced by much coarser collagen (stage 3). This staging of clot development quickly became the basis of a pathological guide to grade thrombi [15]. The current three-stage refinement of the DVT grading scheme indicates that the turnover of erythrocyte-rich to fibrin-rich clot in humans is complete approximately seven days after the initial thrombotic event [16], whereas fibrin deposition commences after one day [17]. Various leukocytes, initially neutrophils and later macrophages, are believed to control this progression of DVTs development from a mass of erythrocytes, to fibrin, and finally to collagen [18]. Infiltrating T-lymphocytes and macrophages conta...

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Altered plasma levels of cytokines, soluble adhesion molecules and matrix metalloproteases in venous thrombosis

Abstract: Plasma biomarker profiling of selected soluble mediators can be used to identify subsets among patients with suspected lower limb thrombosis that differ significantly in their frequencies of DVT.

Cited by 38 publications

References 36 publications

Inflammation in deep vein thrombosis: a therapeutic target?

Inflammation in deep vein thrombosis: a therapeutic target?

Cytokine and chemokine regulation of venous thromboembolism

Resolution of Deep Venous Thrombosis: Proposed Immune Paradigms

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