In patients with idiopathic venous thrombosis, interleukin-10 is decreased and related to endothelial dysfunction

Abstract

The aim of this study was to evaluate the levels of anti-inflammatory interleukin-10 and pro-inflammatory cytokines and their relationship to endothelial function in patients with idiopathic venous thrombosis. Forty-nine eligible patients of both sexes with idiopathic venous thrombosis and 48 matched control subjects were studied. Levels of inflammatory markers were determined. Endothelial function was evaluated by ultrasound measurement of the flow mediated dilatation (FMD) of the brachial artery. Compared to the control group, patients with idiopathic venous thrombosis had significantly lower levels of interleukin-10 1.81 pg/ml (1.53-2.21) versus 2.71 pg/ml (1.84-3.65), p < 0.001. Patients also had increased levels of pro-inflammatory cytokines: interleukin-6 2.37 pg/ml (1.59-4.09) versus 2.03 pg/ml (1.49-2.59), p = 0.025, interleukin-8 3.53 pg/ml (2.94-5.30) versus 2.25 pg/ml (1.77-2.90), p < 0.001. Furthermore, decreased FMD was observed in patients: 5.0% (3.9-6.9) versus 12.7% (10.8-15.6), p < 0.001. FMD was related to levels of interleukin-10 (r = 0.33, p = 0.001) and was inversely related to pro-inflammatory cytokines interleukin-6 (r = -0.34, p = 0.001) and interleukin-8 (r = -0.43, p < 0.001). Patients with idiopathic venous thrombosis have decreased levels of IL-10 and increased levels of pro-inflammatory cytokines. This imbalance indicates that in the stable phase of the disease, patients have an increased systemic inflammatory response. This inflammatory response could be the consequence of the disease, but most probably is involved in the pathogenesis of venous thrombosis.

Abdominal Obesity and the Risk of Venous Thromboembolism Among Women: A Potential Role of Interleukin-6

“…For instance, while some studies, including those with prospective design, demonstrated a significant effect of inflammation, as reflected by increased CRP levels, on the risk of VTE, [19][20][21] others found no link between CRP and a future event of VTE. [22][23][24][25] Previously, we have shown in a case-control study that IL-6 levels were significantly associated with VTE, 26 which agreed with some, [27][28][29] but not all, studies including a prospective cohort. 30,31 Taking into account the close relationship between abdominal obesity and inflammation and the potential role of these conditions in the development of VTE, we have sought to extend our investigation by exploring whether inflammation could contribute to the thrombosis risk from abdominal obesity.…”

“…For instance, although in vitro studies show that CRP and IL-6 are capable of increasing the expression of TF, 35,36 the key inducer of blood coagulation, clinical data on the association of these inflammatory markers with venous thrombotic disease are conflicting and, particularly for IL-6, also limited. Whereas some studies demonstrated that IL-6 is associated with VTE, [27][28][29] others, including a prospective cohort, found no relationship. 30,31 For CRP, there is strong evidence that this acute-phase protein is a predictor of arterial thrombotic events.…”

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

“…Furthermore, previous case-control studies have shown that serum/plasma levels of soluble adhesion molecules derived from immunocompetent or endothelial cells (P-selectin, VCAM-1 and intercellular adhesion molecule 1 (ICAM-1), various proinflammatory cytokines (Interleukin(IL)1-β, IL-6, CXCL-8 (IL-8), IL-10, CCL-2) and tumor necrosis factor α (TNFα) as well as matrix metalloprotease (MMP)-9 are altered in DVT patients [11][12][13][16][17][18] compared with healthy controls [19]. These soluble mediators form a dynamic and interactive network, and it may therefore be more relevant to investigate broader mediator plasma profiles rather than the levels of single mediators.…”

Eosinophilic biomarkers for detection of acute exacerbation of chronic obstructive pulmonary disease with or without pulmonary embolism

“…AECOPD and PE are associated with a wide range of inflammatory cells, mediators and cytokine network components, including P-selectin (11,12), inflammatory cytokines (13,14) and leucocytes (15,16). Previous studies have indicated that eosinophilic airway inflammation is also associated with the development of severe AECOPD (17)(18)(19).…”