The Expression of Surface Tissue Factor Apoprotein by Blood Monocytes in the Course of Infections in Early Infancy

Rivers, R. P. A.; Cattermole, H E J; Wright, Ian

doi:10.1203/00006450-199206000-00006

Cited by 25 publications

(14 citation statements)

References 13 publications

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“…Similarly, in a patient with candidemia, it was found that the monocytes did not express tissue factor. In contrast, monocytes from patients with systemic bacterial infections strongly expressed tissue factor (49). These observations suggest that tissue factor expression is tightly controlled and is induced only in response to specific microbial pathogens.…”

Section: Tissue Factor Endothelial Cells and Infectious Diseasesmentioning

confidence: 56%

Endothelial cells, tissue factor and infectious diseases

Lópes-Bezerra

Filler

2003

Braz J Med Biol Res

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Tissue factor is a transmembrane procoagulant glycoprotein and a member of the cytokine receptor superfamily. It activates the extrinsic coagulation pathway, and induces the formation of a fibrin clot. Tissue factor is important for both normal homeostasis and the development of many thrombotic diseases. A wide variety of cells are able to synthesize and express tissue factor, including monocytes, granulocytes, platelets and endothelial cells. Tissue factor expression can be induced by cell surface components of pathogenic microorganisms, proinflammatory cytokines and membrane microparticles released from activated host cells. Tissue factor plays an important role in initiating thrombosis associated with inflammation during infection, sepsis, and organ transplant rejection. Recent findings suggest that tissue factor can also function as a receptor and thus may be important in cell signaling. The present minireview will focus on the role of tissue factor in the pathogenesis of septic shock, infectious endocarditis and invasive aspergillosis, as determined by both in vivo and in vitro models. Correspondence

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Section: Tissue Factor Endothelial Cells and Infectious Diseasesmentioning

confidence: 56%

Endothelial cells, tissue factor and infectious diseases

Lópes-Bezerra

Filler

2003

Braz J Med Biol Res

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“…This is in good agreement with data available from literature. Rivers et al 21 have shown that the percentage of monocytes expressing surface TF in cord-derived samples taken at birth from apparently uninfected babies ranged between 11% and 24%, and Amirkhosravi et al 22 have shown that adult WB samples contain less than 5% TF positive monocytes. We conclude that the high basal levels of monocytic TF antigen expression contribute to the observed efficient clotting of native cord WB.…”

Section: Discussionmentioning

confidence: 98%

High Availability of Intravascular Tissue Factor in Neonates

Cvirn

Gruber²,

Koestenberger³

et al. 2007

Journal of Pediatric Hematology/Oncology

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In the present study, we compared the levels of intravascular tissue factor (TF) present in cord versus adult whole blood (WB) prior and after lipopolysaccharide (LPS) stimulation. High levels of intravascular TF might help to explain the clinically observed efficient clotting of cord blood despite low levels of procoagulatory factors. Quantitative reverse transcription-polymerase chain reaction revealed same (basal) TF mRNA expression levels in both native cord and adult WB, and approximately same increase in TF mRNA expression owing to LPS incubation in both cord and adult WB (normalized to the housekeeping gene beta-actin). Flow-cytometric (fluorescence activated cell sorting) analysis revealed significantly higher surface TF antigen exposure on the neonatal monocyte membrane in native WB samples, and approximately same ability of neonatal and adult monocytes to express TF upon LPS-stimulation. Thrombelastography revealed significantly shorter clotting times of native cord versus adult WB (527+/-41 vs. 592+/-23 s, P<0.05). Moreover, shortening of clotting times owing to LPS-stimulation was significantly more pronounced in cord versus adult WB (29.65+/-3.35% vs. 12.03+/-6.23%, P<0.05). Because both quantitative reverse transcription-polymerase chain reaction and fluorescence activated cell sorting analysis revealed same capability of both neonatal and adult monocytes to express TF upon LPS-stimulation, this efficient shortening effect in cord WB might be explained by the constitutively high number of monocytes present in neonates. We suggest that the high levels of intravascular TF present in neonates (prior and after LPS-stimulation) might help to explain the clinically observed efficient clotting of cord blood despite low levels of procoagulatory factors.

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“…[15][16][17] In particular, an increase in TF-expressing circulating monocytes has been documented in various conditions, including human lowdose endotoxemia, venous thrombosis accompanying different diseases and disseminated intravascular coagulation (DIC), especially sepsis-associated DIC. [27][28][29][30] In these conditions, the number of blood TF-positive monocytes, as assessed by flow cytometry, was reported to range between 5-60%, the highest values being present in septic patients with DIC. Therefore, an important question to be addressed is whether fibrinolysis can be inhibited by a concentration of TF-expressing cells comparable to that attainable in vivo.…”

Section: Discussionmentioning

confidence: 99%

Tissue factor-expressing monocytes inhibit fibrinolysis through a TAFI-mediated mechanism, and make clots resistant to heparins

Semeraro¹,

Ammollo²,

Semeraro³

et al. 2009

Haematologica

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The online version of this article contains a supplementary appendix. BackgroundThrombin is the main activator of the fibrinolysis inhibitor TAFI (thrombin activatable fibrinolysis inhibitor) and heightened clotting activation is believed to impair fibrinolysis through the increase of thrombin activatable fibrinolysis inhibitor activation. However, the enhancement of thrombin generation by soluble tissue factor was reported to have no effect on plasma fibrinolysis and it is not known whether the same is true for cell-associated tissue factor. The aim of this study was to evaluate the effect of tissue factor-expressing monocytes on plasma fibrinolysis in vitro. Design and MethodsTissue factor expression by human blood mononuclear cells (MNC) and monocytes was induced by LPS stimulation. Fibrinolysis was spectrophotometrically evaluated by measuring the lysis time of plasma clots containing LPS-stimulated or control cells and a low concentration of exogenous tissue plasminogen activator. Results LPS-stimulated MNC (LPS-MNC)prolonged fibrinolysis time as compared to unstimulated MNC (C-MNC) in contact-inhibited but not in normal citrated plasma. A significantly prolonged lysis time was observed using as few as 30 activated cells/µL. Fibrinolysis was also impaired when clots were generated on adherent LPS-stimulated monocytes. The antifibrinolytic effect of LPS-MNC or LPS-monocytes was abolished by an anti-tissue factor antibody, by an antibody preventing thrombin-mediated thrombin activatable fibrinolysis inhibitor activation, and by a TAFIa inhibitor (PTCI). Assays of thrombin and TAFIa in contact-inhibited plasma confirmed the greater generation of these enzymes in the presence of LPS-MNC. Finally, the profibrinolytic effect of unfractionated heparin and enoxaparin was markedly lower (~50%) in the presence of LPS-MNC than in the presence of a thromboplastin preparation displaying an identical tissue factor activity. ConclusionsOur data indicate that LPS-stimulated monocytes inhibit fibrinolysis through a tissue factor-mediated enhancement of thrombin activatable fibrinolysis inhibitor activation and make clots resistant to the profibrinolytic activity of heparins, thus providing an additional mechanism whereby tissue factor-expressing monocytes/macrophages may favor fibrin accumulation and diminish the antithrombotic efficacy of heparins.Key words: monocytes, tissue factor, carboxypeptidase, clot lysis, heparin resistance.Citation: Semeraro F, Ammollo CT, Semeraro N, and Colucci M. Tissue factor-expressing monocytes inhibit fibrinolysis through a TAFI-mediated mechanism, and make clots resistant to heparins. Haematologica 2009; 94:819-826. doi:10.3324/haematol.2008 This is an open-access paper.Tissue factor-expressing monocytes inhibit fibrinolysis through a TAFI-mediated mechanism, and make clots resistant to heparins

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The Expression of Surface Tissue Factor Apoprotein by Blood Monocytes in the Course of Infections in Early Infancy

Cited by 25 publications

References 13 publications

Endothelial cells, tissue factor and infectious diseases

Endothelial cells, tissue factor and infectious diseases

High Availability of Intravascular Tissue Factor in Neonates

Tissue factor-expressing monocytes inhibit fibrinolysis through a TAFI-mediated mechanism, and make clots resistant to heparins

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