Leukocyte procoagulant activity: enhancement of production in vitro by IgG and antigen-antibody complexes.

Rothberger, Henry; Zimmerman, Theodore S.; Spiegelberg, Hans L.; Vaughan, John H.

doi:10.1172/jci108670

Cited by 157 publications

(58 citation statements)

References 23 publications

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“…The coagulation activities (TF/FVIIa binding activity) of the cell supernatants were determined using an mPT assay as previously described (15). This assay is a modification of the classical PT assay, and its principles are also similar with recalcified one-step clotting assay (23,24). In addition, the mPT assay offers a fast, reliable, nonexpensive, and easilyreproducible first screening test of procoagulant activity.…”

Section: Modified Prothrombin Time (Mpt) Assaymentioning

confidence: 99%

C5a and TNF-α Up-Regulate the Expression of Tissue Factor in Intra-Alveolar Neutrophils of Patients with the Acute Respiratory Distress Syndrome

Kambas

Markiewski

Pneumatikos

et al. 2008

The Journal of Immunology

117

111

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Acute respiratory distress syndrome (ARDS) is characterized by the presence of fibrin-rich inflammatory exudates in the intra-alveolar spaces and the extensive migration of neutrophils into alveoli of the lungs. Tissue factor (TF)-dependent procoagulant properties of bronchoalveaolar lavage fluid (BALF) obtained from ARDS patients favor fibrin deposition, and are likely the result of cross-talk between inflammatory mediators and hemostatic mechanisms. However, the regulation of these interactions remains elusive. Prompted by previous findings suggesting that neutrophils, under certain inflammatory conditions, can express functional TF, we investigated the contribution of intra-alveolar neutrophils to the procoagulant properties of BALF from patients with ARDS. Our results confirm that the procoagulant properties of BALF from ARDS patients are the result of TF induction, and further indicate that BALF neutrophils are a main source of TF in intra-alveolar fluid. We also found that BALF neutrophils in these patients express significantly higher levels of TF than peripheral blood neutrophils. These results suggest that the alveolar microenvironment contributes to TF induction in ARDS. Additional experiments indicated that the ability of BALF to induce TF expression in neutrophils from healthy donors can be abolished by inhibiting C5a or TNF-α signaling, suggesting a primary role for these inflammatory mediators in the up-regulation of TF in alveolar neutrophils in ARDS. This cross-talk between inflammatory mediators and the induction of TF expression in intra-alveolar neutrophils may be a potential target for novel therapeutic strategies to limit ARDS-associated disturbances of coagulation.

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Section: Modified Prothrombin Time (Mpt) Assaymentioning

confidence: 99%

C5a and TNF-α Up-Regulate the Expression of Tissue Factor in Intra-Alveolar Neutrophils of Patients with the Acute Respiratory Distress Syndrome

Kambas

Markiewski

Pneumatikos

et al. 2008

The Journal of Immunology

117

111

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“…E xposure of peripheral blood monocytes to a variety of agents leads to the expression of tissue factor, a membrane-bound glycoprotein that plays a critical role in blood coagulation as the cellular receptor and cofactor for factor Vila. 12 The agents include bacterial endotoxin 3 ; antigen-antibody complexes 4 ; activated complement fragments 56 ; and cytokines, such as the T-cell-derived monocyte procoagulant-inducing factor, 7 interleukin-1 (IL-1), 8 -10 and tumor necrosis factor (TNF), 8 -911 although the efficacy of the latter two has been questioned. 7 Monocyte tissue factor expression is thought to be a result of gene transcription and mRNA stabilization.…”

Section: Prostacyclin Analogues Inhibit Tissue Factor Expression In Tmentioning

confidence: 99%

Prostacyclin analogues inhibit tissue factor expression in the human monocytic cell line THP-1 via a cyclic AMP-dependent mechanism.

Crutchley

Solomon

Conanan

1992

Arterioscler Thromb

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Increased expression of tissue factor procoagulant by peripheral blood monocytes has been implicated in a number of thrombotic disorders. The present studies were undertaken to determine whether stable analogues of prostacyclin, a potent endothelium-derived platelet inhibitor and vasodilator, could inhibit tissue factor expression by human monocytic cells. Exposure of monocytic tumor THP-1 cells to 100 ng/ml endotoxin, 2 units/ml interleukin-1 beta, or 5 ng/ml tumor necrosis factor-alpha for 4 hours led to increased tissue factor procoagulant activity. Preincubation for 30 minutes with iloprost, ciprostene, and carbacyclin led to a dose-dependent inhibition of tissue factor expression induced by all three challenging agents. Iloprost was the most potent: 50% inhibition occurred at 5 nM, a concentration close to the reported dissociation constant for iloprost binding to the platelet prostacyclin receptor. An orally active analogue, cicaprost, was equally effective against endotoxin-induced tissue factor expression. Carbacyclin and ciprostene were 100 times less potent. Iloprost prevented the endotoxin-induced expression of tissue factor antigen on the surface of THP-1 cells, as determined by flow cytometry. Iloprost (500 pM-50 nM) increased intracellular levels of cyclic AMP. This effect was potentiated by isobutylmethylxanthine, an inhibitor of phosphodiesterase. The inhibitory effects of iloprost on tissue factor expression were also potentiated by isobutylmethylxanthine and mimicked by forskolin and dibutyryl cyclic AMP but not dibutyryl cyclic GMP. These results suggest that prostacyclin may play a role in downregulating tissue factor expression in monocytes, at least in part via elevation of intracellular levels of cyclic AMP.

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“…Received for publication 9 March 1982 and in revised form 28 April 1982. by a variety of agents-for example, endotoxin (10), immune complexes (11), or complement C5a (12). Although granulocytes or lymphocytes were initially felt to produce this tissue factor activity, more recent studies have established the monocyte as its source (13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Binding of human factor VII and VIIa to monocytes.

Broze¹

1982

J. Clin. Invest.

180

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Leukocyte procoagulant activity: enhancement of production in vitro by IgG and antigen-antibody complexes.

Cited by 157 publications

References 23 publications

C5a and TNF-α Up-Regulate the Expression of Tissue Factor in Intra-Alveolar Neutrophils of Patients with the Acute Respiratory Distress Syndrome

C5a and TNF-α Up-Regulate the Expression of Tissue Factor in Intra-Alveolar Neutrophils of Patients with the Acute Respiratory Distress Syndrome

Prostacyclin analogues inhibit tissue factor expression in the human monocytic cell line THP-1 via a cyclic AMP-dependent mechanism.

Binding of human factor VII and VIIa to monocytes.

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