Immunohistochemical study of tissue factor expression in normal intestine and idiopathic inflammatory bowel disease.

More, L; Sim, R; Hudson, Mark; Dhillon, Amar P.; Pounder, R. E.; Wakefield, Andrew J.

doi:10.1136/jcp.46.8.703

Cited by 33 publications

(21 citation statements)

References 14 publications

(2 reference statements)

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“…TF immunostaining was demonstrated in foci of vasculitis in the intestinal submucosal microvasculature of patients with Crohn's disease (More et al, 1993): this suggests a shift from an anticoagulant to a procoagulant state of the endothelium in this disease. Spontaneous thrombosis occurs in some Crohn's disease patients in association with exacerbations of the illness (Talbot et al, 1986), and we have reported evidence of persistent thrombogenesis in patients with Crohn's disease in this condition (Hudson et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

“…Crohn's disease is associated with widespread granulomatous and lymphocytic microvascular inflammation (Wakefield et al, 1991). Both tissue factor expression (More et al, 1993) and fibrin deposition in foci of endothelial cell injury, with thrombotic occlusion of inflamed blood vessels, are phenotypic features of this condition (Wakefield et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Measles Virus Induction of Human Endothelial Cell Tissue Factor Procoagulant Activity in Vitro

Mazure

Grundy

Nygård

et al. 1994

Journal of General Virology

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Measles Virus Induction of Human Endothelial Cell Tissue Factor Procoagulant Activity in Vitro

Mazure

Grundy

Nygård

et al. 1994

Journal of General Virology

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“…8,9 TF expression on these cells is a characteristic feature of acute and chronic inflammation in conditions such as sepsis, atherosclerosis, Crohn disease, systemic lupus erythematosus, and transplant rejection reactions. [10][11][12][13][14] TF on monocytes and synovial cells promotes leukocyte adhesion and transendothelial migration, potentiating inflammation in joints, 15 while decreased TF activity abrogates the systemic expression of inflammatory mediators in several animal models. 16,17 The antiphospholipid syndrome (APS) is considered a thrombophilic disorder.…”

Section: Introductionmentioning

confidence: 99%

Tissue factor: a link between C5a and neutrophil activation in antiphospholipid antibody–induced fetal injury

Redecha

Tilley

Tencati

et al. 2007

Blood

266

270

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Fetal loss in patients with antiphospholipid (aPL) antibodies has been ascribed to thrombosis of placental vessels. However, we have shown that inflammation, specifically activation of complement with generation of the anaphylotoxin C5a, is an essential trigger of fetal injury. In this study, we analyzed the role of the procoagulant molecule tissue factor (TF) in a mouse model of aPL antibody-induced pregnancy loss. We found that either blockade of TF with a monoclonal antibody in wild-type mice or a genetic reduction of TF prevented aPL antibodyinduced inflammation and pregnancy loss. In response to aPL antibody-generated C5a, neutrophils express TF potentiating inflammation in the deciduas and leading to miscarriages. Importantly, we showed that TF in myeloid cells but not fetal-derived cells (trophoblasts) was associated with fetal injury, suggesting that the site for pathologic TF expression is neutrophils. We found that TF expression in neutrophils contributes to respiratory burst and subsequent trophoblast injury IntroductionThrombosis and inflammation are linked in many clinical conditions. 1 Tissue factor (TF), the major cellular initiator of the coagulation protease cascade, plays important roles in both thrombosis and inflammation. 2 The coagulation cascade is initiated by the complex of TF and factor VIIa (FVIIa). The TF:FVIIa complex activates its substrates factor X and factor IX by limited proteolysis. Activated FX (FXa) then converts prothrombin to thrombin, which cleaves fibrinogen and activates platelets leading to the formation of a hemostatic plug. TF also contributes to inflammation. TF complexes (TF:FVIIa and TF:FVIIa:FXa) induce the expression of TNF-␣, interleukins, and adhesion molecules by cleaving protease activated receptors (PARs). [3][4][5] Monocytes from patients with antiphospholipid (aPL) antibodies express TF and in vitro experiments showed that monocytes incubated with aPL antibodies express TF. 6,7 A variety of inflammatory stimuli, including mitogens, bacterial cell products, components of the complement system, and cytokines, is known to induce the expression of TF on the surface of endothelial cells, monocytes, and neutrophils. 8,9 TF expression on these cells is a characteristic feature of acute and chronic inflammation in conditions such as sepsis, atherosclerosis, Crohn disease, systemic lupus erythematosus, and transplant rejection reactions. 10-14 TF on monocytes and synovial cells promotes leukocyte adhesion and transendothelial migration, potentiating inflammation in joints, 15 while decreased TF activity abrogates the systemic expression of inflammatory mediators in several animal models. 16,17 The antiphospholipid syndrome (APS) is considered a thrombophilic disorder. However, animal studies from our laboratory have shown the importance of inflammation in the pathogenesis of aPL-induced pregnancy loss, a common complication in APS. 18,19 Using a mouse model of APS, we demonstrated that complement activation, through the action of anaphylotoxin C5a, promotes neutrop...

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“…It has been indicated that regional vasculopathy leading to activation of coagulation cascade and local fibrin formation are pathogenic factors in Crohn's disease (Wakefield et al, 1989(Wakefield et al, , 1991. Platelets thrombi linked with fibrin, and expression of tissue factor were also observed in Crohn's intestinal lesions (More et al, 1993;Wakefield et al, 1989). Similarly mucosal capillary thrombi have been identified in UC, but similar changes were also found in self -limited colitis, thus their pathogenic significance in UC is less appreciated (Dhillon et al, 1992).…”

Section: Intestinal Coagulation and Fibrinolytic Disturbancesmentioning

confidence: 81%

Kallikrein – Kinin System and Coagulation System in Inflammatory Bowel Diseases

Stadnicki¹

2011

Ulcerative Colitis - Epidemiology, Pathogenesis and Complications

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Immunohistochemical study of tissue factor expression in normal intestine and idiopathic inflammatory bowel disease.

Cited by 33 publications

References 14 publications

Measles Virus Induction of Human Endothelial Cell Tissue Factor Procoagulant Activity in Vitro

Measles Virus Induction of Human Endothelial Cell Tissue Factor Procoagulant Activity in Vitro

Tissue factor: a link between C5a and neutrophil activation in antiphospholipid antibody–induced fetal injury

Kallikrein – Kinin System and Coagulation System in Inflammatory Bowel Diseases

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