Possible Role of Platelet-Activating Factor in thein VivoExpression of Tissue Factor in Neutrophils

Todoroki, Hidekazu; Higure, Aiichiro; Okamoto, Kohji; Okazaki, Keisuke; Nagafuchi, Yukihisa; Takeda, Satoru; Katoh, Hidenori; Itoh, Hideaki; Ohsato, Keiichi; Nakamura, Shin

doi:10.1006/jsre.1998.5348

Cited by 25 publications

(13 citation statements)

References 28 publications

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“…This is the major reason why neutrophil TF expression is a subject of controversy. Because preinjection of an anti-platelet activating factor drug to rabbits before LPS injection resulted in a pronounced suppression of neutrophil TF expression (Todoroki et al, 1998), platelet activating factor is a requisite factor for neutrophil TF expression in this model. Expression of intercellular adhesion molecule-1 (ICAM-1) increased in the liver endothelial cells of LPS-injected monkeys (Todoroki et al, 2000), thus a neutrophil-endothelial cell interaction via ICAM-1 may be necessary in neutrophil TF expression.…”

Section: Discussionmentioning

confidence: 87%

“…1, A and B) is in vivo evidence that neutrophils express TF in inflammation by immune stimuli as in the case of inflammation by nonspecific stimuli (Higure et al, 1996;Todoroki et al, 1998Todoroki et al, , 2000. Giesen et al (1999) have found TF-bearing neutrophils in ex vivo study using pig arterial media and collagen-coated glass slides exposed to flowing native human blood, while de novo TF production in the neutrophils was not shown.…”

Section: Discussionmentioning

confidence: 99%

“…Taking together the cases of AR and LPS-induced inflammation (Higure et al, 1996;Todoroki et al, 1998Todoroki et al, , 2000, TF expression and presumably elastase fibrinolysis are likely to be general functions of neutrophils in inflammation and may be associated with inflammationinduced hypercoagulability and subsequent bleeding tendency, such as disseminated intravascular coagulation.…”

Section: Discussionmentioning

confidence: 99%

“…We showed previously that infiltrated macrophages induced clotting by expressing TF on the cell membrane, leading to formation of induration (Imamura et al, 1993), a skin lesion characteristic of DTH reaction and associated with fibrin deposition (Colvin and Dvorak, 1975). With regard to inflammation by nonspecific stimuli, we found TF expression on accumulated neutrophils and fibrin clot in liver sinusoid of rabbits and monkeys that had received intravenous injection of bacterial lipopolysaccharides (LPS) (Higure et al, 1996;Todoroki et al, 1998Todoroki et al, , 2000, suggesting participation of neutrophils in Immunohistochemical staining of Arthus reaction (AR) skin tissues using antibodies against either tissue factor (TF) or elastase. A, TF staining of 6-hour AR skin.…”

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confidence: 95%

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New Functions of Neutrophils in the Arthus Reaction: Expression of Tissue Factor, the Clotting Initiator, and Fibrinolysis by Elastase

Imamura

Kaneda

Nakamura

2002

Laboratory Investigation

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SUMMARY:The products of the blood clotting reaction, eg, thrombin and fibrinopeptides, have various proinflammatory activities and are suggested to modulate inflammation. The macrophage expression of tissue factor (TF), the clotting initiator, has been shown to cause clotting in the site of the delayed-type hypersensitivity reaction, a cellular immune response. However, the mechanism of the clotting induction in humoral immune response has been insufficiently studied. Therefore, the Arthus reaction, a model of immune-complex diseases, was produced in monkey skin that was examined for TF expression and fibrin deposition. TF antigen was positive on most of polymorphonuclear leukocytes, which were the main leukocytes in the lesions and were identified as neutrophils with an anti-neutrophil-elastase mAb. TF mRNA was detected in neutrophils by in situ hybridization using TF RNA probes, indicating de novo TF synthesis by the leukocytes. Specific binding of activated factor VII onto TF-positive neutrophils suggested the activity of neutrophil TF to trigger the cascade reaction of clotting. The number of TF-positive neutrophils were correlated in time with the intensity and extent of fibrin deposition that was visualized with an mAb specific for fibrin and peaked in 24 hours. Interestingly, the fibrin deposit was partially positive for an mAb specific for neutrophil elastase-digested fibrin. These results show in vivo evidence of a close relationship between neutrophils and both clotting and fibrinolysis in the Arthus reaction and may suggest that these neutrophil functions contribute to the pathogenesis of this hypersensitivity inflammation. (Lab Invest 2002, 82:1287-1295.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 95%

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New Functions of Neutrophils in the Arthus Reaction: Expression of Tissue Factor, the Clotting Initiator, and Fibrinolysis by Elastase

Imamura

Kaneda

Nakamura

2002

Laboratory Investigation

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“…injections of endotoxin. [28][29][30][31] It has also been demonstrated that neutrophils can promote platelet-mediated fibrin formation, which is attenuated by inhibitors of elastase, thereby revealing a possible role for neutrophils and/or elastase, in coagulation. 32 Neutrophil-platelet interactions influence the level of TF production, which can be reduced by infusing a platelet glycoprotein IIb/IIIa inhibitor.…”

Section: Clinical Aspectsmentioning

confidence: 99%

Disseminated intravascular coagulation

Slofstra¹,

Spek²,

Cate³

2003

Hematol J

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Disseminated Intravascular Coagulation (DIC) is an acquired syndrome representing a hypercoagulable state, haemorrhagic symptoms and multiple organ failure. The clinical relevance of this syndrome is complicated since there is no established way of diagnosing DIC and it is difficult to distinguish whether clinical features are attributable to the underlying disease or DIC. Experimental studies, based on models of gram-negative sepsis and the Generalized Shwartzman Reaction, show that DIC is characterized by strongly enhanced inflammatory activity, activated coagulation and impaired fibrinolysis. In this review we propose that activated neutrophils play a pivotal role in the pathophysiology of DIC, particularly by contributing to inflammation and vascular injury. Additionally, a distinct role for granulocytes in fibrinolysis has also been suggested. Although the underlying procoagulant pathways of DIC and the important role of tissue factor have been unravelled, therapeutic interventions counteracting the mediators of these pathways proved mainly unsuccessful (with the positive exception of activated protein C). Dissecting the molecular interactions at the onset and progression of DIC might therefore help to elucidate the fundamental consequences of DIC, possibly contributing to better diagnostic tools and more effective therapeutic options.

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The Coagulation System in Sepsis

Hack¹

The Sepsis Text

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Possible Role of Platelet-Activating Factor in thein VivoExpression of Tissue Factor in Neutrophils

Cited by 25 publications

References 28 publications

New Functions of Neutrophils in the Arthus Reaction: Expression of Tissue Factor, the Clotting Initiator, and Fibrinolysis by Elastase

New Functions of Neutrophils in the Arthus Reaction: Expression of Tissue Factor, the Clotting Initiator, and Fibrinolysis by Elastase

Disseminated intravascular coagulation

The Coagulation System in Sepsis

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