Inhibition of Il-1 Induced Tissue Factor (Tf) Synthesis and Procoagulant Activity (Pca) in Purified Human Monocytes by Il-4, Il-10 and Il-13

Osnes, Liv; Westvik, Åse-Brit; Joø, Gun Britt; Okkenhaug, Cecilie; Kierulf, Peter

doi:10.1006/cyto.1996.0110

Cited by 58 publications

(48 citation statements)

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“…As mentioned, IL-1 induces tissue factor expression in monocytes/macrophages in vitro (23). Additional studies are needed to test whether this mechanism is relevant in the model.…”

Section: Discussionmentioning

confidence: 93%

“…The enhanced exacerbation due to IL-1 in t-PA Ϫ/Ϫ compared with the exacerbation in t-PA ϩ/ϩ mice suggests that increased fibrin formation somehow forms part of the response in the inflamed joints to IL-1 in this murine arthritis model; this may also be part of the proinflammatory action of IL-1 in rheumatoid disease. In this connection, IL-1 has been widely shown in vitro to induce procoagulant, i.e., tissue factor, activity including in monocytes/macrophages (22,23). Very recently, in two different murine arthritis models, increased expression of genes involved in coagulation and fibrinolysis (e.g., those for tissue factor and u-PA) were noted, and it was suggested that the pattern favored procoagulant activity (24).…”

Section: Discussionmentioning

confidence: 99%

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Tissue-Type Plasminogen Activator Deficiency Exacerbates Arthritis

Yang

Carmeliet

Hamilton

2001

The Journal of Immunology

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Fibrin deposition, cell migration, and tissue remodeling are key components in the lesions of inflammatory joint diseases, such as rheumatoid arthritis. The plasminogen activators (PAs), namely, tissue-type PA (t-PA) and urokinase PA, are implicated in these aspects of an inflammatory response, although their precise roles are yet to be defined. We therefore used gene-deficient mice to explore their role in a two-stage arthritis model involving intraarticular methylated BSA injection, followed by systemic IL-1 treatment. We report in this study that both t-PA and urokinase PA are protective for the mild arthritis induced by intraarticular methylated BSA injection alone, since absence of either of them exacerbates the response; following s.c. IL-1 injection, t-PA−/− mice had particularly severe disease. Fibrin deposition appeared to parallel disease severity under the various conditions, suggesting that PA-mediated fibrinolysis may be normally playing a protective role in inflammatory joint disease.

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“…As mentioned, IL-1 induces tissue factor expression in monocytes/macrophages in vitro (23). Additional studies are needed to test whether this mechanism is relevant in the model.…”

Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Tissue-Type Plasminogen Activator Deficiency Exacerbates Arthritis

Yang

Carmeliet

Hamilton

2001

The Journal of Immunology

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“…IL-1 induces TF activity in endothelial cells (12) and monocytes (62). Injection of IL-1 into experimental animals (baboons) also elicits an initial but transient activation of the fibrinolytic system, followed by a TNF-like shift to a procoagulant state (41,101).…”

Section: Cytokinesmentioning

confidence: 99%

“…The anti-inflammatory cytokines IL-4 and IL-10 inhibit IL-1-and lipopolysaccharide-induced TF activity in monocytes (62), and pretreatment of animals with IL-10 limits the size of thrombi formed in response to stasis-induced venous thrombosis (29).…”

Section: Cytokinesmentioning

confidence: 99%

Biology and Pathogenesis of Thrombosis and Procoagulant Activity in Invasive Infections Caused by Group A Streptococci andClostridium perfringens

Bryant

2003

Clin Microbiol Rev

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Group A streptococcal necrotizing fasciitis/myonecrosis and Clostridium perfringens gas gangrene are two of the most fulminant gram-positive infections in humans. Tissue destruction associated with these infections progresses rapidly to involve an entire extremity. Multiple-organ failure is common, and morbidity and mortality remain high. Systemic activation of coagulation and dysregulation of the anticoagulation pathways contribute to the pathogenesis of many diverse disease entities of infectious etiology, and it has been our hypothesis that microvascular thrombosis contributes to reduced tissue perfusion, hypoxia, and subsequent regional tissue necrosis and organ failure in these invasive gram-positive infections. This article reviews the coagulation, anticoagulation, and fibrinolytic systems from cellular players to cytokines to novel antithrombotic therapies and discusses the mechanisms contributing to occlusive microvascular thrombosis and tissue destruction in invasive group A streptococcal and C. perfringens infections. A thorough understanding of these mechanisms may suggest novel therapeutic targets for patients with these devastating infections

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“…Tissue factor is expressed in all of the major cell types of atherosclerotic lesions, with a preponderance in macrophages (127,128). Tissue factor expression in cultured macrophages is downregulated by the Th2 cytokines IL-4, IL-10, and IL-13, whereas the Th1 cytokine IFN-␥ has the opposite effect (129,130). Some of the effects on tissue factor expression, particularly those of IFN-␥, are differentiation-specific (131,132).…”

Section: Cytokine Regulation Of Coagulation In Atherosclerosismentioning

confidence: 99%

Thematic review series: The Immune System and Atherogenesis. Cytokine regulation of macrophage functions in atherogenesis

Daugherty

Webb

Rateri

et al. 2005

Journal of Lipid Research

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This review will focus on the role of cytokines in the behavior of macrophages, a prominent cell type of atherosclerotic lesions. Once these macrophages have immigrated into the vessel wall, they propagate the development of atherosclerosis by modifying lipoproteins, accumulating intracellular lipids, remodeling the extracellular environment, and promoting local coagulation. The numerous cytokines that have been detected in atherosclerosis, combined with the expression of large numbers of cytokine receptors on macrophages, are consistent with this axis being an important contributor to lesion development. Given the vast literature on cytokine-macrophage interactions, this review will be selective, with an emphasis on the major cytokines that have been detected in atherosclerotic lesions and their effects on properties that are relevant to lesion formation and maturation. There will be an emphasis on the role of cytokines in regulating lipid metabolism by macrophages. We will provide an overview of the major findings in cell culture and then put these in the context of in vivo studies. As noted in Getz's overview (1), lesions contain large numbers of cytokines that can be derived from several cell types. These cytokines may affect the function of many cell types in atherogenesis. The effects of cytokines on endothelial and smooth muscle cells are discussed in Raines and Ferri's contribution to this series (2). The purpose of this review is to focus on the effects of cytokines on macrophages in the evolution of atherosclerotic lesions. This is a vast literature that has necessitated some selectivity in the areas that can be covered. Given the subject area of this journal, we have elected to focus particular attention on the effect of cytokines on lipid metabolism in macrophages. MACROPHAGE FUNCTIONS IN ATHEROSCLEROTIC LESIONSMacrophages are hypothesized to be attracted to the subendothelial space to remove noxious materials deposited at atherosclerosis-prone regions of arteries. The precise chemical identity of the substance that attracts macrophages has not been unequivocally defined, although many candidate molecules are components of modified lipoproteins (3, 4). However, the function of infiltrating cells becomes subverted and leads to their retention within the subendothelial space. In this region, it is proposed that macrophages modify adjacent lipoproteins while also providing major mechanisms of removal for modified materials from the extracellular environment. The combination of lipoprotein modification and uptake leads to macrophages becoming engorged with lipids and resulting in a morphology that is given the descriptive name of "foam cells." Lipid engorgement causes pronounced cellular hypertrophy, with the cell diameter being Ͼ 10 times that of the originating monocyte. Probably as a result of the immense size increase, lipid-laden macrophages are chronically entrapped in the subendothelial space. Trapped macrophages can then invoke processes that perpetuate the continual recruitment of monoc...

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Inhibition of Il-1 Induced Tissue Factor (Tf) Synthesis and Procoagulant Activity (Pca) in Purified Human Monocytes by Il-4, Il-10 and Il-13

Cited by 58 publications

References 0 publications

Tissue-Type Plasminogen Activator Deficiency Exacerbates Arthritis

Tissue-Type Plasminogen Activator Deficiency Exacerbates Arthritis

Biology and Pathogenesis of Thrombosis and Procoagulant Activity in Invasive Infections Caused by Group A Streptococci andClostridium perfringens

Thematic review series: The Immune System and Atherogenesis. Cytokine regulation of macrophage functions in atherogenesis

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