Interferon-γ and Lipopolysaccharide Potentiate Monocyte Tissue Factor Induction by C-Reactive Protein

Nakagomi, Akihiro; Freedman, Ben; Geczy, Carolyn L.

doi:10.1161/01.cir.101.15.1785

Cited by 156 publications

(121 citation statements)

References 38 publications

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“…In addition to activation of the extrinsic coagulation cascade, factor VII binding to TF initiates intracellular signaling in monocytes/macrophages that may potentiate inflammation (17). Although not normally expressed, TF on monocytes/macrophages is induced by mediators of the innate (e.g., LPS, CRP) and cell-mediated immune responses (18), and we showed these to be mutually interactive and proposed that the synergy between CRP and inflammatory mediators could play a prothrombotic role in the pathogenesis of coronary atherosclerosis (19). Lymphocytes, which do not express TF themselves, are required for optimal TF production by monocytes/macrophages (18).…”

Section: Serum Amyloid a Induces Monocyte Tissue Factormentioning

confidence: 78%

“…After the final thaw, PCA of PBMC (100 l) was measured using a one-stage plasma recalcification test with an automatic coagulometer (Diagnostica Stago), as described (19). PCA was calculated from a standard curve using dilutions of rabbit brain extract (Sigma-Aldrich) as standard; results are expressed as mU TF/10 6 cells or as stimulation index (SI) (TF-SI: mU TF of stimulated PBMC divided by mU TF of unstimulated PBMC).…”

Section: Measurement Of Pca and Verification Of Tf Activitymentioning

confidence: 99%

“…Anti-TF IgG (2 g/well) or isotype-matched mouse IgG was added to cells that had been stimulated for 2 h with SAA (100 ng/ml) or LPS (100 ng/ml), and then cells were incubated on ice for 1 h and washed, and supernatants were discarded. Chromogenic assays were performed, as described (19).…”

Section: Measurement Of Pca and Verification Of Tf Activitymentioning

confidence: 99%

“…1B). Compared with SAA, higher amounts of CRP were needed to directly induce TF on PBMC; we used a predetermined amount of 25 g/ml (19) in this study. In marked contrast to SAA, the low levels of PCA induced by CRP were apparent only after 4-to 6-h culture (Fig.…”

Section: Saa Induces Pca With Properties Of Tfmentioning

confidence: 99%

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Serum Amyloid A Induces Monocyte Tissue Factor

Cai

Song

Endoh

et al. 2007

The Journal of Immunology

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107

121

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C-reactive protein (CRP) and serum amyloid A (SAA) increase in the blood of patients with inflammatory conditions and CRP-induced monocyte tissue factor (TF) may contribute to inflammation-associated thrombosis. This study demonstrates that SAA is a potent and rapid inducer of human monocyte TF. SAA induced TF mRNA in PBMC within 30 min and optimal procoagulant activity within 4 h, whereas CRP (25 μg/ml)-induced activity was minimal at this time. Unlike CRP, SAA did not synergize with LPS. Procoagulant activity was inhibited by anti-TF and was dependent on factors VII and X, and TF Ag levels were elevated on CD14+ monocytes. Responses were optimal with lymphocytes, although these were not obligatory. Inhibitor studies indicate activation of NF-κB through the ERK1/2 and p38 MAPK pathways; the cyclo-oxygenase pathway was not involved. SAA-induced TF was partially inhibited by high-density lipoprotein, but not by low-density lipoprotein or by apolipoprotein A-I. SAA is a ligand for the receptor for advanced glycation end products (RAGE), and TF generation was suppressed by ∼50% by a RAGE competitor, soluble RAGE, and by ∼85% by anti-RAGE IgG. However, another RAGE ligand, high mobility group box-1 protein, capable of inducing monocyte chemotactic protein-1 mRNA in 2 h, did not induce TF within 24 h. Cross-linking studies confirmed SAA binding to soluble RAGE. Elevated SAA is a marker of disease activity in patients with rheumatoid arthritis, and PBMC from patients with rheumatoid arthritis were more sensitive to SAA than normals, suggesting a new link between inflammation and thrombosis.

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Section: Serum Amyloid a Induces Monocyte Tissue Factormentioning

confidence: 78%

Section: Measurement Of Pca and Verification Of Tf Activitymentioning

confidence: 99%

Section: Measurement Of Pca and Verification Of Tf Activitymentioning

confidence: 99%

Section: Saa Induces Pca With Properties Of Tfmentioning

confidence: 99%

See 2 more Smart Citations

Serum Amyloid A Induces Monocyte Tissue Factor

Cai

Song

Endoh

et al. 2007

The Journal of Immunology

Self Cite

107

121

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“…Several other inflammatory markers for prediction of coronary accidents in healthy men and women and in patients with stable angina, acute coronary diseases and in follow up of cardiovascular accident have been studied. These markers include Values are mean ± SD; P [ 0.05 not significant; P \ 0.0001 highly significant interleukin (IL-6) [20,21], serum amyloid A (SAA) [22], Tumour necrosis factor-a (TNF-a) [23], CD40 ligand [24]. Among these markers CRP has emerged as most powerful inflammatory marker of future cardiovascular risk [25][26][27].…”

Section: Discussionmentioning

confidence: 99%

Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease

Datta¹,

Iqbal²,

Prasad³

2011

Ind J Clin Biochem

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Acute myocardial Infarction is one of the major causes of morbidity & mortality in world and atherosclerosis is the major cause of ischemic heart disease. In order to determine the better clinical marker of atherosclerosis, we estimated serum low-density lipoprotein (LDL-C) and high sensitivity C-reactive protein (hsCRP). Hundred patients of myocardial infarction and 100 controls irrespective of age and sex were studied for these parameters over a period of 2 years. The statistical analysis showed that the serum hsCRP was significantly raised in myocardial infarction cases than controls (P \ 0.01) but LDL-C was not (P [ 0.05). We conclude that the serum hsCRP has better predictive value for risk of atherosclerosis.

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Inflammatory Biomarkers, Hormone Replacement Therapy, and Incident Coronary Heart Disease

Pradhan¹,

Manson²,

Rossouw³

et al. 2002

JAMA

601

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Context Postmenopausal hormone replacement therapy (HRT) has been shown to elevate C-reactive protein (CRP) levels. Several inflammatory biomarkers, including CRP, are associated with increased cardiovascular risk. However, whether the effect of HRT on CRP represents a clinical hazard is unknown. Objectives To assess the association between baseline levels of CRP and interleukin 6 (IL-6) and incident coronary heart disease (CHD) and to examine the relationship between baseline use of HRT, CRP, and IL-6 levels as they relate to subsequent vascular risk. Design, Setting, and Participants Prospective, nested case-control study of postmenopausal women, forming part of the Women's Health Initiative, a large, nationwide, observational study. Among 75343 women with no history of cardiovascular disease or cancer, 304 women who developed incident CHD were defined as cases and matched by age, smoking status, ethnicity, and follow-up time with 304 study participants who remained event free during a median observation period of 2.9 years. Main Outcome Measure Incidence of first myocardial infarction or death from CHD. Results Median baseline levels of CRP (0.33 vs 0.25 mg/dL; interquartile range [IQR], 0.14-0.71 vs 0.10-0.47; PϽ.001) and IL-6 (1.81 vs 1.47 pg/mL; IQR, 1.30-2.75 vs 1.05-2.15; PϽ.001) were significantly higher among cases compared with controls. In matched analyses, the odds ratio (OR) for incident CHD in the highest vs lowest quartile was 2.3 for CRP (95% confidence interval [CI], 1.4-3.7; P for trend=.002) and 3.3 for IL-6 (95% CI, 2.0-5.5; P for trend Ͻ.001). After additional adjustment for lipid and nonlipid risk factors, both inflammatory markers were significantly associated with a 2-fold increase in odds for CHD events. As anticipated, current use of HRT was associated with significantly elevated median CRP levels. However, there was no association between HRT and IL-6. In analyses comparing individuals with comparable baseline levels of either CRP or IL-6, those taking or not taking HRT had similar CHD ORs. In analyses stratified by HRT, we observed a positively graded relationship between plasma CRP levels and the OR for CHD among both users and nonusers of HRT across the full spectrum of baseline CRP. Conclusions These prospective findings indicate that CRP and IL-6 independently predict vascular events among apparently healthy postmenopausal women and that HRT increases CRP. However, use or nonuse of HRT had less importance as a predictor of cardiovascular risk than did baseline levels of either CRP or IL-6.

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Interferon-γ and Lipopolysaccharide Potentiate Monocyte Tissue Factor Induction by C-Reactive Protein

Cited by 156 publications

References 38 publications

Serum Amyloid A Induces Monocyte Tissue Factor

Serum Amyloid A Induces Monocyte Tissue Factor

Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease

Inflammatory Biomarkers, Hormone Replacement Therapy, and Incident Coronary Heart Disease

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