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1.
Circ J ; 82(5): 1418-1427, 2018 04 25.
Artigo em Inglês | MEDLINE | ID: mdl-29225295

RESUMO

BACKGROUND: Smoking increases the risk of atherothrombotic events. Tissue factor (TF) mainly expressed on monocytes plays an important role in thrombosis and atherosclerosis. Metabolic syndrome (MetS) is being increasingly recognized as a major atherothrombotic risk factor, but the effects of smoking on monocyte TF activity (MTFA), carotid atherosclerosis estimated on carotid intima-media thickness (CIMT), and long-term prognosis in MetS remain unclear.Methods and Results:A total of 301 MetS patients lacking any known cardiovascular disease were prospectively investigated and classified into 4 groups according to smoking status at entry and at 12 months as follows: never smokers, past smokers, quitters, and persistent smokers. Peripheral blood mononuclear cells (PBMC) were isolated, and MTFA was measured using a coagulation assay. Linear trends for higher baseline MTFA and CIMT were observed among persistent smokers, quitters, and past smokers compared with never smokers. At 12 months, MTFA and CIMT decreased in never and past smokers and quitters but increased in persistent smokers. Six acute myocardial infarctions and 8 strokes occurred during a median follow-up of 66.0 months. Persistent smoking was associated with an increased risk of events (P<0.001). CONCLUSIONS: Smoking is associated with upregulated MTFA and progression of CIMT, which may be related to the risk of atherothrombotic events in MetS patients.


Assuntos
Doenças das Artérias Carótidas/metabolismo , Síndrome Metabólica/metabolismo , Monócitos/metabolismo , Infarto do Miocárdio/metabolismo , Fumar/metabolismo , Acidente Vascular Cerebral/metabolismo , Tromboplastina/metabolismo , Idoso , Doenças das Artérias Carótidas/diagnóstico , Doenças das Artérias Carótidas/patologia , Feminino , Humanos , Masculino , Síndrome Metabólica/diagnóstico , Síndrome Metabólica/patologia , Pessoa de Meia-Idade , Monócitos/patologia , Infarto do Miocárdio/diagnóstico , Infarto do Miocárdio/patologia , Prognóstico , Fumar/efeitos adversos , Acidente Vascular Cerebral/diagnóstico , Acidente Vascular Cerebral/patologia
2.
J Atheroscler Thromb ; 23(6): 713-27, 2016 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-26782970

RESUMO

AIM: Malnutrition has been identified to be an independent predictor of morbidity and mortality in patients with chronic heart failure (CHF). However, the pathophysiological mechanisms underlying this pathway remain unclear. METHODS: Nutritional screening was performed using the controlling nutritional status (CONUT) score, which was calculated using the serum albumin and total cholesterol levels and lymphocyte number, in 114 CHF patients with a mean left ventricular ejection fraction of 26.6%±6.4%. The carotid intima-media thickness (CIMT) is correlated with carotid atherosclerosis and is a significant predictor of future cardiovascular events. Peripheral blood mononuclear cells (PBMCs) were isolated, and the production of monocyte tumor necrosis factor (TNF)-α was measured and expressed as mean±SD (pg/mL/10(6) PBMCs). RESULTS: A multivariate linear regression analysis showed that the production of monocyte TNF-α (ß coefficient=0.434, p<0.001) and mean CIMT (ß coefficient=0.204, p=0.006) were independent determinants of the CONUT score. During a median follow-up of 67.5 months, 45 patients experienced cardiac events, including 16 cardiac deaths and 29 readmissions for worsening CHF. A multivariate Cox hazard analysis demonstrated that a monocyte TNF-α level of ≥4.1 pg/mL/10(6) PBMCs (hazard ratio (HR), 14.10; 95% confidence interval (CI), 2.55-77.92; p=0.002) and CONUT score of ≥3 (HR, 11.97; 95% CI, 2.21-64.67; p=0.004) were independently associated with the incidence of cardiac events. CONCLUSIONS: These data indicate that a poor nutritional status as assessed using the CONUT score and atherosclerosis as indicated by CIMT is significantly associated with inflammation and predicts poor outcomes in patients with CHF.


Assuntos
Espessura Intima-Media Carotídea , Insuficiência Cardíaca/complicações , Inflamação/etiologia , Monócitos/patologia , Estado Nutricional , Idoso , Biomarcadores/análise , Doença Crônica , Feminino , Insuficiência Cardíaca/fisiopatologia , Humanos , Inflamação/metabolismo , Inflamação/patologia , Leucócitos Mononucleares/metabolismo , Leucócitos Mononucleares/patologia , Masculino , Pessoa de Meia-Idade , Monócitos/metabolismo , Prognóstico , Estudos Prospectivos , Taxa de Sobrevida , Fator de Necrose Tumoral alfa/metabolismo
4.
Antioxid Redox Signal ; 14(9): 1589-600, 2011 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-21142608

RESUMO

S100A8 is implicated in the pathogenesis of inflammatory diseases. S100A8 is upregulated in macrophages by Toll-like receptors (TLR)-3, 4, and 9 agonists in an IL-10-dependent manner, and by corticosteroids in vitro and in vivo, and scavenges oxidants generated by activated phagocytes. Because if its elevated expression in various lung disorders, we asked whether S100A8 was protective in allergic inflammation. S100A8, but not Cys(41)-Ala S100A8, in which the single reactive Cys residue was replaced by Ala, reduced mast cell (MC) degranulation and production of particular cytokines (IL-6, IL-4, and granulocyte macrophage colony-stimulating factor) in response to IgE-crosslinking in vitro, likely by inhibiting intracellular reactive oxygen species production, thereby reducing downstream linker for activation of T cells and extracellular signal regulated kinase/mitogen-activated protein kinase phosphorylation. In lungs of mice with acute asthma, S100A8, but not Cys(41)-Ala S100A8, reduced MC degranulation, production of eosinophil chemoattractants (IL-5, eotaxin, and monocyte chemoattractant protein-1), and eosinophil infiltration. Suppression of IL-6 and IL-13 could have contributed to reduced mucus production seen in lungs of S100A8-treated mice. IgE production was unaffected. In asthma, there is an imbalance of anti-oxidant systems that are generally protective. Our results strongly support a protective role for S100A8 in allergic inflammation by modulating MC activation and eosinophil recruitment, and by scavenging oxidants generated by activated leukocytes, in processes reliant on its thiol-scavenging capacity.


Assuntos
Asma/metabolismo , Calgranulina A/metabolismo , Movimento Celular/fisiologia , Eosinófilos/citologia , Mastócitos/citologia , Animais , Apoptose/efeitos dos fármacos , Asma/genética , Movimento Celular/genética , Células Cultivadas , Quimiocina CCL2/genética , Feminino , Fator Estimulador de Colônias de Granulócitos e Macrófagos/genética , Interleucina-10/genética , Interleucina-13/genética , Interleucina-4/genética , Interleucina-5/genética , Interleucina-6/genética , Mastócitos/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Fosforilação , Reação em Cadeia da Polimerase , Espécies Reativas de Oxigênio/metabolismo , Fator de Crescimento Transformador beta/genética , Fator de Necrose Tumoral alfa/genética
5.
J Immunol ; 178(3): 1852-60, 2007 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-17237436

RESUMO

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 mug/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-kappaB 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 approximately 50% by a RAGE competitor, soluble RAGE, and by approximately 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.


Assuntos
Monócitos/metabolismo , Proteína Amiloide A Sérica/fisiologia , Tromboplastina/genética , Idoso , Artrite Reumatoide/sangue , Proteína C-Reativa , Células Cultivadas , Feminino , Regulação da Expressão Gênica , Humanos , Lipoproteínas/farmacologia , Masculino , Pessoa de Meia-Idade , NF-kappa B/metabolismo , RNA Mensageiro , Receptor para Produtos Finais de Glicação Avançada , Receptores Imunológicos/metabolismo , Proteína Amiloide A Sérica/metabolismo , Transdução de Sinais , Trombofilia
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