Elevated Levels of Interleukin-6 in Unstable Angina

Biasucci, Luigi M.; Vitelli, Alessandra; Liuzzo, Giovanna; Altamura, Sergio; Caligiuri, Giuseppina; Monaco, Claudia; Rebuzzi, Antonio Giuseppe; Ciliberto, Gennaro; Maseri, Attilio

doi:10.1161/01.cir.94.5.874

Cited by 654 publications

(365 citation statements)

References 25 publications

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“…7 IL-6 plays a key role in driving the acute inflammatory response and orchestrates the production of acute phase proteins. 8 Elevated levels of IL-6 are found in patients with coronary syndromes 9 and have been associated with increased risk of future myocardial infarction in an apparently healthy population. 10 A relationship between IL-6 and EH may be hypothesised for a number of reasons.…”

Section: Introductionmentioning

confidence: 99%

The −174 G/C polymorphism of the interleukin-6 gene promoter and essential hypertension in an elderly Italian population

et al. 2002

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Several studies have proposed a relationship between blood pressure and inflammation. Interleukin-6 (IL-6) is a multifunctional cytokine involved in inflammation and tissue injury and potentially influencing blood pressure. Recently, a common polymorphism of the IL-6 gene, associated with differences in the transcription rate of the protein, has been described. The aim of this study was to investigate a possible association between genetic variations of the −174GC polymorphism of the IL-6 gene promoter and hypertension in humans. IL-6 gene promoter polymorphism was evaluated by polymerase chain reaction followed by restriction enzyme analysis in 210 elderly Italian patients affected by essential

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Section: Introductionmentioning

confidence: 99%

The −174 G/C polymorphism of the interleukin-6 gene promoter and essential hypertension in an elderly Italian population

et al. 2002

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“…13,27 IL-6 induces CRP production in hepatocytes and it is the only cytokine that can stimulate the synthesis of all other acute-phase proteins. [28][29][30] Thus, some authors proposed IL-6 as a useful prognostic marker of CVD outcome [31][32][33][34][35][36][37] and suggested a central role for IL-6 in the pathogenesis of CHD. [38][39][40] However, the estimated heritability for IL-6 ranged between 0.17 and 0.57 in the literature 16,41,42 and previous studies concerning the heritability of CRP and IL-6 have to be interpreted carefully (Table 1).…”

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confidence: 99%

“…In previous studies, plasma CRP levels strongly correlated with those of IL-6, suggesting that measuring CRP may also have been indirectly measuring plasma IL-6 levels. 35,40,62 It was demonstrated that healthy subjects with increased plasma IL-6 levels have a twofold risk of death and CVD events, 32,33 independent of traditional cardiovascular risk factors but additive to that for CRP. 31 Some authors even proposed that elevated plasma IL-6 levels are a stronger predictor of cardiovascular mortality than CRP 63 and IL-6 seems to be the main circulating cytokine in systemic inflammation.…”

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confidence: 99%

Genetic and environmental contributions to plasma C-reactive protein and interleukin-6 levels – a study in twins

et al. 2006

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Elevated baseline levels of acute-phase proteins such as C-reactive protein (CRP) or cytokines like interleukin-6 (IL-6) are known risk factors for atherosclerosis and cardiovascular disease (CVD) events. However, until today, there is only controversial information about the contribution of genetic and environmental factors. Therefore, we performed an open prospective study in 108 monozygotic (MZ) and 60 same-sex dizygotic (DZ) twin pairs to analyse the genetic and environmental contributions to plasma CRP and IL-6 levels. Heritability of IL-6 was 0.61, indicating that plasma IL-6 levels are to a major part influenced by genetic determinants; however, for CRP, heritability was only 0.22, pointing to a moderate genetic influence. Plasma CRP levels were strongly influenced by female gender, older age and especially the body mass index. Our data underline the central role of IL-6 in low-grade inflammation contributing to atherosclerosis and CVD. Genes and Immunity (2006) Keywords: twin pairs; heritability; interleukin-6; C-reactive protein; body mass index Low-grade inflammation is thought to play an essential role in the pathogenesis of atherosclerosis and cardiovascular disease (CVD) events. 1,2 As a highly sensitive C-reactive protein (CRP) measurement is possible, several large epidemiological studies have demonstrated association between elevated plasma CRP levels reflecting low-grade inflammation and the development of CVD events such as coronary heart disease (CHD), stroke or peripheral arterial disease. 3-7 CRP represents not only a sensitive marker for systemic inflammation, but also contributes to the complex interaction occurring between endothelial dysfunction, lipid accumulation, cell activation and inflammatory response in the pathogenesis of atherosclerosis. [8][9][10][11] Family studies have suggested that 35-45% of the variations in plasma baseline CRP levels are genetically determined [12][13][14][15] and twin studies revealed a heritability of 20-52% for CRP. [16][17][18] In addition, it is known that (environmental) factors such as obesity, older age, female gender, smoking, diabetes mellitus, chronic infections, lower socio-economic status, greater alcohol consumption and medications such as oral contraceptives are involved in a low-grade inflammatory response with elevated plasma CRP levels. 6,[19][20][21][22][23][24][25][26] An aim of determining plasma CRP levels could be related to polymorphisms in upstream cytokines such as interleukin (IL)-6. 13,27 IL-6 induces CRP production in hepatocytes and it is the only cytokine that can stimulate the synthesis of all other acute-phase proteins. [28][29][30] Thus, some authors proposed IL-6 as a useful prognostic marker of CVD outcome 31-37 and suggested a central role for IL-6 in the pathogenesis of CHD. [38][39][40] However, the estimated heritability for IL-6 ranged between 0.17 and 0.57 in the literature 16,41,42 and previous studies concerning the heritability of CRP and IL-6 have to be interpreted carefully (Table 1). The design and exact an...

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“…Unstable angina is associated with activation of systemic circulating neutrophils 16 and with elevated inflammatory markers such as C-reactive protein and IL-6 levels. [17][18][19] The magnitude of this elevation predicts poor outcome and is not merely secondary to the presence of myocardial necrosis or ischemia. 20 We have recently detected a functional polymorphism 174 bp upstream from the start of transcription of the IL-6 gene.…”

mentioning

confidence: 99%

Stromelysin-1 and Interleukin-6 Gene Promoter Polymorphisms Are Determinants of Asymptomatic Carotid Artery Atherosclerosis

Rauramaa

Väisänen²,

Luong³

et al. 2000

ATVB

193

109

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Abstract-The functional 5A/6A polymorphism of the stromelysin-1 promoter has been implicated as a potential genetic marker for the progression of angiographically determined atherosclerosis in patients with coronary artery disease. Recently, a novel interleukin-6 (IL-6) gene functional G/C polymorphism at Ϫ174 in the promoter has also been reported. In this study, we analyzed the relation of these two polymorphisms with carotid artery atherosclerosis in 109 randomly selected, middle-aged men without exercise-induced ischemia. Atherosclerosis was quantified as intimamedia thickness (IMT) by high-resolution ultrasonography. Univariately, stromelysin genotype was significantly (Pϭ0.015) associated with IMT, and this relation remained (Pϭ0.033) after adjustments for age, cardiorespiratory fitness, body mass index, smoking, LDL cholesterol, and systolic blood pressure and for sonographers. The 5A/6A polymorphism independently explained 7% of the variance in carotid bifurcation IMT. The IL-6 polymorphism was also significantly associated (Pϭ0.036) with increased IMT, with men homozygous for the G allele having IMT that was 11% greater than men homozygous for the C allele. Men who were homozygous for both the 6A and G alleles had an covariate adjusted IMT that was 36% greater than men who were homozygous for neither allele (PϽ0.003). These data suggest that genetic factors that predispose to reduced matrix remodeling (stromelysin 6A allele) and to increased inflammation (IL-6 G allele) combine to increase susceptibility for intima-media thickening in the carotid bifurcation, a predilection site for atherosclerosis. Key Words: stromelysin-1 Ⅲ interleukin-6 Ⅲ DNA polymorphism Ⅲ B-mode ultrasonography Ⅲ carotid atherosclerosis Ⅲ population sample

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Elevated Levels of Interleukin-6 in Unstable Angina

Cited by 654 publications

References 25 publications

The −174 G/C polymorphism of the interleukin-6 gene promoter and essential hypertension in an elderly Italian population

The −174 G/C polymorphism of the interleukin-6 gene promoter and essential hypertension in an elderly Italian population

Genetic and environmental contributions to plasma C-reactive protein and interleukin-6 levels – a study in twins

Stromelysin-1 and Interleukin-6 Gene Promoter Polymorphisms Are Determinants of Asymptomatic Carotid Artery Atherosclerosis

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