Interleukin-1 Receptor Antagonist Gene Polymorphism and Coronary Artery Disease

Francis, Sheila; Camp, Nicola J.; Dewberry, Rachael; Gunn, Julian; Syrris, Petros; Carter, Nicholas D.; Jeffery, Stephen; Kaski, Juan Carlos; Cumberland, D.C.; Duff, Gordon W.; Crossman, David C.

doi:10.1161/01.cir.99.7.861

Cited by 205 publications

(170 citation statements)

References 33 publications

Supporting

Mentioning

152

Contrasting

Unclassified

Order By: Relevance

“…In our hands, the frequency of the TNF-a -308A allele in the control group was similar to that observed in CAD patients. The lack of association between -308 TNF-a polymorphism and CAD is consistent with other studies (24,28), and confirm the results of Francis et al (29) who found no association between TNF-a -308A allele and clinically or angiographically-documented coronary stenosis. Our data confirm some previous studies that investigated Caucasian populations and failed to demonstrate that this locus could be a marker for greater risk of CAD.…”

Section: Discussionsupporting

confidence: 91%

–308G>A and –1031T>C tumor necrosis factor gene polymorphisms in Tunisian patients with coronary artery disease

Ghazouani

Khalifa²,

Abboud³

et al. 2009

Clinical Chemistry and Laboratory Medicine

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 91%

–308G>A and –1031T>C tumor necrosis factor gene polymorphisms in Tunisian patients with coronary artery disease

Ghazouani

Khalifa²,

Abboud³

et al. 2009

Clinical Chemistry and Laboratory Medicine

View full text Add to dashboard Cite

“…Previously defined examples include polymorphisms in TNF␣ and IL-1ra that have been shown to have certain prognostic significance in malaria and ischaemic heart disease respectively. 24,25 Similarly, a number of polymorphisms in TNF␣ and IL-1␤ have been reported to be associated with rheumatoid arthritis severity. [26][27][28] The novel Mif gene polymorphism that we have identified is associated with reduced MIF promoter activity, and the presence of this genotype in the homozygous state appears to be associated with a reduced risk of severe rheumatoid arthritis.…”

Section: Discussionmentioning

confidence: 99%

A functional promoter polymorphism in the macrophage migration inhibitory factor (MIF) gene associated with disease severity in rheumatoid arthritis

et al. 2002

View full text Add to dashboard Cite

show abstract

“…Furthermore, IL-1ra levels are increased in patients with angina, and specific polymorphisms in the IL-1ra gene are associated with coronary artery disease. 13,14 Studies with IL-1 antagonists would be required to test the causality of these associations. This study does not rule out contribution by other important proinflammatory and anti-inflammatory cytokines, and it is possible that the IL-1ra simply acts as a surrogate marker for some other cytokine or mediator that causes endothelial dysfunction.…”

Section: Aspirin Pretreatment Preserves Endothelial Functionmentioning

confidence: 99%

Prevention of Inflammation-Induced Endothelial Dysfunction

Kharbanda

Walton²,

Allen³

et al. 2002

Circulation

155

101

View full text Add to dashboard Cite

Background — Inflammation and infection may initiate and promote atherosclerosis or its complications by adverse effects on the vascular endothelium. The mechanisms by which aspirin reduces cardiovascular risk might involve anti-inflammatory actions or direct effects on the endothelium in addition to its antiplatelet action. We investigated the role of aspirin in modulating endothelial dysfunction induced by an experimental inflammatory stimulus. Methods and Results — An inflammatory response was generated in healthy volunteers by Salmonella typhi vaccination. Venous occlusion plethysmography was used to assess resistance vessel responses (16 hours before and 8 hours after vaccination) to the endothelium-dependent dilator bradykinin (BK) and the endothelium-independent dilator glyceryl-trinitrate (GTN). Twelve subjects were randomized to receive either aspirin 1.2 g orally or placebo 2 hours before vaccination. After vaccination alone there was suppression of the response to BK in the placebo group ( P =0.01), with no change in response to GTN. In the aspirin group there was no change in the response to either BK or GTN after vaccination. Aspirin treatment prevented vaccine-induced elevation of interleukin-1 receptor antagonist but enhanced the generation of tumor necrosis factor-α compared with placebo. In an additional 5 individuals, local intrabrachial aspirin (10 mg/min for 15 minutes) failed to restore responses to BK after vaccination. Conclusions — Experimental inflammation produces endothelial dysfunction, which can be prevented by pretreatment with aspirin. Locally administered aspirin does not reverse vaccine-induced endothelial dysfunction once established. The protective effects of aspirin on inflammation-induced endothelial dysfunction may be through modulation of the cytokine cascade.

show abstract

Interleukin-1 Receptor Antagonist Gene Polymorphism and Coronary Artery Disease

Abstract: IL-1RN*2 was significantly associated with SVD. A difference in genetic association between SVD and MVD was also apparent.

Cited by 205 publications

References 33 publications

–308G>A and –1031T>C tumor necrosis factor gene polymorphisms in Tunisian patients with coronary artery disease

–308G>A and –1031T>C tumor necrosis factor gene polymorphisms in Tunisian patients with coronary artery disease

A functional promoter polymorphism in the macrophage migration inhibitory factor (MIF) gene associated with disease severity in rheumatoid arthritis

Prevention of Inflammation-Induced Endothelial Dysfunction

Contact Info

Product

Resources

About