Abstract
BackgroundInterleukin-1B (IL-1B) is a key pro-inflammatory cytokine that has been associated with the development of atherosclerosis and myocardial infarction. However, the prospective associations between functional single nucleotide polymorphisms (SNPs) in IL1B and incident acute coronary syndrome (ACS) have not been thoroughly investigated. The aims of this study were to examine the associations between individual SNPs in and SNP haplotypes of the promoter region of IL1B and incident ACS in a prospective study. Furthermore, we wanted to explore potential interactions with other risk factors for ACS on an additive scale.Methodology/Principal FindingsThe present study was based on the Danish prospective study Diet, Cancer and Health comprising more than 57 000 participants aged 50–64 at baseline. During a median follow-up of 7.2 years we identified 989 cases of incident ACS (755 men and 234 women). All cases were validated by review of medical records, and information on covariates was collected by study technicians. The study was conducted according to a case-cohort study design including ACS cases and a sex-stratified sub cohort of 1663 participants drawn randomly from the entire cohort. Weighted Cox proportional hazard models with age as time axis were used in the statistical analyses. Individual IL1B SNPs, SNP haplotypes, or haplotype combinations were not significantly associated with incident ACS, and, likewise, we found no evidence of interaction on an additive scale between IL1B haplotypes and risk factors, respectively.Conclusions/SignificanceGenetic variation in the promoter region of IL1B may not be associated with incident ACS in men or women above the age of 50 years.
Highlights
Interleukin-1B (IL-1B) is a key pro-inflammatory cytokine that induces the production of other cytokines, adhesion molecules, and metalloproteinases [1,2]
In a human case-control study, the -511T single nucleotide polymorphism (SNP) in IL1B was associated with a lower release of IL-1B from human mononuclear cells and a relatively low risk of myocardial infarction at young age [7]
Potential biological interaction on an additive scale between SNP haplotypes and obesity (BMI, WC adjusted for HC, HC adjusted for WC) or the NFKB1 -94 ATTG ins/del polymorphism was explored as the relative excess risk due to interaction (RERI) and calculated as suggested by Rothman [25]
Summary
Interleukin-1B (IL-1B) is a key pro-inflammatory cytokine that induces the production of other cytokines, adhesion molecules, and metalloproteinases [1,2]. The IL-1 signaling pathway has been associated with the development of atherosclerosis in animal studies[3,4,5], and IL-1B mRNA is increased in human atherosclerotic arteries [6]. In a human case-control study, the -511T single nucleotide polymorphism (SNP) in IL1B was associated with a lower release of IL-1B from human mononuclear cells and a relatively low risk of myocardial infarction at young age [7]. IL1B polymorphisms may interact with obesity, as the effect of obesity on plaque development is partly mediated by the release of inflammatory cytokines from adipose tissue compartments [11]. Interleukin-1B (IL-1B) is a key pro-inflammatory cytokine that has been associated with the development of atherosclerosis and myocardial infarction. The prospective associations between functional single nucleotide polymorphisms (SNPs) in IL1B and incident acute coronary syndrome (ACS) have not been thoroughly investigated. We wanted to explore potential interactions with other risk factors for ACS on an additive scale
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