Background: Cytokines regulate the expression of inflammatory molecules which destabilize the atheromatic plaques. This study focuses on studying the association of inflammatory cytokine polymorphisms like TNF-α -308 (G/A), TNF-β +252 (A/G), IL-6 -174 (G/C) and IL-6 -597 (G/A), and IFN-ɣ +874 (T/A) with coronary artery disease (CAD) among north Indian patients.
Materials and methods: 143 CAD and 137 normal healthy controls were recruited in this study. DNA extraction was carried out by high salting out method. TNF-α -308 (G/A) (rs1800797), TNF-β +252 (A/G) (rs909253), IL-6 -174 (G/C) (rs1800795), IL6 -597 (G/A) (rs1800797), and IFN-ɣ +874 (T/A) (rs2430561) SNPs were genotyped by TaqMan®SNP genotyping assays. Different statistical analyses were performed using SPSS v 22.0 and SNPStats. p≤0.05 was considered significant.
Results: Significant risk association with CAD was found for TNF-α -308 (G/A) “A” allele (OR =5.6, CI 1.8-17.4, p=0.001) and TNF-β +252 (A/G) “G” allele (OR=3.4, CI=1.9-6.0, p<0.001). However, no statistical significance was found for IL-6 -174 (G/C) or IL6 -597 (G/A), with CAD. TNF-α -308 (G/A), and TNF-β +252 (A/G) haplotype “GG” “AG” increased CAD risk significantly (GG haplotype, adjusted OR = 2.6, CI 1.4-5.0, p=0.003 and AG haplotype OR =8.5, CI 2.2-33.35, p=0.002) after adjustments for age, sex, TC, TG, HDL, APOB, smoking and diet.
Discussion: The present study found significant risk association for TNF-α -308 (G/A), and TNF-β +252 (A/G) genotypes, alleles and haplotypes, with CAD in a North Indian Population.
Funding
Authors acknowledge the financial support from Loughborough University and the Society for the Study of Human Biology (SSHB) (Undergraduate bursary award to M. Kirby).
History
School
Sport, Exercise and Health Sciences
Published in
Gene
Citation
MASTANA, S.S. ...et al., 2017. Genetic association of pro-inflammatory cytokine gene polymorphisms with coronary artery disease (CAD) in a North Indian population. Gene, 628, pp. 301–307.
This work is made available according to the conditions of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) licence. Full details of this licence are available at: https://creativecommons.org/licenses/by-nc-nd/4.0/
Acceptance date
2017-07-17
Publication date
2017
Notes
This paper was published in the journal Gene and the definitive published version is available at https://doi.org/10.1016/j.gene.2017.07.050.