The association of interleukin-16 gene polymorphisms with susceptibility of coronary artery disease

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Abstract

Objectives: Recent studies have shown that interleukin (IL)-16 is an immunomodulatory cytokine, which plays an important role in some inflammatory and autoimmune diseases. We aimed to investigate the association between the IL-. 16 gene polymorphisms and presence of coronary artery disease (CAD) where inflammatory processes are involved. Designs and Methods: This case-control study enrolled 651 CAD patients confirmed by coronary angiography and 428 controls. Four tag single nucleotide polymorphisms (rs8034928-rs3848180-rs4577037-rs1131445) within the IL-. 16 gene and the related haplotypes were genotyped by using polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP). Plasma IL-. 16 concentration was measured by enzyme-linked immunosorbent assay. Results: In patients with CAD, the plasma concentration of IL-. 16 was significantly higher than in controls (97.6 ± 10.7, 66.5 ± 9.6, respectively P < 0.001). By using multivariate logistic regression analysis, the allele and genotype frequencies of rs8034928 were different between CAD and control groups (P < 0.001). However, the associations of the polymorphisms rs3848180, rs4577037, and rs1131445 with CAD were not observed. The haplotypes TTTT and TGGT significantly increased risk to CAD (OR, 95% CI: 1.43, 1.26-1.63; 1.47, 1.16-1.85; respectively), whereas the haplotypes CTTT and TTGT referred to protection of CAD (OR, 95% CI: 0.45, 0.33-0.62; 0.50, 0.33-0.76; respectively). Conclusion: The study indicated that the IL-. 16 rs8034928 T/C polymorphism and haplotypes were associated with the presence of CAD in Chinese Han population. The IL-. 16 gene polymorphisms may be a useful predictor to the susceptibility of CAD. © 2012 The Canadian Society of Clinical Chemists.

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Huang, H., Zeng, Z., Zhang, L., Liu, R., Li, X., Qiang, O., … Chen, Y. (2013). The association of interleukin-16 gene polymorphisms with susceptibility of coronary artery disease. Clinical Biochemistry, 46(3), 241–244. https://doi.org/10.1016/j.clinbiochem.2012.11.009

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