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Fadl, M. A., & algalil, S. S. N. (2020). IL1β exon5 3954 C/T Polymorphism: A Potential Genetic Risk Factor of Heart Diseases predisposition in Sudanese Patients. Sudan Journal of Medical Sciences (SJMS), 15(4), 399–407. https://doi.org/10.18502/sjms.v15i4.8162
https://doi.org/10.18502/sjms.v15i4.8162
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Manal A. Fadl
Manal A. Fadl
Dept of biochemistry and molecular biology-Faculty of Science and Technology-AlNeelain University
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Sahar S. Noor algalil
Sahar S. Noor algalil
Dept of biochemistry and molecular biology-Faculty of Science and Technology-AlNeelain University
Published Date
- Dec 31, 2020
IL1β exon5 3954 C/T Polymorphism: A Potential Genetic Risk Factor of Heart Diseases predisposition in Sudanese Patients
Abstract
IL-1β was known to cause an inflammation in heart tissue leading to progressive loss of contractile tissues. The aim of this study was to evaluate “for the first time” the relationship between IL-1β polymorphism (rs1143634) and the risk of heart diseases (HDs) in Sudanese patients. Methods: Fifty patients with HD and 65 healthy controls were enrolled in this cross-sectional study. The IL-1β (rs1143634) polymorphism was detected by PCR-RFLP using TaqI restriction enzyme. Results: About 82% of the HD cases were aged >40 years. No gender difference was reported between the two groups (P = 0.28). 24% of the cases had a previous history of heart attack. Family history of HD was associated with a six-fold increased risk of HD. The analysis provides evidence that the mutant genotype (CT + TT) of the IL1β polymorphism is significantly associated with HD, with up to four-fold increased risk of the disease (P = 0.015, OR = 3.8). The mutant allele T was significantly higher in HD patients as compared to the controls (P = 0.023). The frequency of the CT genotype among patient who have family history, previous attack of HD, hypertension, and diabetes was 79%, 33%, 81%, and 90% respectively. Conclusion: The IL1β (rs1143634) polymorphism was associated with the increased risk of HD in our samples. The carriage of the mutant allele among those who have family history of HD, previous attack, hypertension, and diabetes might be a predictive factor for the onset of clinical manifestation of HD in Sudanese patients.
Key words: heart diseases’ risk factors, gene polymorphisms, Interleukin (IL)-1 β
References
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[4] Vosberg, H. P. (1994). Identification of gene defects by linkage analysis: use in inherited cardiomyopathies. European Heart Journal, vol. 15, Supplement D, pp. 20–23.
[5] Evans, E., Poirier, O., Kee, F., et al. (1994). Polymorphisms of the angiotensin-converting-enzyme gene in subjects who die from coronary heart disease. International Journal of Medicine, vol. 87, no. 4, pp. 211–214.
[6] Yokota, M., Ichihara, S., Lin, T.L., et al. (2000). Association of a T29-->C polymorphism of the transforming growth factor-beta1 gene with genetic susceptibility to myocardial infarction in Japanese. Circulation, vol. 101, no. 24, pp. 2783–2787.
[7] Andreotti, F., Porto, I., Crea, F., et al. (2002). Inflammatory gene polymorphisms and ischaemic heart disease: review of population association studies. Heart, vol. 87, no. 2, pp. 7–12.
[8] Nordlie, M. A., Wold, L. E., and Kloner, R. A. (2005). Genetic contributors toward increased risk for ischemic heart disease. Journal of Molecular and Cellular Cardiology, vol. 39, no. 4, pp. 667–679.
[9] Xuan, Y., Wang, L., Zhi, H., et al. (2016). Association between 3 IL-10 gene polymorphisms and cardiovascular disease risk systematic review with meta-analysis and trial sequential analysis. Medicine, vol. 95, no. 6, p. e2846.
[10] Greenberg, M. J., Daily, N. J., Wang, A., et al. (2018). Genetic and tissue engineering approaches to modeling the mechanics of human heart failure for drug discovery. Front Cardiovascular Medicine, vol. 5, p. 120.
[11] Kofler, S., Nickel, T., and Weis, M. (2005). Role of cytokines in cardiovascular diseases: a focus on endothelial responses to inflammation. Clinical Science, vol. 108, no. 3, pp. 205–213.
[12] Wu, J., Wang, Y., and Zhang, Y. (2011). Association between interleukin-16 polymorphisms and risk of coronary artery disease. DNA Cell Biology, vol. 30, no.5, pp. 305–308.
[13] Elsaid, A., Abdel-Aziz, A. F., Elmougy, R., et al. (2014). Association of polymorphisms G(-174)C in IL-6 gene and G(-1082)A in IL-10 gene with traditional cardiovascular risk factors in patients with coronary artery disease. Indian Journal of Biochemistry and Biophysics, vol. 51, no.4, pp. 282–292.
[14] Zuo, H. P., Che, L., and Wu, X. Z. (2014). Correlation between the polymorphism of C-592A in interleukin-10 gene and genetic susceptibility to coronary heart disease. Experimental Clinical Cardiology, vol. 20, no.8, pp. 3440–3454.
[15] Buraczynska, M., Zukowski, P., Drop, B., et al. (2016). Effect of G(-174)C polymorphism in interleukin-6 gene on cardiovascular disease in type 2 diabetes patients. Cytokine, vol. 79, pp. 7–11.
[16] Hongmei, Y., Yongping, J., and Jiyuan, L. V. (2016). Interleukin-6 polymorphisms and risk of coronary artery diseases in a Chinese population: a case-control study. Pakistan Journal of Medical Science, vol. 32, no. 4, pp. 880–885.
[17] Gupta, S., Markham, D. W., Drazner, M. H., et al. (2008). Fulminant myocarditis. Nature Clinical Practice Cardiovascular Medicine, vol. 5, no. 11, pp. 693–706.
[18] Dinarello, C. A. (1996). Biologic basis for interleukin-1 in disease. Blood, vol. 87, no. 6, pp. 2095–20147.
[19] Marculescu, R., Endler, G., Schillinger, M., et al. (2002). Interleukin-1 receptor antagonist genotype is associated with coronary atherosclerosis in patients with type 2 diabetes. Diabetes, vol. 51, no.12, pp. 3582–3585.
[20] Geismar, K., Enevold, C., Sørensen, L. K., et al. (2008). Involvement of interleukin-1 genotypes in the association of coronary heart disease with periodontitis. Journal of Periodontology, vol. 79, no. 12, pp. 2322–2330.
[21] Zee, R. Y., Hennessey, H., Michaud, S. E., et al. (2008). Genetic variants within the interleukin-1 gene cluster, and risk of incident myocardial infarction, and ischemic stroke: a nested case-control approach. Atherosclerosis, vol. 201, no.1, pp. 124–129.
[22] Zhou, L., Cai, J., Liu, G., et al. (2012). Associations between interleukin-1 gene polymorphisms and coronary heart disease risk: a meta-analysis. PLOS ONE, vol. 7, no. 9, p. e45641.
[23] Zou, L., Zhao, H., Gong, X., et al. (2015).The association between three promoter polymorphisms of IL-1 and stroke: a meta-analysis. Gene, vol. 567, no. 1, pp. 36–44.
[24] Momiyama, Y., Ohmori, R., and Ohsuzu, F. (2005). Association between IL-1beta gene polymorphism and myocardial infarction. Arteriosclerosis, Thrombosis and Vascular Biology, vol. 25, no. 4, p. e36.
[25] Soylu, O., Yildirim, A., Coker, A., et al. (2008). Interleukin-1B (-511) gene polymorphism is associated with acute coronary syndrome in the Turkish population. European Cytokine Network, vol. 19, no.1, pp. 42–48.
[26] Dinarello, C. A. (2011). Interleukin-1 in the pathogenesis and treatment of inflammatory diseases. Blood, vol. 117, no. 14, pp. 3720–3732.
[27] Van Tassell, B. W., Raleigh, J. M., and Abbate, A. (2015). Targeting interleukin-1 in heart failure and inflammatory heart disease. Current Heart Failure Report, vol. 12, no. 1, pp. 33–41.
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[29] Yassin, K., Elfil, A., Hamid, H., et al. (2015). Epidemiology of cardiac disease during pregnancy in Khartoum Hospital, Sudan. Journal of Women's Health Care, vol. 4, no. 2, p. 227.
[30] Ali, S., Domi, S. B., Elfaki, A. M. H., et al. (2017). The echocardiographic prevalence of rheumatic heart disease in North Kordofan and initiation of a control program. Sudan Medical Journal, vol. 53, no. 2, pp. 63–68.
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[32] Iacoviello, L., Di Castelnuovo, A., Gattone, M., et al. (2005). Polymorphisms of the interleukin-1beta gene affect the risk of myocardial infarction and ischemic stroke at young age and the response of mononuclear cells to stimulation in vitro. Arteriosclerosis and Thrombosis and Vascular Biology, vol. 25, Issue1, pp. 222–227.
[33] Vohnout, B., Di Castelnuovo, A., Trotta, R., et al. (2003). Interleukin-1 gene cluster polymorphisms and risk of coronary artery disease. Haematologica, vol. 88, no.1, pp. 54–60.
[34] Liang, Z., Cai, J., Liu, G., et al. (2012). Associations between interleukin-1 gene polymorphisms and coronary heart disease risk: a meta-analysis. PLOS ONE, vol. 7, no. 9, p. e45641.
[35] Wang, S., Dai, Y. X., Chen, L. L., et al. (2015). Effect of IL-1β, IL-8, and IL-10 polymorphisms on the development of myocardial infarction. Genetic Molecular Research, vol. 14, no. 4, pp. 12016–12021.
[36] World Health Organization. (2009). Global Health Risks: Mortality and Burden of Disease Attributable to Selected Major Risks. Geneva: WHO.
[37] Allen, L., Cobiac, L., and Townsend, N. (2017). Quantifying the global distribution of premature mortality from non-communicable diseases. Journal of Public Health, vol. 39, no. 4, pp. 698–703.