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IL-8 -251A/T polymorphism contributes to coronary artery disease susceptibility in a Chinese population

Interleukin-8 (IL-8) is a mediator of inflammation and plays an important role in regulating immune responses. To date, several studies have tested the association between IL-8 gene polymorphisms and development of coronary artery disease (CAD), but their results have proved to be inconsistent. We c...

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Bibliographic Details
Published in:Genetics and molecular research 2017-02, Vol.16 (1)
Main Authors: Zhang, R J, Li, X D, Zhang, S W, Li, X H, Wu, L
Format: Article
Language:English
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Summary:Interleukin-8 (IL-8) is a mediator of inflammation and plays an important role in regulating immune responses. To date, several studies have tested the association between IL-8 gene polymorphisms and development of coronary artery disease (CAD), but their results have proved to be inconsistent. We conducted an investigation to assess the relationship between the IL-8 -251A/T (rs4073) sequence variant and CAD in a Chinese population. Between April 2013 and January 2015, 217 patients with coronary angiography-confirmed CAD were enrolled in our study, along with 245 control subjects. IL-8 -251A/T genotyping was performed using a polymerase chain reaction-restriction fragment length polymorphism assay. A chi-square test revealed that IL-8 -251A/T genotype distributions significantly differed between CAD patients and control subjects (chi-square = 8.29, P < 0.02). Moreover, multiple-logistic regression analysis showed that individuals carrying TA [odds ratio (OR) = 1.59, 95% confidence interval (CI) = 1.01-2.57] and AA (OR = 2.06, 95%CI = 1.21-3.52) genotypes were at increased risk of CAD compared to those with the TT genotype. Under dominant (OR = 1.75, 95%CI = 1.13-2.73) and recessive (OR = 1.54, 95%CI = 1.02-2.37) genetic models, the IL-8 -251A/T polymorphism also significantly correlated with CAD. In conclusion, our results suggest that this variant is an independent risk factor for CAD development under codominant, dominant, and recessive models.
ISSN:1676-5680
1676-5680
DOI:10.4238/gmr16018224