Abstract
AimThe role of interleukin 17A (IL-17A) in the inflammatory process has caused interest in the potential significance of IL-17A as a biomarker for coronary artery disease (CAD). The aim of the present study was to evaluate the role of IL-17A gene polymorphisms as susceptibility markers for CAD in the Mexican population.MethodsFour IL-17A gene polymorphisms (rs8193036, rs3819024, rs2275913 and rs8193037) were genotyped by 5’ exonuclease TaqMan assays in a group of 900 patients with premature CAD and 667 healthy controls (with negative calcium score by computed tomography), seeking associations with CAD and other metabolic and cardiovascular risk factors using logistic regression analyses.ResultsNo single IL-17A polymorphism was associated with premature CAD, however two haplotypes (CAGG and TAGA) were significantly associated with increased risk of premature CAD (OR = 1.35, 95% CI: 1.00–1.84, P = 0.018 and OR = 2.09, 95% CI: 1.16–3.76, P = 0.003, respectively). Moreover, rs3819024 was associated with increased levels of visceral abdominal fat (P = 0.002) and rs8193036 was significantly associated with risk of central obesity (P = 0.020), hypertriglyceridemia (P = 0.027), and metabolic syndrome (P = 0.027) in the premature CAD group, under dominant models adjusted by age, gender, BMI, smoking history, alcohol consumption, and treatment.ConclusionThe results suggest that IL-17A haplotypes are involved in the risk of developing premature CAD and some IL-17A polymorphisms are associated with cardiovascular risk factors in Mexican individuals with premature CAD.
Highlights
Coronary artery disease (CAD) is a complex multifactorial and polygenic disorder resulting from an excessive inflammatory response to various forms of injurious stimuli to the arterial wall [1,2,3]
No single IL-17A polymorphism was associated with premature coronary artery disease (CAD), two haplotypes (CAGG and TAGA) were significantly associated with increased risk of premature CAD (OR = 1.35, 95% CI: 1.00–1.84, P = 0.018 and OR = 2.09, 95% CI: 1.16–3.76, P = 0.003, respectively)
The results suggest that IL-17A haplotypes are involved in the risk of developing premature CAD and some IL-17A polymorphisms are associated with cardiovascular risk factors in Mexican individuals with premature CAD
Summary
Coronary artery disease (CAD) is a complex multifactorial and polygenic disorder resulting from an excessive inflammatory response to various forms of injurious stimuli to the arterial wall [1,2,3]. Interleukin-17A (IL-17A) is the most widely studied member of the IL-17 cytokine family. It is mainly produced by T-helper (Th)-17 lymphocytes, but is secreted by natural killer T (NKT) cells, γδ T cells (γδ-17), cytotoxic CD8+ T cells (Tc17), and neutrophils [5,6,7]. IL-17A plays a proatherogenic inflammatory role during atherogenesis by promoting monocyte/macrophage recruitment into the aortic wall in the mouse model [12], while the administration of IL-17A neutralizing antibodies to apolipoprotein E (ApoE−/−) knockout mice markedly reduced early atherosclerotic lesion area and vulnerability [13]. Other studies have reported the proatherogenic effect of IL-17A [16,17] These findings have suggested that IL-17A might play a role in the development of cardiovascular diseases
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