RESULTS A significant association between IL-8 gene -251 A/T polymorphism and CAD risk was found in the dominant model (OR 1.42, 95% CI 1.16-1.76, P<0.001), recessive model (OR 1.30, 95% CI 1.12-1.52, P<0.001), allelic model (OR 1.28, 95% CI 1.12-1.47, P<0.001), homozygote model (OR 1.59, 95% CI 1.21-2.08, P<0.001), and heterozygote model (OR 1.35, 95% CI 1.11-1.64, P=0.002).
The aim of this study was to assess the effects of TMZ on interleukin-2 (IL-2) and interleukin-8 (IL-8) serum concentrations in 156 patients with stable coronary artery disease.
We conducted a case-control study to investigate the genetic variants Interleukin-1β(IL-1β) +3953 C/T (rs1143634), IL-6 -174G/C (rs1800795), IL-8-251T/A (rs4073), and IL-10 -1082A/G (rs1800896) and -819C/T (rs1800871) in the development of coronary artery disease (CAD).
Compared to controls, there were no associations between circulating levels of IL-8, lipocalin-2, nerve growth factor (NGF), RANTES, CD-163, GPX-3, monocyte chemotactic protein-1 (MCP-1)/CCL2, leptin, soluble vascular endothelial growth factor receptor-1 (sFLT1), fatty acid binding protein-4 (FABP-4), and plasminogen activator inhibitor-1 (PAI-1) and increases in their gene expression in EAT adjacent to CAD.
We also detected higher levels of CCL2 and CXCL8 in supernatants of oxLDL-stimulated PBMCs from CAD patients than in corresponding supernatants from controls.
Our main findings were: (i) patients with stable (n = 40) and unstable (n = 40) angina had elevated plasma levels of CXCL16 compared with controls (n = 20); (ii) low-dose simvastatin (20 mg qd, n = 15) and high-dose atorvastatin (80 mg qd, n = 9) down-regulated plasma levels of CXCL16 during 6 months of therapy; (iii) in vitro, atorvastatin significantly decreased the interleukin (IL)-1beta-mediated release of CXCL16 from PBMC and endothelial cells; (iv) attenuating effect of atorvastatin on the IL-1beta-mediated release of CXCL16 in PBMC seems to involve post-transcriptional modulation as well as down-regulation of CXCL16 release through inhibition of the protease a disintegrin and metalloproteinase 10 (ADAM10); (v) soluble CXCL16 increased the release of IL-8, monocyte chemoattractant peptide 1, and matrix metalloproteinases in vascular SMC and increased the release of IL-8 and monocyte chemoattractant peptide 1 in PBMC, with particularly enhancing effects in cells from CAD patients.
We investigated the potential influence of two common polymorphisms of the interleukin-8 gene, -251A/T, and 781C/T on susceptibility to coronary artery disease.
We investigated the potential influence of two common polymorphisms of the interleukin-8 gene, -251A/T, and 781C/T on susceptibility to coronary artery disease.