IL-10 and other pro-inflammatory interleukins were analyzed in 90 subjects divided into 3 groups: group 1 (n = 30), patients with MetS without severe CAD; group 2 (n = 30), patients with MetS and severe CAD (history of myocardial infarction or revascularization performed through surgery or percutaneous transluminal coronary angioplasty with or without stent placement); and group 3 (n = 30), healthy individuals.
Compared with control group, the levels of heart rate, left ventricular end-diastolic pressure, TNF-α, and IL-6 were increased in each group of rats with MI (all p < 0.05), while the levels of systolic blood pressure, diastolic blood pressure, mean arterial pressure, left ventricular systolic pressure, and IL-10 were significantly decreased (all p < 0.05).
Although both interleukin (IL)-4 and IL-10 were reported to promote CD206<sup>+</sup> macrophage-mediated cardiac repair after MI, IL-10- but not IL-4-stimulated CD11b<sup>+</sup>Ly6G<sup>-</sup> cells could differentiate into OPN-producing galectin-3<sup>hi</sup>CD206<sup>+</sup> macrophages and showed enhanced phagocytic ability.
Consistently, the implantation of Ad.IL10-MSCs into MI animals resulted in more reductions in myocardial infarct size, cardiac impairment, and cell apoptosis, compared to the individual treatments of either MSC or IL10 administration.
We found that synovial fluid levels of VEGF and IL-6 were significantly higher in patients with OA than in patients with MI, and IL-10 was lower in patients with OA compared to MI patients (p<0.05).
GoM allowed to identify a population of subjects negative forIL-10 -824T allele, 74.4% of which were diabetic patients characterised by vascular damages (Chronic kidney failure and/or Myocardial Infarction), reduction of haematocrit, increase of blood urea nitrogen, creatinin and monocyte levels.
In patients, IL-10 predicted a crude risk increase of death/MI, with the highest risk observed in the fourth quartile (adjusted odds ratio 1.7 (95% confidence interval 1.2 to 2.3)).
We investigated variation in inflammation-related genes - interleukin (IL)-1beta, IL-6, C-reactive protein (CRP), IL-10, IL-18, and the tumor necrosis factor (TNF) superfamily [lymphotoxin(LT)-alpha, TNF-alpha, LT-beta] - with respect to nonfatal incident myocardial infarction (MI) or ischemic stroke risk.
In addition, a predominance of the -1082ACC/ATA IL-10 genotype in the myocardial infarction group compared with the unstable angina group and the -874 A/A IFN-gamma genotype in the stable angina group compared with the unstable angina and the myocardial infarction group, was found.
In our study, association of interleukin-10 (IL-10) and CD14 polymorphisms and environmental factors with the risk of myocardial infarction was studied.
In patients with ST-se AMI, the serum IL-10 level is a major independent predictor of 30-day mortality and should be used for early risk stratification following acute myocardial infarction.
In this paper we review the evidence for a possible role of genetic polymorphisms of the most important inflammatory cytokines (IL-6, TNF-alpha, IL-10) and immune receptors (CD14 receptor and TLR-4) in modulating the incidence or the prognosis of MI, with a special focus in ageing population.
Opposite effects of interleukin 10 common gene polymorphisms in cardiovascular diseases and in successful ageing: genetic background of male centenarians is protective against coronary heart disease.
We investigated the possibility that single nucleotide polymorphisms of the genes encoding TNF-alpha (-863C/A, -308G/A), LT-alpha (252G/A), and IL-10 (-1082G/A, -819C/T, and -592C/A) are associated with the incidence of restenosis, death, or myocardial infarction (MI) after coronary stenting.