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 our study, association of interleukin-10 (IL-10) and CD14 polymorphisms and environmental factors with the risk of myocardial infarction was studied.
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 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.
The aim of the study was to assess whether these IL-10 and TNF gene polymorphisms are related to the risk of coronary artery disease (CAD) and myocardial infarction (MI).
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.
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 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).
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 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.
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.
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.
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.