Polymorphisms of −174G>C and −572G>C in the Interleukin 6 (IL-6) Gene and Coronary Heart Disease Risk: A Meta-Analysis of 27 Research Studies

OBJECTIVE: Elevated serum IL-6 level is a risk factor for coronary heart disease (CHD). The -174 G>C and -572 G>C polymorphisms in the IL-6 gene have previously been shown to modulate IL-6 levels. But the association between the -174 G>C and -572 G>C polymorphisms and the risk of CHD is still unclear. A meta-analysis of all eligible studies was carried out to clarify the role of IL-6 gene polymorphisms in CHD. METHODS AND RESULTS: PubMed, EMBASE, Vip, CNKI and CBM-disc were searched for eligible articles in English and Chinese that were published before October 2010. 27 studies involving 11580 patients with CHD and 17103 controls were included. A meta-analysis was performed for the included articles using the RevMan 5.0 and Stata 10.0 softwares. Overall, the -174 C allele was not significantly associated with CHD risk (ORs = 1.04, 95%CI = 0.98 to 1.10) when compared with the -174 G allele in the additive model, and meta-analysis under other genetic models (dominant, recessive, CC versus GG, and GC versus GG) also did not reveal any significant association. On the contrary, the -572 C allele was associated with a decreased risk of CHD when compared with the -572 G allele (ORs = 0.79, 95%CI = 0.68 to 0.93). Furthermore, analyses under the recessive model (ORs = 0.69, 95% = 0.59 to 0.80) and the allele contrast model (genotype of CC versus GG, ORs = 0.49, 95% = 0.35 to 0.70) yielded similar results. However, statistical significance was not found when the meta-analysis was restricted to studies focusing on European populations, studies with large sample size, and cohort studies by using subgroup analysis. CONCLUSIONS: The -174 G>C polymorphism in the IL-6 gene is not significantly associated with increased risks of CHD. However, The -572 G>C polymorphism may contribute to CHD development. Future investigations with better study design and large number of subjects are needed

Association between COX-2 rs 6681231 Genotype and Interleukin-6 in Periodontal Connective Tissue. A Pilot Study

This study was partially undertaken at the UCL Eastman Dental Institute, which received a proportion of funding from the Department of Health’s National Institute of Health Research (NIHR) Biomedical Research Centres funding scheme

Genetic variation and exercise-induced muscle damage: implications for athletic performance, injury and ageing.

Prolonged unaccustomed exercise involving muscle lengthening (eccentric) actions can result in ultrastructural muscle disruption, impaired excitation-contraction coupling, inflammation and muscle protein degradation. This process is associated with delayed onset muscle soreness and is referred to as exercise-induced muscle damage. Although a certain amount of muscle damage may be necessary for adaptation to occur, excessive damage or inadequate recovery from exercise-induced muscle damage can increase injury risk, particularly in older individuals, who experience more damage and require longer to recover from muscle damaging exercise than younger adults. Furthermore, it is apparent that inter-individual variation exists in the response to exercise-induced muscle damage, and there is evidence that genetic variability may play a key role. Although this area of research is in its infancy, certain gene variations, or polymorphisms have been associated with exercise-induced muscle damage (i.e. individuals with certain genotypes experience greater muscle damage, and require longer recovery, following strenuous exercise). These polymorphisms include ACTN3 (R577X, rs1815739), TNF (-308 G>A, rs1800629), IL6 (-174 G>C, rs1800795), and IGF2 (ApaI, 17200 G>A, rs680). Knowing how someone is likely to respond to a particular type of exercise could help coaches/practitioners individualise the exercise training of their athletes/patients, thus maximising recovery and adaptation, while reducing overload-associated injury risk. The purpose of this review is to provide a critical analysis of the literature concerning gene polymorphisms associated with exercise-induced muscle damage, both in young and older individuals, and to highlight the potential mechanisms underpinning these associations, thus providing a better understanding of exercise-induced muscle damage

Prognostic value of plasma interleukin-6 concentrations and the -174 G > C and -572 G > C promoter polymorphisms of the interleukin-6 gene in patients with acute myocardial infarction treated with thrombolysis.

The present study was performed to investigate the prognostic value of plasma interleukin-6 (IL-6) concentrations and promoter polymorphisms of the IL-6 gene in patients with acute myocardial infarction treated with thrombolysis. Two hundred and eight patients with myocardial infarction treated with thrombolysis were included and followed for 2-5 years. Plasma concentrations of IL-6 were measured at admission and 48 h after admission. Genotyping for the -174 G > C and -572 G > C IL-6 polymorphisms was performed. Patients who died of cardiovascular causes or suffered a new myocardial infarction during follow-up had increased plasma concentrations of IL-6 at admission (P < 0.002) and at 48 h after admission (P < 0.05) compared with patients who had an uneventful course. IL-6 levels above the median at admission were independently associated with a worse prognosis. No associations were found between IL-6 levels and the promoter polymorphisms. The -174 G > C polymorphism was not associated with cardiovascular death or a new myocardial infarction, whereas the -572 G > C polymorphism showed a borderline significant increase in risk (P = 0.05) in univariate analysis. In conclusion, the early IL-6 response during myocardial infarction is associated with prognosis in patients with Q-wave myocardial infarction, whereas no associations were found between IL-6 genotype and phenotype

Identification and Predictive Value of IL6(+)IL10(+)Cytokine Patterns in ST-Elevation AcuteMyocardial Infarction

none19siE. Ammirati; C.V. Cannistraci; N.A.Cristell; V. Vecchio; A.G. Palini; P. Tornvall; A.M. Paganoni; E.A. Miendlarzewska; L.M. Sangalli; A. Monello; J. Pernow; M. Björnstedt Bennermo; G. Marenzi; D. Hu; N.G. Uren; T. Ravasi; D. Cianflone; A.A. Manfredi; A. Maseri;E., Ammirati; C. V., Cannistraci; N. A., Cristell; V., Vecchio; A. G., Palini; P., Tornvall; Paganoni, ANNA MARIA; E. A., Miendlarzewska; Sangalli, LAURA MARIA; A., Monello; J., Pernow; M., Björnstedt Bennermo; G., Marenzi; D., Hu; N. G., Uren; T., Ravasi; D., Cianflone; A. A., Manfredi; A., Maser