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Published on: November 14, 2017
CD14 C260T promoter polymorphism and the risk of cerebrovascular diseases: a meta-analysis
1Institute of Biochemistry, Swiss Federal Institute of Technology (ETH), Zurich, Switzerland. indranil@bc.biol.ethz.ch
Insights
This meta-analysis found no significant link between the CD14 C260T gene variant and cerebrovascular disease (CVD) risk. Further research in diverse populations is needed to confirm these findings on CVD susceptibility.
Area of Science:
- Genetics
- Neuroscience
- Cardiovascular Science
Background:
- Cerebrovascular diseases (CVD) stem from blood vessel issues in the brain, with atherosclerosis and inflammation being key contributors.
- Monocyte/macrophage activation, potentially mediated by lipopolysaccharide (LPS) via CD14, is an inflammatory pathway in atherogenesis.
- The CD14 C260T single-nucleotide polymorphism (SNP) has been investigated for its potential role in CVD.
Purpose of the Study:
- To conduct a comprehensive meta-analysis of genetic association studies.
- To evaluate the role of the CD14 C260T polymorphism in cerebrovascular disease (CVD) risk.
Main Methods:
- Systematic literature search for case-control studies on CD14 C260T and CVD.
- Inclusion of 7 studies with 1488 patients and 1600 controls.
- Calculation of odds ratios (ORs) using fixed and random effects models for alleles, genotypes, and genetic models.
Main Results:
- No significant association was found between the CD14 C260T polymorphism (T allele) and CVD risk.
- Odds ratios (ORs) for the T allele were 0.99 (95% CI [0.89, 1.09]) and 0.99 (95% CI [0.88, 1.11]) under fixed and random effects models, respectively.
- Similar non-significant results were observed for homozygotes and dominant/recessive models.
Conclusions:
- The CD14 C260T polymorphism does not appear to be a significant risk factor for cerebrovascular diseases.
- Further investigation in ethnically diverse populations is recommended to reliably assess the role of this SNP in CVD susceptibility.
Abstract:
Cerebrovascular diseases (CVD) are dysfunctions of the brain, resulting from diseases of blood vessels supplying the brain. Atherosclerosis is one of the major underlying causes of CVD, in which inflammation plays a crucial role. One of the inflammatory mechanisms contributing to atherogenesis is the activation of monocytes and macrophages, which could be mediated by the bacterial endotoxin lipopolysaccharide (LPS) via its receptor CD14. The C260T (rs2569190) single-nucleotide polymorphism (SNP) in the promoter region of the CD14 gene was implicated in CVD. To assess the role of this SNP in CVD, a comprehensive meta-analysis of the available genetic data was conducted. All the case-control association studies evaluating the role of CD14 C260T in CVD were identified. Of these, 7 studies (comprising a total of 1488 patients and 1600 control subjects) were included in this meta-analysis. To measure the strength of genetic association for the gene variant, the odds ratios (ORs) were calculated using both fixed and random effects for comparisons of the alleles, the genotypes, and the dominant and recessive genotype models. The results showed there was no significant association between the T allele of C260T and the risk of CVD under the fixed effects model, OR = 0.99 (95% CI (0.89, 1.09)), P = 0.84; or the random effects model, OR = 0.99 (95% CI (0.88, 1.11)), P = 0.83. Similar results were obtained for the homozygotes and the dominant and recessive models. In conclusion, the results of this meta-analysis suggest the CD14 C260T polymorphism is not a risk factor for CVD. However, more studies in ethnically varied populations are needed to evaluate in a reliable manner the role of this SNP in CVD susceptibility.
