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CD14 C(-260)T gene polymorphism, circulating soluble CD14 levels and arteriosclerosis
Jacques Amar1, Jean-Bernard Ruidavets, Claire Bal dit Sollier
1Service de Médecine Interne et d'Hypertension Artérielle, CHU Toulouse, France.
Journal of Hypertension
|July 17, 2004
Summary
The CD14 C260T gene polymorphism is linked to soluble CD14 (sCD14) levels but not early atherosclerosis markers. Smoking status modifies this association, suggesting a potential impact on vascular events.
Area of Science:
- Cardiovascular Science
- Genetics
- Immunology
Background:
- The CD14 pathway links infection and inflammation.
- Previous studies show conflicting results on CD14 C260T polymorphism, soluble CD14 (sCD14) levels, and atherosclerosis.
- Investigating these relationships in a population-based sample is crucial.
Purpose of the Study:
- To examine the association between CD14 C260T gene polymorphism, sCD14 blood levels, and arterial wall status.
- To determine if CD14 C260T polymorphism correlates with early atherosclerosis markers like intima-media thickness and plaque presence.
Main Methods:
- Analysis of 899 subjects from the Toulouse MONICA center with complete data.
- Measurement of sCD14 levels using an immuno-enzymatic method.
- Assessment of carotid intima-media thickness (IMT) and arterial plaques via ultrasonography, alongside genotypic analysis for CD14 C260T polymorphism.
Main Results:
- Subjects with the 't' allele showed increased sCD14 expression (P < 0.01).
- No significant association was found between the CD14 C260T polymorphism and IMT, plaque presence, or pulse wave velocity.
- A significant interaction (P < 0.05) between the C260T polymorphism and smoking was observed, where the 't' allele did not affect sCD14 levels in current smokers.
Conclusions:
- The CD14 C260T polymorphism is associated with sCD14 expression but not with early atherosclerosis markers in this population.
- This polymorphism influences plasma sCD14 levels, with an interaction observed concerning current smoking status.
- Further research is warranted to elucidate the role of this interaction in smoking-related vascular events.