کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2894844 | 1172443 | 2007 | 6 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Association between TNF and IL-1 bloc polymorphisms and plasma MCP-1 concentration Association between TNF and IL-1 bloc polymorphisms and plasma MCP-1 concentration](/preview/png/2894844.png)
BackgroundCirculating MCP-1 concentration was found to be increased in cardiovascular diseases and is of high interest in the list of biomarkers of atherosclerosis. TNF-α, LT-α, IL-1α and IL-1β are four proinflammatory cytokines that regulate MCP-1 concentration in vitro. We hypothesized that specific genetic polymorphisms in TNF, LTA, IL-1A and IL-1B genes could modulate plasma MCP-1 concentration.MethodsPlasma MCP-1 concentration was quantified with a biochip array analyzer in 395 adults from the Stanislas family study. TNF −308G > A, LTA 252A > G (A = TNFB2, G = TNFB1), IL-1A −889C > T and IL-1B 3954C > T were genotyped with a prototypic multilocus genotyping assay.ResultsAmong the four polymorphisms studied only LTA 252A > G and TNF −308G > A were significantly associated with plasma MCP-1 concentration (p = 0.005 and p = 0.038, respectively) after adjustment for covariates (age, sex, smoking, monocyte count and hematocrit). Carriers of the 252A allele or the −308G had lower MCP-1 concentrations than carriers of the 252G or the −308A alleles, respectively. Moreover, as TNF and LTA genes were in linkage disequilibrium, the TNF bloc haplotypes were compared with respect to MCP-1 concentration, and a significant association (p = 0.021) was observed, due only to the LTA polymorphism. This association remained significant even after adjustment for TNF-α and hs-CRP concentrations.ConclusionA functional polymorphism within the TNF bloc could modulate MCP-1 concentration and seems more likely to be near to the LTA 252A > G polymorphism than to the TNF −308G > A one. In addition, the association found in healthy French adults is independent of other actors of inflammation such as TNF-α and hs-CRP.
Journal: Atherosclerosis - Volume 192, Issue 2, June 2007, Pages 348–353