Effects of statins on @entity1198 modulating cytokines in XXXX subjects.

@entity1 @entity2993 @entity1198 @entity8671 @entity1780 @entity8923 @entity731 @entity20300 @entity8673 @entity165
Background. Activation of the innate immune system by @entity165 accelerates @entity731 . High levels or modified forms of @entity165 stimulate release of the inflammatory cytokines IL-12 and @entity8923 that synergistically stimulate T lymphocytes to produce the atherogenic cytokine interferon-y. While activation of the innate immune system by @entity165 is well-described in animal models and @entity1 subjects with high @entity165 levels or known @entity731 , the interaction of @entity165 and lipoproteins with the innate immune system in @entity1 subjects without known @entity731 is less well-described. The goal of our study was to assess the @entity1198 modulating cytokines IL-12 p40 and @entity8923 , and their counter regulatory cytokines @entity8923 binding protein and @entity20300 , to determine if their levels are linked to @entity165 levels or other factors. Methods. We performed a blinded, randomized hypothesis-generating study in @entity1 subjects without known @entity731 . We measured serum lipids, lipoprotein levels, and collected plasma samples at baseline. Subjects were randomized to two weeks of therapy with @entity2993 , @entity8673 , or @entity8671 . Lipids and cytokine levels were measured after two weeks of statin treatment. Subjects were given a four-week statin-free period. At the end of the four-week statin-free period, venous blood was sampled again to determine if serum lipids returned to within 5% of their pre-statin levels. When lipid levels returned to baseline, subjects were again treated with the next statin in the randomization scheme. IL-12, @entity8923 , @entity8923 binding protein, and @entity20300 were measured at baseline and after each statin treatment to determine effects of @entity1780 treatment on their blood levels, and identify correlations with lipids and lipoproteins. Results. Therapy with statins revealed no significant change in the levels of IL-12, @entity8923 , @entity8923 binding protein or @entity20300 levels. We found that @entity8923 levels positively correlate with total @entity165 levels (r (2) = 0.15, p < 0.03), but not HDL or LDL @entity165 . In contrast, IL-12 p40 levels inversely correlated with total @entity165 (r (2) = -0.17, p < 0.008), HDL @entity165 (r (2) = -0.22, p < 0.002), and apolipoprotein A1 (r (2) = -0.21, p < 0.002). Similarly, @entity8923 binding protein levels inversely correlated with apolipoprotein A1 levels (r (2) = -0.13, p < 0.02). Conclusions. Our findings suggest that total @entity165 levels positively regulate @entity8923 , while HDL @entity165 and apolipoprotein A1 may reduce IL-12 p40 and @entity8923 binding protein levels. Additional studies in a larger @entity1 population are needed to confirm these findings, and verify mechanistically whether HDL @entity165 can directly suppress IL-12 p40 and @entity8923 binding protein levels in @entity1 subjects.
