918). In the group CP-673451 datasheet with high expressors, the cytokine answer decreases after glutamine supplementation on average by 17% (Table 2). The IL-2 release in

whole blood samples after stimulation with PMA and ionomycin in relation to the IL-2 genotypes with and without glutamine supplementation is shown in Table 3. The T/T genotype was detected in 47% of the probands, the G/T genotype in 46% and the G/G genotype in 7% of the cases (Table 6). Glutamine supplementation increased IL-2 release in the first tertile of low cytokine expressors. The increase in IL-2 release could not be attributed to a clear distribution of genotypes in this expressor group. A similar situation is also found in the statistics of the medium expressors in the second tertile. The addition of glutamine increased the cytokine release compared to the IL-2 release without glutamine supplementation but it appears that also in this tertile the genotype does not increase the sensitivity of the cytokine release to glutamine. When analysing of the third tertile with high expressors, the glutamine supplementation decreases the release of cytokines, and the genotype does not affect the release of IL-2 either with or without glutamine supplementation. In summary, one can say that there is no significant interaction of the genotype

to the IL-2 release. In addition to this, there is no significant relationship JQ1 order between the interaction of IL-2 genotypes and the IL-2 release under the influence of glutamine in our collective (n = 91). A stimulating effect of glutamine on the IL-2 release in the first and second tertile of low and medium expressors was HSP90 independent of the genotype identified. The TNF-α release in dependence of glutamine supplementation is shown in Table 4. Depending on the level of low, medium and high cytokine release, the TNF-α release was also divided into tertiles with low, medium and high cytokine expressors. The analysis of the tertiles shows that the TNF-α release is increased by a glutamine supplementation in the first

tertile (low expressors) by 23% and decreases in the second and third tertile (medium and high expressors) by 9% and 11% (Table 4). The variations of the TNF-α release are very large in all tertiles, so no clear correlation between the amount of glutamine concentration and the levels of a TNF-α cytokine release can be determined. The glutamine supplementation effects on the entire subject panel (n = 87), a reduction in TNF-α release of 6%. No effect of glutamine on the TNF-α release can be shown. The TNF-α release in whole blood after stimulation with PMA and ionomycin in relation to the TNF-α genotypes with and without glutamine supplementation is shown in Table 5. In 66% of the cases in our collective, the G/G genotype was found. The G/A genotype was detected in 28% and the A/A genotype in 6% of the cases (Table 6).