Increased proliferation, however, does not necessarily means a positive response because even cells from tolerant mice are able to respond vigorously to mitogen stimulus [38].

The LPS of gram-negative bacteria is a potent stimulator of macrophages. Binding of LPS to toll-like receptor 4 in the cell surface triggers various inflammatory events such as the synthesis of inducible NO synthase and the production of both proinflammatory and anti-inflammatory cytokines. It is well find more known that IFN-γ acts synergistically with LPS in triggering these events in adaptive immune response. Our results show that peritoneal macrophages from mice of all experimental groups were similarly responsive selleck chemical to LPS + IFN-γ, producing comparable levels of nitrite, TNF-α, and IL-10 in culture supernatants. However, peritoneal macrophages from mice fed FOS released significant lower levels of IL-1β, thus indicating that yacon consumption may induce an anti-inflammatory state in macrophages, because IL-1β production is one of the first intracelular events after macrophage stimulation

[39]. Several studies convey the importance of healthy microbiota in maintaining the intestinal tract’s physiological and immunologic functions, including inducing tolerance to exogenous antigens such as those present in the diet [40]. The immune response against pathogens is characterized by the recognition of molecular patterns combined with strong innate responses, followed by an adaptive response to eliminate the offending agent, which often results in damage to the host’s tissues. The response toward components of the symbiotic microbiota, however, is characterized by a complex integrated system of microbial recognition and inhibition of immune effector activation [36]. This process involves both the maintenance of a significant number of macrophages and dendritic cells

in a state of immaturity and an appropriate balance between regulatory T lymphocytes and “inflammatory” T-lymphocyte subsets such as Th1 and Th17 [41]. It is possible that yacon FOS binds directly Low-density-lipoprotein receptor kinase to dendritic cells present in the intestinal mucosa and modulate its activity to a tolerogenic profile. Although literature data indicate this possibility [42], we have no evidence yet to confirm these data. Despite that yacon is being used in folk medicine for long time, well-designed clinical studies testing the effects of regular yacon consumption in humans are still necessary. In conclusion, the results support our hypothesis that regular consumption of yacon improves the balance of the peripheral immune system in the mouse. This conclusion is based on the increased levels of intestinal IgA in mice and a reduced production of the inflammatory cytokine IL-1β in peritoneal macrophages.

The mean RSS for the five-parameter fitted curve was < 0.001 (n = 26) which was significantly better than our acceptability criterion of RSS = 0.01 ( Fig. 2B). The error for the back-calculated values of the standards was within 30%, except for the lowest concentration (0.006 μg/mL). The CV was < 10% for concentrations above 0.011 μg/mL and the dynamic range of the assay was two orders of magnitude. To establish the LOB, blank samples were tested (negative control, 0 μg/mL) along with the standard CHIR-99021 nmr curve. The mean proportion value of the shifted area (immune complexes) over the total area

determined from the blanks was 0.011 ± 0.003 (n = 60). The LOB was thus calculated to be 0.015 (mean + 1.645 × SD) and the extrapolated PARP inhibitor ATI concentration from the standard curve was 0.006 μg/mL ( Table 1). To determine the LOD, the extrapolated value of the lowest standard concentration (0.006 μg/mL) was obtained as 0.014 ± 0.003 μg/mL (n = 26). The LOD was calculated from the LOB and the SD from the lowest concentration in the standard curve with < 30% error: LOD = LOB + 1.645 × SD(low concentration sample) which was 0.012 μg/mL. The LLOQ for

the ATI-HMSA assay was 0.011 μg/mL, which was determined by the interpolated concentrations of replicates of the low ATI concentration with CV < 30%. The ULOQ for the ATI-HMSA assay was 0.54 μg/mL, which was similarly determined by the interpolated concentrations of replicates of the high ATI concentration with CV < 20%. The effective serum concentrations corresponding to the LLOQ and the ULOQ for the ATI-HMSA were determined by multiplying

the concentration with the dilution factor (50), which corresponded to 0.56 μg/mL and 27 μg/mL, respectively. The performance characteristics of the IFX-HMSA standard curve in the concentration range of 0.03–3.75 μg/mL were similarly assessed over 38 experiments by multiple analysts using different instruments on different days (Table 2). The same methods were used to determine the LOB, LOD, stiripentol LLOQ, and ULOQ as described for the ATI-HMSA. The LOB, LOD, LLOQ, and ULOQ for the IFX-HMSA were 0.0027, 0.0074, 0.039, and 1.36 μg/mL, respectively. The effective IFX serum concentration for the LLOQ and ULOQ were 0.98 and 34 μg/mL (dilution factor = 25). To assess the precision and accuracy of the ATI-HMSA and the IFX-HMSA, two methods were used. First, we used the high, mid, and low QC samples in both assays to determine their recovery rate. As shown in Table 3, the ATI-HMSA intra-assay precision had a CV < 4% and the accuracy rate was < 12% error. The intra-assay precision and accuracy for the IFX-HMSA were < 6% and < 10% error, respectively (Table 4). Second, we tested the high, mid, and low control samples over different runs and instruments and by multiple analysts.