Effects of High-Forage Diets Containing Raw Flaxseeds or Soybean on In Vitro Ruminal Fermentation, Gas Emission, and Microbial Profile.

Lipid metabolism plays an important role in the energy economy of ruminants. However, its interactions of fat, rumen fermentation, gas emission, and microorganisms are not yet clear. This study evaluated the effect of adding raw oilseeds to high-forage diets on in vitro ruminal fermentation, gas composition, and microbial profile. Three isoenergetic and isoproteic experimental diets were designed and used as fermentation substrate: control treatment (CON group) was the basal diet lacking oilseeds, the other two treatments were the basal diet supplemented by 100 g/kg dry matter (DM) raw whole soybean (S group) and 50 g/kg DM raw flaxseed (F group), respectively. Data showed that the acetate, butyrate, and total VFA concentration of culture fluids in the S group were lower (p < 0.05) than in the F group. There was a tendency to a higher level (p = 0.094) of propionate concentration in the F group compared with the other two groups. The gas production in the F group was higher (p < 0.05) than in the control group. There was a lower abundance of Sutterella (p < 0.05) and a greater abundance of Butyrivibrio (p < 0.05) in both of the two oilseed treatments. Methanobrevibacter (p = 0.078) in the F group was the lowest. Our results suggested that CH4 emission could be inhibited with flaxseed supplementation by propionate production metabolism, biohydrogenation of unsaturated fatty acid (FA), and toxicity to Methanobrevibacter, while regarding soybean seed supplementation, the emission of CH4 was more likely to be reduced through biohydrogenation of unsaturated FA modulated by Butyrivibrio.

Expression profile of PU.1 in CD4+T cells from patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with complex genetic predisposing factors involved. PU.1 is an important member of the ETS transcription factors family which has diverse functions such as regulating the proliferation, differentiation of immune cells and multiple inflammatory cytokines. Previous studies preliminary explored the relation between PU.1 and SLE. To further explain the potential role of PU.1 in the pathogenesis of SLE, 40 SLE patients and 20 age-sex matched healthy controls (HC) were recruited in this study. Flow cytometry was used to test the percentages of CD4+PU.1+T cells in peripheral blood mononuclear cells (PBMCs) from patients with SLE and HC. Expression levels of PU.1 mRNA in CD4+T cells from SLE patients and HC were analyzed by real-time transcription-polymerase chain reaction. Expression levels of plasma IL-1ß, IL-9, IL-18, IL-6, IFN-α, TNF-α, IL-10 and TGF-ß1 were measured by enzyme-linked immunosorbent assay. The percentage of CD4+PU.1+T cells in PBMCs from patients with SLE was significantly higher than that from HC (P < 0.001). In addition, the PU.1 mRNA expression in CD4+T cells from SLE patients was increased than that from HC (P = 0.002). In SLE patients, no significant correlation was found between the percentage of CD4+PU.1+T cells and the expression of PU.1 mRNA in CD4+T cells (P > 0.05). Associations of PU.1 mRNA expression in CD4+T cells with major clinical and laboratory parameters of SLE patients were also analyzed, but no significant correlations were found. Consistent with previous studies, SLE patients had increased IL-1ß, IL-18, IL-6, IFN-α, TNF-α and IL-10 plasma concentrations than HC (P < 0.01). The expression level of plasma TGF-ß1 was significantly decreased in SLE patients than in HC (P < 0.001). In SLE patients, the expression level of IL-1ß was positive correlated with PU.1 mRNA expression in CD4+T cells (P = 0.001). Our study first time evaluated the expression profile of PU.1 in CD4+T cells from SLE patients confirming that PU.1 may participate in the pathogenesis of SLE.

Negative Correlation Between miR-326 and Ets-1 in Regulatory T Cells from new-Onset SLE Patients.

To analyze the relationship between miR-326 and Ets-1 mRNA levels in Treg cells and clinical manifestations in patients with SLE and explore the role of miR-326 and Ets-1 in the pathogenesis and activity of SLE. Twenty-five new-onset SLE patients without treatment, twenty-eight inactive SLE patients (SLEDA ≤ 4) and twenty-two healthy controls were included in the present study. Clinical data of SLE patients were recorded. Treg cells were purified by MACS from 20 ml peripheral blood, in which the quantity of miR-326 and Ets-1 mRNA were assessed by real-time PCR. Data were analyzed using SPSS Version 17.0. The nonparametric Mann-Whitney U test was used to compare the groups, The Spearman test was used for correlation analyses. Two-tailed p values <0.05 were considered statistically significant. 1.The level of miR-326 was significantly higher in Treg cells from SLE patients [1.98(0.592,6.148)] than that in healthy controls [0.921(0.345, 1.879)] (p = 0.032). The difference between new-onset SLE patients [6.192(0.673, 15.298)] and healthy controls was significant (p = 0.019). Significant difference of the miR-326 expression was found between new-onset SLE patients with serous cavity effusion and new-onset SLE patients without it(P<0.05). Significant positive correlation was found between the expression of miR-326 mRNA in Treg cells with CRP and anti-C1q antibody from new-onset SLE patients. 2. The level of Ets-1 mRNA was decreased in SLE patients [0.382(0.232, 0.572)] compared to healthy controls(p = 0.013). The difference was also found in new-onset SLE patients [0.222(0.125, 0.296)] while compared to healthy controls. Also, the level in new-onset SLE patients was lower than that in inactive SLE patients [0.482(0.398, 0.512)] (p = 0.001). 3. Negative correlation was found between miR-326 and Ets-1 mRNA expression in Treg cells from new-onset SLE patients (r = -0.583 p = 0.01). 4. There was no correlation of miR-326 or Ets-1 mRNA expression with SLEDAI. The increase of miR-326 expression in Treg cells from SLE patients may inhibit the expression of Ets-1 to participate in the pathological process of SLE.