Surface co-stimulatory molecule expression was analyzed by gating on CD11c cell populations by FACS

A, representative histograms showing the percentage of co-stimulatory molecules expression by CD11c+ cells. Solid lines, specific staining; shaded histograms, appropriate isotype controls. B, Average Mean Fluorescent Intensity (MFI) of co-stimulatory markers. Data are representative of three independent experiments.<p><b>Copyright information:</b></p><p>Taken from "CD11c+ antigen presenting cells from the alveolar space, lung parenchyma and spleen differ in their phenotype and capabilities to activate naïve and antigen-primed T cells"</p><p>http://www.biomedcentral.com/1471-2172/9/48</p><p>BMC Immunology 2008;9():48-48.</p><p>Published online 13 Aug 2008</p><p>PMCID:PMC2527294.</p><p></p

ER stress modulates the immune regulatory ability in gut M2 cells of patients with ulcerative colitis

Summary: This study aims to characterize the impaired immune regulatory function of Mφ obtained from UC patient colon lavage fluid (CLF). Mφs were the largest proportion (21.3 4.0%) of the CLF-derived cellular components. Less abundant and weaker immune suppressive function were observed in M2 Mφs (M2 cells) of the ulcerative colitis (UC) group. High levels of endoplasmic reticulum (ER) stress associated molecules were detected in UC M2 cells. The spliced X box binding protein-1 (XBP1) gene was negatively correlated with programmed death ligand-1 (PD-L1) in UC M2 cells. XBP1 promoted the expression of ring-finger protein 20 (Rnf20) in M2 cells. Rnf20 reduced PD-L1 abundance in UC M2 cells and impaired the immune suppressive ability. Inhibition of Rnf20 restored the immune regulating capacity of M2 cells and suppressed experimental colitis

CD11c APC populations were isolated from BAL, lung parenchyma and the spleen and pulsed with M

Tb CF protein or infected with live mycobacteria. APCs were then co-cultured with CD4+ or CD8+ T cells that were purified from the mice that were infected by live mycobacteria for 17 days (diagram). Cells were co-cultured for 24 h and IFN-γ-secreting T cells were determined by ELISPOT assay. A, IFN-γ-secreting CD4+ T cells. B, IFN-γ-secreting CD8+ T cells. Data are expressed as the mean value ± SD of triplicate samples and representative of two independent experiments. ‡p < 0.05 compared to the corresponding mycobacterial BCG-infected APCs; #p < 0.05 compared to the corresponding spleen data.<p><b>Copyright information:</b></p><p>Taken from "CD11c+ antigen presenting cells from the alveolar space, lung parenchyma and spleen differ in their phenotype and capabilities to activate naïve and antigen-primed T cells"</p><p>http://www.biomedcentral.com/1471-2172/9/48</p><p>BMC Immunology 2008;9():48-48.</p><p>Published online 13 Aug 2008</p><p>PMCID:PMC2527294.</p><p></p

Probiotics and AC regulates the intestinal microbial composition and diversity.

<p>(A) PCA in the 50^th day, the 100^th day and the 150^th day were performed based on the genera abundance of the microbial genomes. (B) Main genus composition was a percentage of total assigned sequences. (C) Bacterial phyla distribution as a percentage of total sequences. (D) Heatmap represents a sample of a color, abundance of a genus is a longitudinal sample clustering situation, reflecting on the case of multiple samples at the level of community composition similarity. All presented results are statistically significant (p<0.05) as assessed by the Wilcoxon test.</p

Serum TC, TG, HDL, LDL, and FFA concentrations in SD rats fed the experimental diets.

<p>TC, total cholesterol; TG, total triacylglycerol; LDL, low-density lipoprotein; HDL, high-density lipoprotein; FFA, free fatty acid.</p><p>Results are expressed as mean±SD, n = 6. Means within a row with different superscript letters are significantly different (P<0.05).</p><p>Serum TC, TG, HDL, LDL, and FFA concentrations in SD rats fed the experimental diets.</p

Probiotics combined with AC ameliorated blood glucose levels and IR.

<p>(A) Intraperitoneal glucose tolerance test. (B) Fasting blood glucose levels. (C) Fasting plasma insulin levels, and (D) HOMA-IR were assessed. The data are shown as mean±SD, n = 6. Means within a row with different superscript letters are significantly different (P<0.05).</p

Co-Administration of Cholesterol-Lowering Probiotics and Anthraquinone from <i>Cassia obtusifolia L</i>. Ameliorate Non-Alcoholic Fatty Liver

<div><p>Non-alcoholic fatty liver disease (NAFLD) has become a common liver disease in recent decades. No effective treatment is currently available. Probiotics and natural functional food may be promising therapeutic approaches to this disease. The present study aims to investigate the efficiency of the anthraquinone from <i>Cassia obtusifolia L</i>. (AC) together with cholesterol-lowering probiotics (P) to improve high-fat diet (HFD)-induced NAFLD in rat models and elucidate the underlying mechanism. Cholesterol-lowering probiotics were screened out by MRS-cholesterol broth with ammonium ferric sulfate method. Male Sprague–Dawley rats were fed with HFD and subsequently administered with AC and/or P. Lipid metabolism parameters and fat synthesis related genes in rat liver, as well as the diversity of gut microbiota were evaluated. The results demonstrated that, compared with the NAFLD rat, the serum lipid levels of treated rats were reduced effectively. Besides, cholesterol 7α-hydroxylase (CYP7A1), low density lipoprotein receptor (LDL-R) and farnesoid X receptor (FXR) were up-regulated while the expression of 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMGCR) was reduced. The expression of peroxisome proliferator activated receptor (PPAR)-α protein was significantly increased while the expression of PPAR-γ and sterol regulatory element binding protein-1c (SREBP-1c) was down-regulated. In addition, compared with HFD group, in AC, P and AC+P group, the expression of intestinal tight-junction protein occludin and zonula occluden-1 (ZO-1) were up-regulated. Furthermore, altered gut microbiota diversity after the treatment of probiotics and AC were analysed. The combination of cholesterol-lowering probiotics and AC possesses a therapeutic effect on NAFLD in rats by up-regulating CYP7A1, LDL-R, FXR mRNA and PPAR-α protein produced in the process of fat metabolism while down-regulating the expression of HMGCR, PPAR-γ and SREBP-1c, and through normalizing the intestinal dysbiosis and improving the intestinal mucosal barrier function.</p></div