36 research outputs found

    Barcharts of <i>IL23A</i> median fold change by RT-qPCR in AGS and MKN-28 (n=4).

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    <p>BCM-300, P1, M1, and M2 are <i>H. pylori</i> strains. Both BCM-300 and P1 (wild-type) are CagA strains, whereas M1 and M2 are P1-derived isogenic mutants lacking CagA and VirB7, respectively. Generally, higher expression levels were seen in AGS more than MKN-28 cells. Significant upregulation of <i>IL23A</i> was seen in both cells with BCM-300, P1 (the highest), and M1 strain (P<.05), whereas no alteration was seen after M2 infection (non-functional T4SS) similar to that of the non-infected control samples (CO).</p

    Correlation of <i>IL23A</i> with <i>IL8</i> and <i>EBI3</i> after infection with different <i>H. pylori</i> strains.

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    <p>Scatterplots of log-transformed fold changes of transcripts by RT-qPCR illustrate the relationship of <i>IL23A</i> with both <i>IL8</i> (panel A) and <i>EBI3</i> (panel B) transcripts after infection with different <i>H. pylori</i> strains using pair-wise Spearmen’s <i>rho</i> correlations. Robust regression line using an M estimator was plotted as well (red line). BCM-300, P1, M1, and M2 are <i>H. pylori</i> strains. Both BCM-300 and P1 (wild-type) are CagA strains, whereas M1 and M2 are P1-derived isogenic mutants lacking CagA and VirB7, respectively. BCM-300+Fi is infection with <i>H. pylori</i> BCM-300 bacteria after application of 0.22µm filter cap to prevent any physical contact with the cells, while permitting their secretory factors to pass through. Asterisks represent the significance levels (*P<.05, **<.01, ***<.001).</p

    Boxplots of raw Cqs of the detected transcripts by RT-qPCR in non-infected AGS and MKN-28.

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    <p>Each box represents the lower quartile, the median, and the upper quartile score (vertical lines of the box). Means (small white squares) and outliers are also shown (black dots). Expression levels of detected transcripts were ordered in AGS cell line from highest (<i>ACTB</i>) to lowest (<i>IL23R</i>) based on their median values. Similar ranking order was seen in MKN-28 cells except for the least four abundant transcripts: <i>IL23A</i>, <i>IL12A</i>, <i>EBI3</i>, and <i>IL23R</i>.</p

    Schematic diagram of IL-12 family.

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    <p>The diagram illustrates the currently known 5 chains (the innermost zone), composite cytokines with their proposed functions (the middle zone), and their receptors (the outermost zone). The five color-coded chains are either α chains (p19, p35, and p28) or β chains (p40 and Ebi3). Each functional cytokine is made of one α and one β chain. IL-12 (p35/p40) is a proinflammatory Th1 activator and stabilizer. Similarly, IL-23 (p19/p40) is a proinflammatory Th1 activator and Th17 stabilizer. On the other hand, IL-27 (p28/Ebi3) is an immunoregulatory cytokine mainly with an anti-inflammatory capacity. IL-35 (p35/Ebi3) is again anti-inflammatory and secreted by Treg cells. Therefore, the four cytokines with their divergent functions can promote a representative model of the immunological spectrum ranging from inflammation to tolerance. The unknown cytokine is a theoretical one and symbolizes the possibility of unraveling other unknown family members in the future. Each chain (p19, p40, p35, Ebi3, p28) binds to its specific receptor (IL23R, IL12RB1, IL12RB2, IL6ST, and IL27RA, respectively) and is coded with the same color of the corresponding chain (receptor names are not shown). Typically, a composite cytokine would require a β chain receptor for high affinity binding and an α chain receptor for signal transduction. For alternative terminology of IL-12 family members refer to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0075192#pone-0075192-t001" target="_blank">Table 1</a>.</p

    Detection of IL-1β-induced nuclear translocation of NF-κB by immunofluorescence in C3842 cells (A–D) and SW1353 cells (E-H).

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    <p>In untreated cells and cells treated with Curcumin or Curcumin+IL-1β, NF-κB was detected in the cytoplasm, not in the nucleus (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0099296#pone-0099296-g006" target="_blank">Figure 6</a>). In cells treated with IL-1β nuclear translocation of NF-κB was evident.</p

    Immunohistochemical analysis of IL-12, p19, and Ebi3 in human gastric mucosa.

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    <p>Microscopic images from a typical case of <i>H. pylori</i> negative gastritis are shown in A-D (antrum) and E-H (corpus). The antrum mucosa (A) contains few immune cells (hematoxylin-eosin). Both immune and epithelial cells were stained with IL-12 in the antrum mucosa (B). Immunostaining of p19 was detected in both immune and epithelial cells with a tendency to be more localized in the superficial epithelial cells and glandular neck zone of the antrum mucosa (C; arrowheads). Immunostaining of Ebi3 was exclusively found in the glandular neck zone of the antrum mucosa (D). The corpus mucosa (E) contains also few immune cells and is rich in parietal cells (hematoxylin-eosin). Both immune and epithelial cells of the corpus mucosa were stained with IL-12 (F). Immune cells, foveolar epithelium, and corpus glands with parietal cells were all immunostained with p19 (G). No Ebi3 staining was detected in the corpus mucosa (H). Microscopic findings in <i>H. pylori</i> gastritis are shown in I-L (antrum) and M-P (corpus). The antrum mucosa in <i>H. pylori</i> gastritis (I) contains higher amounts of immune cells (hematoxylin-eosin). No clear difference in IL-12 immunostaining was detected in epithelial cells (J) as compared to that of uninfected antrum mucosa (B). In contrast, a stronger immunostaining of p19 was observed in the foveolar epithelium and in immune cells including a lymph follicle (K). Ebi3 staining was only detected in the glandular neck zone of the antrum mucosa (L), similar to <i>H. pylori</i> negative mucosa (D). The corpus mucosa (M) contains increased immune cells (hematoxylin-eosin). No clear difference in IL-12 immunostaining was detected in epithelial cells (N) as compared to that of uninfected corpus mucosa (F). In contrast, a stronger immunostaining of p19 was observed in the foveolar epithelium, corpus glands with parietal cells, and immune cells (O). No Ebi3 staining was detected in the corpus mucosa (P). Scale bar=50µm.</p

    Relative expression of genes associated with NF-κB. RNA was extracted from C3842 cells treated with IL-1β (10 ng/ml), Curcumin (20 µmol/l) or both.

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    <p>qRT-PCR was performed using the NF-κB primer library (RealTimePrimers, Elkins Park, PA, USA).</p><p>See Material and Methods section for details. The gene expression levels were normalized to the expression of ribosomal protein 13a (RPL13a). The Curcumin effect on IL-1β-induced gene expression was calculated as ratio of the gene expression in cells treated with IL-1β+Curcumin and cells treated with IL-1β alone. Relative changes higher than 2-fold are marked bold. Relative changes lower than 0.5-fold are marked italic. Putative housekeeping genes other than RPL13a are indicated by italics.</p

    Effect of Curcumin on VEGF-A expression.

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    <p>IL-1β-induced VEGF-A expression is blocked in C3842 and SW1353 chondrosarcoma cells after incubation with Curcumin.</p
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