recombinant human soluble il 6r protein  (R&D Systems)

 
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    Name:
    Recombinant Human IL 6 IL 6 R alpha Protein Chimera CF
    Description:
    The Recombinant Human IL 6 IL 6 R alpha Protein Chimera from R D Systems is derived from HEK293 The Recombinant Human IL 6 IL 6 R alpha Protein Chimera has been validated for the following applications Bioactivity
    Catalog Number:
    8954-SR-025/CF
    Price:
    329
    Category:
    Proteins and Enzymes
    Source:
    HEK293-derived Recombinant Human IL-6/IL-6 R alpha Protein Chimera
    Applications:
    Bioactivity
    Purity:
    >90%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie« Blue Staining.
    Conjugate:
    Unconjugated
    Size:
    25 ug
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    Structured Review

    R&D Systems recombinant human soluble il 6r protein
    The Recombinant Human IL 6 IL 6 R alpha Protein Chimera from R D Systems is derived from HEK293 The Recombinant Human IL 6 IL 6 R alpha Protein Chimera has been validated for the following applications Bioactivity
    https://www.bioz.com/result/recombinant human soluble il 6r protein/product/R&D Systems
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    recombinant human soluble il 6r protein - by Bioz Stars, 2021-05
    94/100 stars

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    other:

    Article Title: Inflammatory biomarkers, geriatric assessment, and treatment outcomes in acute myeloid leukemia
    Article Snippet: Plasma concentrations of six inflammatory biomarkers were analyzed: Interleukin-6 [IL-6], IL-6 soluble receptor [IL-6 sR], tumor necrosis factor alpha [TNFα], TNFα soluble receptor 1[TNFα sR1], interleukin- 3 [IL-3], and C-reactive protein [CRP].

    Enzyme-linked Immunosorbent Assay:

    Article Title: The Anti-Inflammatory Activity of HMGB1 A Box Is Enhanced When Fused with C-Terminal Acidic Tail
    Article Snippet: .. Measurement of TNF-α and IL-6 TNF-α and IL-6 levels were determined by enzyme-linked immunosorbent assay (ELISA) kits (R & D System, USA) according to the instructions of the manufacturer. .. The concentrations of the two cytokines were calculated with reference to standard curves of purified recombinant TNF-α and IL-6 at various dilutions.

    Recombinant:

    Article Title: The classic signalling and trans‐signalling of interleukin‐6 are both injurious in podocyte under high glucose exposure
    Article Snippet: Differentiated podocytes were exposed to media containing high glucose (HG, final glucose concentration 30 mmol/l) or 19.9 mmol/l mannitol as osmotic control. .. After individual pre‐treatment with gp130 antibody (2 μg/ml, R & D Systems, Minneapolis, MN, USA), IL‐6 antibody (1 μg/ml, R & D Systems, Minneapolis, MN, USA), recombinant sgp130 (1 μg/ml, R & D Systems, Minneapolis, MN, USA), recombinant human IL‐6 (20 ng/ml, Peprotech, Rocky Hill, NJ, USA) or complex of IL‐6 and recombinant human soluble IL‐6R protein (30 ng/ml, R & D Systems, Minneapolis, MN, USA), podocytes were exposed to HG or osmotic control for 24 hrs. .. shRNA transfection For RNA interference, recombinant lentivirus vector harbouring a short‐hairpin RNA sequence targeting on IL‐6R (IL‐6R shRNA) and gp130 (gp130 shRNA) was obtained from JikaiGene (Shanghai, China) and the scrambled shRNA was used as control.

    Marker:

    Article Title: The Roles of Physical Activity and Inflammation in Mortality, Cognition, and Depressive Symptoms Among Older Mexican Americans
    Article Snippet: CRP levels were measured with the CRP Ultra Wide Range Reagent Kit latex-enhanced immunoassay (Equal Diagnostics, Exton, Pennsylvania); levels of IL-6 and TNF-α and their receptors were determined using the Quantiglo Chemiluminescent Immunoassay (R & D Systems, Minneapolis, Minnesota). .. Since the distributions of inflammatory markers were found to be nonnormal and highly skewed, for each marker, we used the quartile 3 cutpoint as a cutoff for the marker among participants who had baseline CRP levels less than 10 mg/L (CRP: 5.1 mg/L; IL-6: 5.2 pg/mL; IL-6 receptor: 44,009.2 pg/mL; TNF-α: 4.8 pg/mL; TNF-α receptor 1: 1,822.1 pg/mL; TNF-α receptor 2: 2,880.9 pg/mL). .. Participants who had baseline CRP levels greater than or equal to 10 mg/L were placed in the high-CRP group, under the assumption that a CRP concentration greater than or equal to 10 mg/L indicates clinically relevant acute inflammation.

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  • 99
    R&D Systems human recombinant soluble il 6 receptor
    Effects of <t>IL-6</t> on capsaicin-evoked CGRP release from adult DRG neurons in culture. A. Adult cultured DRGs were treated with capsaicin (30 nM) alone (i.e.; Control), TB-2-081 (5 μM) followed by capsaicin (TB-2-081), IL-6 (20 ng/ml) followed by
    Human Recombinant Soluble Il 6 Receptor, supplied by R&D Systems, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human recombinant soluble il 6 receptor/product/R&D Systems
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    human recombinant soluble il 6 receptor - by Bioz Stars, 2021-05
    99/100 stars
      Buy from Supplier

    94
    R&D Systems recombinant human soluble il 6 receptor
    IL-17 Enhances <t>IL-6-mediated</t> SOCS3 Expression in Primary Astrocytes, and SOCS3 is a Negative Regulator of the Synergistic Effect of IL-6 and IL-17 A , Astrocytes were treated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 2 - 8 h, and levels of SOCS3 mRNA expression were determined by QRT-PCR. B and C, Astrocytes were transfected with SOCS3 siRNA (100 nM) or siRNA control (100 nM) for 48 h. Transfected cells were then treated with medium (UN) or IL-6/R plus IL-17 for 4 h. Levels of SOCS3 (B) and IL-6 (C) mRNA expression was determined by QRT-PCR. D, Astrocytes were transfected with SOCS3 siRNA or siRNA control for 48 h. Transfected cells were then treated with medium (UN) or IL-6/R plus IL-17 for 24 h, and supernatants analyzed for IL-6 protein by ELISA. E, SOCS3 floxed astrocytes were infected with GFP as control or GFP-Cre for deletion. After 48 h in culture, cells were harvested. Digestion of genomic DNA distinguishes the full-length (fl) and excised alleles ( Δ ). F, SOCS3 floxed astrocytes were infected with GFP as control or GFP-Cre for deletion. After 48 h in culture, the cells were treated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 4 h, and levels of IL-6 mRNA expression determined by QRT-PCR. G, SOCS3 floxed astrocytes were infected with GFP as control or GFP-Cre for deletion. After 48 h in culture, cells were incubated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 16 or 24 h, and supernatants analyzed for IL-6 protein by ELISA. All data are the mean ± SD of three experiments. *, p ≤ 0.05;**, p ≤ 0.01.
    Recombinant Human Soluble Il 6 Receptor, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant human soluble il 6 receptor/product/R&D Systems
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    recombinant human soluble il 6 receptor - by Bioz Stars, 2021-05
    94/100 stars
      Buy from Supplier

    99
    R&D Systems recombinant human sil 6r
    TNF-α interacts with microglia to recruit soluble IL-6 receptor. A , Release of IL-6 soluble receptor (sIL6-R) into the supernatant of BV2 mouse microglia cells within 2 h of stimulation ( n = 6). Basal release (control, 26.0 ± 3.9 pg/ml, mean ± SEM) decreased insignificantly in the presence of minocycline. TNF-α increased <t>sIL-6R</t> release significantly, an effect inhibited by minocycline. There was no additional release of sIL-6R by IL-6. x indicates a significant difference between the indicated groups ( p
    Recombinant Human Sil 6r, supplied by R&D Systems, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant human sil 6r/product/R&D Systems
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    recombinant human sil 6r - by Bioz Stars, 2021-05
    99/100 stars
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    Effects of IL-6 on capsaicin-evoked CGRP release from adult DRG neurons in culture. A. Adult cultured DRGs were treated with capsaicin (30 nM) alone (i.e.; Control), TB-2-081 (5 μM) followed by capsaicin (TB-2-081), IL-6 (20 ng/ml) followed by

    Journal: Pain

    Article Title: Reversal of pancreatitis-induced pain by an orally available, small molecule interleukin-6 receptor antagonist

    doi: 10.1016/j.pain.2010.05.022

    Figure Lengend Snippet: Effects of IL-6 on capsaicin-evoked CGRP release from adult DRG neurons in culture. A. Adult cultured DRGs were treated with capsaicin (30 nM) alone (i.e.; Control), TB-2-081 (5 μM) followed by capsaicin (TB-2-081), IL-6 (20 ng/ml) followed by

    Article Snippet: Ninety-six well-plates (Nunc) were coated with 500 ng/mL of human recombinant soluble IL-6 receptor (R & D Systems) overnight at 4°C.

    Techniques: Cell Culture

    A. Structure of TB-2-081. B Saturation of IL-6 at human recombinant sIL-6R. Half saturation concentration is 960 pM. C. Competitive binding of TB-2-081 to IL-6R (IC 50 = 29.4 pM). D. TB-2-081 inhibits the growth of IL-6 dependent cell line TF-1(IC 50 =

    Journal: Pain

    Article Title: Reversal of pancreatitis-induced pain by an orally available, small molecule interleukin-6 receptor antagonist

    doi: 10.1016/j.pain.2010.05.022

    Figure Lengend Snippet: A. Structure of TB-2-081. B Saturation of IL-6 at human recombinant sIL-6R. Half saturation concentration is 960 pM. C. Competitive binding of TB-2-081 to IL-6R (IC 50 = 29.4 pM). D. TB-2-081 inhibits the growth of IL-6 dependent cell line TF-1(IC 50 =

    Article Snippet: Ninety-six well-plates (Nunc) were coated with 500 ng/mL of human recombinant soluble IL-6 receptor (R & D Systems) overnight at 4°C.

    Techniques: Recombinant, Concentration Assay, Binding Assay

    Pancreatitis-induced changes in IL-6 expression in the pancreas and DRG. A. Time-course of changes in levels of IL-6 in pancreata of naïve, ethanol vehicle or DBTC-treated animals (*indicates significant difference from naïve group, P

    Journal: Pain

    Article Title: Reversal of pancreatitis-induced pain by an orally available, small molecule interleukin-6 receptor antagonist

    doi: 10.1016/j.pain.2010.05.022

    Figure Lengend Snippet: Pancreatitis-induced changes in IL-6 expression in the pancreas and DRG. A. Time-course of changes in levels of IL-6 in pancreata of naïve, ethanol vehicle or DBTC-treated animals (*indicates significant difference from naïve group, P

    Article Snippet: Ninety-six well-plates (Nunc) were coated with 500 ng/mL of human recombinant soluble IL-6 receptor (R & D Systems) overnight at 4°C.

    Techniques: Expressing

    IL-17 Enhances IL-6-mediated SOCS3 Expression in Primary Astrocytes, and SOCS3 is a Negative Regulator of the Synergistic Effect of IL-6 and IL-17 A , Astrocytes were treated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 2 - 8 h, and levels of SOCS3 mRNA expression were determined by QRT-PCR. B and C, Astrocytes were transfected with SOCS3 siRNA (100 nM) or siRNA control (100 nM) for 48 h. Transfected cells were then treated with medium (UN) or IL-6/R plus IL-17 for 4 h. Levels of SOCS3 (B) and IL-6 (C) mRNA expression was determined by QRT-PCR. D, Astrocytes were transfected with SOCS3 siRNA or siRNA control for 48 h. Transfected cells were then treated with medium (UN) or IL-6/R plus IL-17 for 24 h, and supernatants analyzed for IL-6 protein by ELISA. E, SOCS3 floxed astrocytes were infected with GFP as control or GFP-Cre for deletion. After 48 h in culture, cells were harvested. Digestion of genomic DNA distinguishes the full-length (fl) and excised alleles ( Δ ). F, SOCS3 floxed astrocytes were infected with GFP as control or GFP-Cre for deletion. After 48 h in culture, the cells were treated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 4 h, and levels of IL-6 mRNA expression determined by QRT-PCR. G, SOCS3 floxed astrocytes were infected with GFP as control or GFP-Cre for deletion. After 48 h in culture, cells were incubated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 16 or 24 h, and supernatants analyzed for IL-6 protein by ELISA. All data are the mean ± SD of three experiments. *, p ≤ 0.05;**, p ≤ 0.01.

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Interleukin-17 Enhancement of the Interleukin-6 Signaling Cascade in Astrocytes

    doi: 10.4049/jimmunol.1000142

    Figure Lengend Snippet: IL-17 Enhances IL-6-mediated SOCS3 Expression in Primary Astrocytes, and SOCS3 is a Negative Regulator of the Synergistic Effect of IL-6 and IL-17 A , Astrocytes were treated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 2 - 8 h, and levels of SOCS3 mRNA expression were determined by QRT-PCR. B and C, Astrocytes were transfected with SOCS3 siRNA (100 nM) or siRNA control (100 nM) for 48 h. Transfected cells were then treated with medium (UN) or IL-6/R plus IL-17 for 4 h. Levels of SOCS3 (B) and IL-6 (C) mRNA expression was determined by QRT-PCR. D, Astrocytes were transfected with SOCS3 siRNA or siRNA control for 48 h. Transfected cells were then treated with medium (UN) or IL-6/R plus IL-17 for 24 h, and supernatants analyzed for IL-6 protein by ELISA. E, SOCS3 floxed astrocytes were infected with GFP as control or GFP-Cre for deletion. After 48 h in culture, cells were harvested. Digestion of genomic DNA distinguishes the full-length (fl) and excised alleles ( Δ ). F, SOCS3 floxed astrocytes were infected with GFP as control or GFP-Cre for deletion. After 48 h in culture, the cells were treated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 4 h, and levels of IL-6 mRNA expression determined by QRT-PCR. G, SOCS3 floxed astrocytes were infected with GFP as control or GFP-Cre for deletion. After 48 h in culture, cells were incubated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 16 or 24 h, and supernatants analyzed for IL-6 protein by ELISA. All data are the mean ± SD of three experiments. *, p ≤ 0.05;**, p ≤ 0.01.

    Article Snippet: Recombinant human IL-6, recombinant human soluble IL-6 Receptor (sIL-6R) and recombinant mouse IL-17 were from R & D Systems (Minneapolis, MN).

    Techniques: Expressing, Quantitative RT-PCR, Transfection, Enzyme-linked Immunosorbent Assay, Infection, Incubation

    Proposed Model of IL-17 Enhancement of the IL-6 Signaling Cascade in Astrocytes A, IL-6/R and IL-17 activate the NF-κB and MAPK pathway, which then induce IL-6 gene expression. The synergistic effect of these two mediators depends on NF-κB, p38 and JNK MAPK activity. Activated NF-κB p65, c-Fos and c-Jun bind to the IL-6 promoter. Concurrent with NF-κB and MAPK recruitment, IL-6/R and IL-17 leads to the recruitment of coactivators CBP and p300, modifications in AcH3 and AcH4, and recruitment of RNA Pol II to the IL-6 promoter, which results in transcriptional activation of the IL-6 gene. IL-17 can also enhance IL-6/R induced SOCS3 expression, and SOCS3 inhibits IL-6/R plus IL-17-induced NF-κB and MAPK activation, which results in a reduction of IL-6 gene expression in astrocytes. B , Naive CD4 + T cells, after activation by signaling through the T cell receptor and co-stimulatory molecules, can differentiate into Th17 cells in the presence of IL-6, TGF-β, IL-1 and IL-23. IL-17 together with IL-6/R triggers a positive-feedforward loop of IL-6 expression in astrocytes, which may also influence Th17 cell differentiation. SOCS3 participates in these processes as a negative feedback regulator. See text for details.

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Interleukin-17 Enhancement of the Interleukin-6 Signaling Cascade in Astrocytes

    doi: 10.4049/jimmunol.1000142

    Figure Lengend Snippet: Proposed Model of IL-17 Enhancement of the IL-6 Signaling Cascade in Astrocytes A, IL-6/R and IL-17 activate the NF-κB and MAPK pathway, which then induce IL-6 gene expression. The synergistic effect of these two mediators depends on NF-κB, p38 and JNK MAPK activity. Activated NF-κB p65, c-Fos and c-Jun bind to the IL-6 promoter. Concurrent with NF-κB and MAPK recruitment, IL-6/R and IL-17 leads to the recruitment of coactivators CBP and p300, modifications in AcH3 and AcH4, and recruitment of RNA Pol II to the IL-6 promoter, which results in transcriptional activation of the IL-6 gene. IL-17 can also enhance IL-6/R induced SOCS3 expression, and SOCS3 inhibits IL-6/R plus IL-17-induced NF-κB and MAPK activation, which results in a reduction of IL-6 gene expression in astrocytes. B , Naive CD4 + T cells, after activation by signaling through the T cell receptor and co-stimulatory molecules, can differentiate into Th17 cells in the presence of IL-6, TGF-β, IL-1 and IL-23. IL-17 together with IL-6/R triggers a positive-feedforward loop of IL-6 expression in astrocytes, which may also influence Th17 cell differentiation. SOCS3 participates in these processes as a negative feedback regulator. See text for details.

    Article Snippet: Recombinant human IL-6, recombinant human soluble IL-6 Receptor (sIL-6R) and recombinant mouse IL-17 were from R & D Systems (Minneapolis, MN).

    Techniques: Expressing, Activity Assay, Activation Assay, Cell Differentiation

    IL-17 Synergizes with IL-6/R for Activation of the NF-κB and MAPK Pathways A , Astrocytes were incubated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 15 and 30 min, and then cell lysates were immunoblotted with antibodies against IκBα and GAPDH. The basal level of the untreated sample was set at 100, and the percentage change of IκBα upon IL-6/R, IL-17 or IL-6/R + IL-17 treatment compared with the basal value. B , Astrocytes were incubated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 30 and 60 min, and then cell lysates were immunoblotted with antibodies against phospho-p65 Ser 536, p65 and GAPDH. C , Astrocytes were incubated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 15 and 30 min, and then cell lysates were immunoblotted with antibodies against phospho-ERK1/2, ERK1/2 and GAPDH. D , Astrocytes were incubated with medium (UN), IL-6/R, IL-17 or IL-6/R and IL-17 for 30 min and 60 min, and then cell lysates were immunoblotted with antibodies against phospho-p38, p38 and GAPDH. E , Astrocytes were incubated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 30 and 60 min, and then cell lysates were immunoblotted with antibodies against phospho-JNK, JNK and GAPDH. The basal level of the untreated sample was set at 1.0 and fold activation upon IL-6/R, IL-17 or IL-6/R + IL-17 treatment was compared with that value ( B , C , D and E ). Representative of at least three experiments.

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Interleukin-17 Enhancement of the Interleukin-6 Signaling Cascade in Astrocytes

    doi: 10.4049/jimmunol.1000142

    Figure Lengend Snippet: IL-17 Synergizes with IL-6/R for Activation of the NF-κB and MAPK Pathways A , Astrocytes were incubated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 15 and 30 min, and then cell lysates were immunoblotted with antibodies against IκBα and GAPDH. The basal level of the untreated sample was set at 100, and the percentage change of IκBα upon IL-6/R, IL-17 or IL-6/R + IL-17 treatment compared with the basal value. B , Astrocytes were incubated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 30 and 60 min, and then cell lysates were immunoblotted with antibodies against phospho-p65 Ser 536, p65 and GAPDH. C , Astrocytes were incubated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 15 and 30 min, and then cell lysates were immunoblotted with antibodies against phospho-ERK1/2, ERK1/2 and GAPDH. D , Astrocytes were incubated with medium (UN), IL-6/R, IL-17 or IL-6/R and IL-17 for 30 min and 60 min, and then cell lysates were immunoblotted with antibodies against phospho-p38, p38 and GAPDH. E , Astrocytes were incubated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 30 and 60 min, and then cell lysates were immunoblotted with antibodies against phospho-JNK, JNK and GAPDH. The basal level of the untreated sample was set at 1.0 and fold activation upon IL-6/R, IL-17 or IL-6/R + IL-17 treatment was compared with that value ( B , C , D and E ). Representative of at least three experiments.

    Article Snippet: Recombinant human IL-6, recombinant human soluble IL-6 Receptor (sIL-6R) and recombinant mouse IL-17 were from R & D Systems (Minneapolis, MN).

    Techniques: Activation Assay, Incubation

    IL-17 and IL-6/R Induction of IL-6 Depends on NF-κB, p38 and JNK MAPK Activity A , Astrocytes were cultured in absence or presence of IL-17 followed by IL-6/R treatment for 4 h. Actinomycin D (5 ng/ml) was then added, and cells harvested at 0, 30, 60, 120, and 240 min after addition. The abundance of IL-6 mRNA was determined by QRT-PCR. B , C , DMSO vehicle, BAY 11 (5 μM), U0126 (10 μM), SB203580 (10 μM) or JNKi II (10 μM) were added to cultures 1 h before cytokine addition, and then astrocytes were incubated with medium, IL-6/R, IL-17 or IL-6/R plus IL-17 for 4 h. Levels of IL-6 mRNA expression were determined by QRT-PCR. All data are the mean ± SD of three experiments. **, p ≤ 0.01; NS = not significant.

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Interleukin-17 Enhancement of the Interleukin-6 Signaling Cascade in Astrocytes

    doi: 10.4049/jimmunol.1000142

    Figure Lengend Snippet: IL-17 and IL-6/R Induction of IL-6 Depends on NF-κB, p38 and JNK MAPK Activity A , Astrocytes were cultured in absence or presence of IL-17 followed by IL-6/R treatment for 4 h. Actinomycin D (5 ng/ml) was then added, and cells harvested at 0, 30, 60, 120, and 240 min after addition. The abundance of IL-6 mRNA was determined by QRT-PCR. B , C , DMSO vehicle, BAY 11 (5 μM), U0126 (10 μM), SB203580 (10 μM) or JNKi II (10 μM) were added to cultures 1 h before cytokine addition, and then astrocytes were incubated with medium, IL-6/R, IL-17 or IL-6/R plus IL-17 for 4 h. Levels of IL-6 mRNA expression were determined by QRT-PCR. All data are the mean ± SD of three experiments. **, p ≤ 0.01; NS = not significant.

    Article Snippet: Recombinant human IL-6, recombinant human soluble IL-6 Receptor (sIL-6R) and recombinant mouse IL-17 were from R & D Systems (Minneapolis, MN).

    Techniques: Activity Assay, Cell Culture, Quantitative RT-PCR, Incubation, Expressing

    IL-6/R plus IL-17 Enhances Recruitment of p65, P-p65, c-Jun, c-Fos, CBP, p300, and RNA Pol II to the IL-6 Promoter A, Primary astrocytes were treated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 90 min, and then cells were cross-linked with formaldehyde. Soluble chromatin was subjected to immunoprecipitation with Abs against p65, P-p65, c-Fos, c-Jun, or normal rabbit IgG. PCR analysis of the positive control (input) indicates that soluble chromatin samples obtained from each time point had equal amounts of chromatin fragments containing the IL-6 promoter. B, Primary astrocytes were treated as above. Soluble chromatin was subjected to immunoprecipitation with Abs against histone acetylation (Ac-H3 and Ac-H4), p300, CBP, RNA Pol II or normal rabbit IgG. The basal level of the untreated sample was set at 1.0 and fold activation upon IL-6/R, IL-17 or IL-6/R plus IL-17 treatment was compared with that value. Representative of at least three experiments.

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Interleukin-17 Enhancement of the Interleukin-6 Signaling Cascade in Astrocytes

    doi: 10.4049/jimmunol.1000142

    Figure Lengend Snippet: IL-6/R plus IL-17 Enhances Recruitment of p65, P-p65, c-Jun, c-Fos, CBP, p300, and RNA Pol II to the IL-6 Promoter A, Primary astrocytes were treated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 90 min, and then cells were cross-linked with formaldehyde. Soluble chromatin was subjected to immunoprecipitation with Abs against p65, P-p65, c-Fos, c-Jun, or normal rabbit IgG. PCR analysis of the positive control (input) indicates that soluble chromatin samples obtained from each time point had equal amounts of chromatin fragments containing the IL-6 promoter. B, Primary astrocytes were treated as above. Soluble chromatin was subjected to immunoprecipitation with Abs against histone acetylation (Ac-H3 and Ac-H4), p300, CBP, RNA Pol II or normal rabbit IgG. The basal level of the untreated sample was set at 1.0 and fold activation upon IL-6/R, IL-17 or IL-6/R plus IL-17 treatment was compared with that value. Representative of at least three experiments.

    Article Snippet: Recombinant human IL-6, recombinant human soluble IL-6 Receptor (sIL-6R) and recombinant mouse IL-17 were from R & D Systems (Minneapolis, MN).

    Techniques: Immunoprecipitation, Polymerase Chain Reaction, Positive Control, Activation Assay

    Enhanced Activation of NF-κB and MAPK Pathways in SOCS3 Deficient Astrocytes To evaluate NF-κB and MAPK activation in the absence or presence of SOCS3, SOCS3 floxed astrocytes were infected with GFP as control or GFP-Cre for deletion. After 48 h in culture, cells were treated with medium (UN) or IL-6/R plus IL-17 for 15, 30, 60 or 120 min, and then cell lysates were immunoblotted with antibodies against phospho-p65 Ser 536, p65, phospho-p38, p38, phospho-JNK, JNK or GAPDH. The basal level of the untreated GFP infected sample was set at 1.0 and fold activation upon IL-6/R plus IL-17 treatment compared with that value. Representative of at least three experiments.

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Interleukin-17 Enhancement of the Interleukin-6 Signaling Cascade in Astrocytes

    doi: 10.4049/jimmunol.1000142

    Figure Lengend Snippet: Enhanced Activation of NF-κB and MAPK Pathways in SOCS3 Deficient Astrocytes To evaluate NF-κB and MAPK activation in the absence or presence of SOCS3, SOCS3 floxed astrocytes were infected with GFP as control or GFP-Cre for deletion. After 48 h in culture, cells were treated with medium (UN) or IL-6/R plus IL-17 for 15, 30, 60 or 120 min, and then cell lysates were immunoblotted with antibodies against phospho-p65 Ser 536, p65, phospho-p38, p38, phospho-JNK, JNK or GAPDH. The basal level of the untreated GFP infected sample was set at 1.0 and fold activation upon IL-6/R plus IL-17 treatment compared with that value. Representative of at least three experiments.

    Article Snippet: Recombinant human IL-6, recombinant human soluble IL-6 Receptor (sIL-6R) and recombinant mouse IL-17 were from R & D Systems (Minneapolis, MN).

    Techniques: Activation Assay, Infection

    IL-17 Enhances IL-6/sIL-6R-mediated IL-6 Expression in Primary Astrocytes A , IL-17RA and IL-17RC mRNA expression was determined by RT-PCR in RAW264.7 cells (positive control), and primary astrocytes, in duplicate. B , Primary astrocytes were treated with medium (UN), IL-6/R (IL-6, 10 ng/ml and sIL-6R, 25 ng/ml), IL-17 (25 ng/ml) or IL-6/R plus IL-17 for up to 24 h, and levels of IL-6 and GAPDH mRNA expression were determined by RT-PCR and QRT-PCR. C , Primary astrocytes were treated with medium (UN), IL-6/R, different concentrations of IL-17 (1-50 ng/ml) or IL-6/R + IL-17 (1-50 ng/ml) for 4 h, and levels of IL-6 mRNA expression were determined by QRT-PCR. D , Primary astrocytes were treated with medium (UN), IL-6, sIL-6R or IL-17 in various combinations for 4 h, and levels of IL-6 mRNA expression were determined by QRT-PCR. E , Primary astrocytes were treated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 2 - 48 h, and supernatants were analyzed for IL-6 protein using ELISA. Experiments shown are representative of at least three experiments. All data are the mean ± SD of three experiments. *, p ≤0.05; **, p ≤0.01.

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Interleukin-17 Enhancement of the Interleukin-6 Signaling Cascade in Astrocytes

    doi: 10.4049/jimmunol.1000142

    Figure Lengend Snippet: IL-17 Enhances IL-6/sIL-6R-mediated IL-6 Expression in Primary Astrocytes A , IL-17RA and IL-17RC mRNA expression was determined by RT-PCR in RAW264.7 cells (positive control), and primary astrocytes, in duplicate. B , Primary astrocytes were treated with medium (UN), IL-6/R (IL-6, 10 ng/ml and sIL-6R, 25 ng/ml), IL-17 (25 ng/ml) or IL-6/R plus IL-17 for up to 24 h, and levels of IL-6 and GAPDH mRNA expression were determined by RT-PCR and QRT-PCR. C , Primary astrocytes were treated with medium (UN), IL-6/R, different concentrations of IL-17 (1-50 ng/ml) or IL-6/R + IL-17 (1-50 ng/ml) for 4 h, and levels of IL-6 mRNA expression were determined by QRT-PCR. D , Primary astrocytes were treated with medium (UN), IL-6, sIL-6R or IL-17 in various combinations for 4 h, and levels of IL-6 mRNA expression were determined by QRT-PCR. E , Primary astrocytes were treated with medium (UN), IL-6/R, IL-17 or IL-6/R plus IL-17 for 2 - 48 h, and supernatants were analyzed for IL-6 protein using ELISA. Experiments shown are representative of at least three experiments. All data are the mean ± SD of three experiments. *, p ≤0.05; **, p ≤0.01.

    Article Snippet: Recombinant human IL-6, recombinant human soluble IL-6 Receptor (sIL-6R) and recombinant mouse IL-17 were from R & D Systems (Minneapolis, MN).

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Positive Control, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

    Potentiation of IL-6 effects on P-gp expression by adding its specific α receptor subunits. Addition of soluble IL-6R induced a major potentiation of rmIL-6 whatever the concentration of the factor used.

    Journal: BMC Cell Biology

    Article Title: Astroglial expression of the P-glycoprotein is controlled by intracellular CNTF

    doi: 10.1186/1471-2121-3-20

    Figure Lengend Snippet: Potentiation of IL-6 effects on P-gp expression by adding its specific α receptor subunits. Addition of soluble IL-6R induced a major potentiation of rmIL-6 whatever the concentration of the factor used.

    Article Snippet: Recombinant rat CNTF (rrCNTF, Boehringer Mannheim, Germany), recombinant human Leukemia Inhibitory Factor and human Cardiotrophin-1 (rhLIF and rhCT-1, Dr Gascan, Angers), Tumor Necrosis Factor alpha (TNFα), Nerve Growth Factor (NGF, Promega, France), Retinoic Acid (RA, Sigma Aldrich, France), dibutyryl cyclic AMP (dBcAMP, Sigma Aldrich), bacterial lipopolysaccharides (LPS, Sigma Aldrich), Transforming Growth Factor alpha (rhTGFα, Promega, France), recombinant human Interleukin-1β (rhIL-1β, Sigma), Interferon-β (IFN-β, Promega, France), recombinant human Interferon-γ (rhIFN-γ, R & D systems, United Kingdom), recombinant mouse Interleukin-6 (rmIL-6, R & D systems, United Kingdom), recombinant human soluble Il-6 receptor (R & D systems) were used in these experiments.

    Techniques: Expressing, Concentration Assay

    Effect of cytokines of the IL-6 family on P-gp intracellular content in CNTF-/- astrocytes. Only rrCNTF (250 ng/ml) provoked a significant increase in P-gp intracellular content (+43.8 % ± 20, factorial ANOVA significant at 95%, t-test p

    Journal: BMC Cell Biology

    Article Title: Astroglial expression of the P-glycoprotein is controlled by intracellular CNTF

    doi: 10.1186/1471-2121-3-20

    Figure Lengend Snippet: Effect of cytokines of the IL-6 family on P-gp intracellular content in CNTF-/- astrocytes. Only rrCNTF (250 ng/ml) provoked a significant increase in P-gp intracellular content (+43.8 % ± 20, factorial ANOVA significant at 95%, t-test p

    Article Snippet: Recombinant rat CNTF (rrCNTF, Boehringer Mannheim, Germany), recombinant human Leukemia Inhibitory Factor and human Cardiotrophin-1 (rhLIF and rhCT-1, Dr Gascan, Angers), Tumor Necrosis Factor alpha (TNFα), Nerve Growth Factor (NGF, Promega, France), Retinoic Acid (RA, Sigma Aldrich, France), dibutyryl cyclic AMP (dBcAMP, Sigma Aldrich), bacterial lipopolysaccharides (LPS, Sigma Aldrich), Transforming Growth Factor alpha (rhTGFα, Promega, France), recombinant human Interleukin-1β (rhIL-1β, Sigma), Interferon-β (IFN-β, Promega, France), recombinant human Interferon-γ (rhIFN-γ, R & D systems, United Kingdom), recombinant mouse Interleukin-6 (rmIL-6, R & D systems, United Kingdom), recombinant human soluble Il-6 receptor (R & D systems) were used in these experiments.

    Techniques:

    TNF-α interacts with microglia to recruit soluble IL-6 receptor. A , Release of IL-6 soluble receptor (sIL6-R) into the supernatant of BV2 mouse microglia cells within 2 h of stimulation ( n = 6). Basal release (control, 26.0 ± 3.9 pg/ml, mean ± SEM) decreased insignificantly in the presence of minocycline. TNF-α increased sIL-6R release significantly, an effect inhibited by minocycline. There was no additional release of sIL-6R by IL-6. x indicates a significant difference between the indicated groups ( p

    Journal: The Journal of Neuroscience

    Article Title: Involvement of Spinal IL-6 Trans-Signaling in the Induction of Hyperexcitability of Deep Dorsal Horn Neurons by Spinal Tumor Necrosis Factor-Alpha

    doi: 10.1523/JNEUROSCI.4159-15.2016

    Figure Lengend Snippet: TNF-α interacts with microglia to recruit soluble IL-6 receptor. A , Release of IL-6 soluble receptor (sIL6-R) into the supernatant of BV2 mouse microglia cells within 2 h of stimulation ( n = 6). Basal release (control, 26.0 ± 3.9 pg/ml, mean ± SEM) decreased insignificantly in the presence of minocycline. TNF-α increased sIL-6R release significantly, an effect inhibited by minocycline. There was no additional release of sIL-6R by IL-6. x indicates a significant difference between the indicated groups ( p

    Article Snippet: According to experimental protocols, recombinant rat TNF-α (ImmunoTools), recombinant rat IL-6 (Life Technologies), recombinant sgp130, recombinant human IL-6, and/or recombinant human sIL-6R (R & D Systems) were then applied directly in Tyrode's solution onto the spinal cord surface into the trough over the recording site at a concentration of 1 μg/ml.

    Techniques:

    Effect of minocycline on TNF-α-induced hyperexcitability. A , There were no changes of neuronal responses to mechanical stimulation after application of minocycline only and no increase after subsequent application of minocycline plus TNF-α ( n = 11), but there was an increase of the responses after TNF-α plus sIL-6R in the presence of minocycline ( n = 7). Data are shown as the mean number of action potentials per 15 s (mean APs/15 s) ± SEM for intervals of 30 min. Baseline values (in APs/15 s) in the minocycline/TNF-α group: innocuous pressure knee 288.3 ± 105.2, noxious pressure knee 636.8 ± 113.0, innocuous pressure ankle 260.9 ± 69.8, noxious pressure ankle 482.9 ± 84.8. Baseline values (in APs/15 s) in the minocycline/TNF-α/sIL-6R group: innocuous pressure knee 42.3 ± 28.2, noxious pressure knee 326.1 ± 98.7, innocuous pressure ankle 112.3 ± 60.3, noxious pressure ankle 554.9 ± 160.5. Asterisks with arrow indicate the start of significant increases of responses or significant increase of responses at the specific time point ( p

    Journal: The Journal of Neuroscience

    Article Title: Involvement of Spinal IL-6 Trans-Signaling in the Induction of Hyperexcitability of Deep Dorsal Horn Neurons by Spinal Tumor Necrosis Factor-Alpha

    doi: 10.1523/JNEUROSCI.4159-15.2016

    Figure Lengend Snippet: Effect of minocycline on TNF-α-induced hyperexcitability. A , There were no changes of neuronal responses to mechanical stimulation after application of minocycline only and no increase after subsequent application of minocycline plus TNF-α ( n = 11), but there was an increase of the responses after TNF-α plus sIL-6R in the presence of minocycline ( n = 7). Data are shown as the mean number of action potentials per 15 s (mean APs/15 s) ± SEM for intervals of 30 min. Baseline values (in APs/15 s) in the minocycline/TNF-α group: innocuous pressure knee 288.3 ± 105.2, noxious pressure knee 636.8 ± 113.0, innocuous pressure ankle 260.9 ± 69.8, noxious pressure ankle 482.9 ± 84.8. Baseline values (in APs/15 s) in the minocycline/TNF-α/sIL-6R group: innocuous pressure knee 42.3 ± 28.2, noxious pressure knee 326.1 ± 98.7, innocuous pressure ankle 112.3 ± 60.3, noxious pressure ankle 554.9 ± 160.5. Asterisks with arrow indicate the start of significant increases of responses or significant increase of responses at the specific time point ( p

    Article Snippet: According to experimental protocols, recombinant rat TNF-α (ImmunoTools), recombinant rat IL-6 (Life Technologies), recombinant sgp130, recombinant human IL-6, and/or recombinant human sIL-6R (R & D Systems) were then applied directly in Tyrode's solution onto the spinal cord surface into the trough over the recording site at a concentration of 1 μg/ml.

    Techniques:

    Increase of spinal IL-6 release during peripheral stimulation in the presence of spinally applied TNF-α and neuronal effects of IL-6 and IL-6/sIL-6R. A , Spinal IL-6 release (means ± SEM) into the spinal cord supernatant in the course of the stimulation protocol and spinal TNF-α application. Samples were extracted after 1 h of baseline (control) and 1 and 2 h after TNF-α application ( n = 10). *Significant increase after TNF-α compared with control before TNF-α ( p

    Journal: The Journal of Neuroscience

    Article Title: Involvement of Spinal IL-6 Trans-Signaling in the Induction of Hyperexcitability of Deep Dorsal Horn Neurons by Spinal Tumor Necrosis Factor-Alpha

    doi: 10.1523/JNEUROSCI.4159-15.2016

    Figure Lengend Snippet: Increase of spinal IL-6 release during peripheral stimulation in the presence of spinally applied TNF-α and neuronal effects of IL-6 and IL-6/sIL-6R. A , Spinal IL-6 release (means ± SEM) into the spinal cord supernatant in the course of the stimulation protocol and spinal TNF-α application. Samples were extracted after 1 h of baseline (control) and 1 and 2 h after TNF-α application ( n = 10). *Significant increase after TNF-α compared with control before TNF-α ( p

    Article Snippet: According to experimental protocols, recombinant rat TNF-α (ImmunoTools), recombinant rat IL-6 (Life Technologies), recombinant sgp130, recombinant human IL-6, and/or recombinant human sIL-6R (R & D Systems) were then applied directly in Tyrode's solution onto the spinal cord surface into the trough over the recording site at a concentration of 1 μg/ml.

    Techniques:

    Model of the cooperation of TNF-α and IL-6 in the generation of spinal hyperexcitability. TNF-α leads to IL-6 release mainly from neurons and acts on microglia to provide sIL-6R for IL-6 trans -signaling by ADAM10/17-protease-dependent cleavage of IL-6R, which is not present in neurons. Interaction of IL-6-bound IL-6R or IL-6/sIL-6R complex with ubiquitously expressed and homodimerized gp130 is required for IL-6 signaling.

    Journal: The Journal of Neuroscience

    Article Title: Involvement of Spinal IL-6 Trans-Signaling in the Induction of Hyperexcitability of Deep Dorsal Horn Neurons by Spinal Tumor Necrosis Factor-Alpha

    doi: 10.1523/JNEUROSCI.4159-15.2016

    Figure Lengend Snippet: Model of the cooperation of TNF-α and IL-6 in the generation of spinal hyperexcitability. TNF-α leads to IL-6 release mainly from neurons and acts on microglia to provide sIL-6R for IL-6 trans -signaling by ADAM10/17-protease-dependent cleavage of IL-6R, which is not present in neurons. Interaction of IL-6-bound IL-6R or IL-6/sIL-6R complex with ubiquitously expressed and homodimerized gp130 is required for IL-6 signaling.

    Article Snippet: According to experimental protocols, recombinant rat TNF-α (ImmunoTools), recombinant rat IL-6 (Life Technologies), recombinant sgp130, recombinant human IL-6, and/or recombinant human sIL-6R (R & D Systems) were then applied directly in Tyrode's solution onto the spinal cord surface into the trough over the recording site at a concentration of 1 μg/ml.

    Techniques:

    Induction of hyperexcitability of deep dorsal horn neurons by TNF-α via IL-6/sIL-6R. A , Hypothetical flow chart of an upstream function of TNF-α initiating the release of IL-6 and sIL-6R from different sources to form the downstream IL-6/sIL-6R complex for IL-6 trans -signaling. Indicated are the action sites of specific inhibitors. B , Increases of neuronal responses to mechanical stimulation by spinal application of IL-6/sIL-6R ( n = 6) and spinal application of IL-6/sIL-6R plus etanercept ( n = 6) for 2 h, shown as mean number of action potentials per 15 s (mean APs/15 s) ± SEM for intervals of 30 min. Baseline values (in APs/15 s) in the IL-6/sIL-6R group: innocuous pressure knee 154.5 ± 23.2, noxious pressure knee 357.8 ± 43.1, innocuous pressure ankle 67.0 ± 28.7, noxious pressure ankle 470.4 ± 80.7. Baseline values (in APs/15 s) in the IL-6/sIL-6R plus etanercept group: innocuous pressure knee 81.6 ± 47.8, noxious pressure knee 298.3 ± 84.6, innocuous pressure ankle 53.8 ± 44.0, noxious pressure ankle 322.7 ± 135.4. C , Increases of neuronal responses to mechanical stimulation by spinal application of TNF-α plus minocycline ( n = 11) or IL-6/sIL-6R plus minocycline ( n = 8) for 2 h, shown as mean number of action potentials per 15 s (mean APs/15 s) ± SEM for intervals of 30 min. Baseline values (in APs/15 s) in the TNF-α plus minocycline group: innocuous pressure knee 288.3 ± 105.2, noxious pressure knee 636.8 ± 113.0, innocuous pressure ankle 260.9 ± 69.8, noxious pressure ankle 482.9 ± 84.8. Baseline values (in APs/15 s) in the IL-6/sIL-6R plus minocycline group: innocuous pressure knee 98.4 ± 34.4, noxious pressure knee 292.5 ± 53.1, innocuous pressure ankle 56.4 ± 36.1, noxious pressure ankle 261.2 ± 54.4. Asterisks with arrow indicate the start of significant increases of responses or significant increase of responses at the specific time point ( p

    Journal: The Journal of Neuroscience

    Article Title: Involvement of Spinal IL-6 Trans-Signaling in the Induction of Hyperexcitability of Deep Dorsal Horn Neurons by Spinal Tumor Necrosis Factor-Alpha

    doi: 10.1523/JNEUROSCI.4159-15.2016

    Figure Lengend Snippet: Induction of hyperexcitability of deep dorsal horn neurons by TNF-α via IL-6/sIL-6R. A , Hypothetical flow chart of an upstream function of TNF-α initiating the release of IL-6 and sIL-6R from different sources to form the downstream IL-6/sIL-6R complex for IL-6 trans -signaling. Indicated are the action sites of specific inhibitors. B , Increases of neuronal responses to mechanical stimulation by spinal application of IL-6/sIL-6R ( n = 6) and spinal application of IL-6/sIL-6R plus etanercept ( n = 6) for 2 h, shown as mean number of action potentials per 15 s (mean APs/15 s) ± SEM for intervals of 30 min. Baseline values (in APs/15 s) in the IL-6/sIL-6R group: innocuous pressure knee 154.5 ± 23.2, noxious pressure knee 357.8 ± 43.1, innocuous pressure ankle 67.0 ± 28.7, noxious pressure ankle 470.4 ± 80.7. Baseline values (in APs/15 s) in the IL-6/sIL-6R plus etanercept group: innocuous pressure knee 81.6 ± 47.8, noxious pressure knee 298.3 ± 84.6, innocuous pressure ankle 53.8 ± 44.0, noxious pressure ankle 322.7 ± 135.4. C , Increases of neuronal responses to mechanical stimulation by spinal application of TNF-α plus minocycline ( n = 11) or IL-6/sIL-6R plus minocycline ( n = 8) for 2 h, shown as mean number of action potentials per 15 s (mean APs/15 s) ± SEM for intervals of 30 min. Baseline values (in APs/15 s) in the TNF-α plus minocycline group: innocuous pressure knee 288.3 ± 105.2, noxious pressure knee 636.8 ± 113.0, innocuous pressure ankle 260.9 ± 69.8, noxious pressure ankle 482.9 ± 84.8. Baseline values (in APs/15 s) in the IL-6/sIL-6R plus minocycline group: innocuous pressure knee 98.4 ± 34.4, noxious pressure knee 292.5 ± 53.1, innocuous pressure ankle 56.4 ± 36.1, noxious pressure ankle 261.2 ± 54.4. Asterisks with arrow indicate the start of significant increases of responses or significant increase of responses at the specific time point ( p

    Article Snippet: According to experimental protocols, recombinant rat TNF-α (ImmunoTools), recombinant rat IL-6 (Life Technologies), recombinant sgp130, recombinant human IL-6, and/or recombinant human sIL-6R (R & D Systems) were then applied directly in Tyrode's solution onto the spinal cord surface into the trough over the recording site at a concentration of 1 μg/ml.

    Techniques: Flow Cytometry