il 17  (R&D Systems)

 
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    Name:
    Recombinant Human IFN alpha I alpha 17 Protein
    Description:
    The Recombinant Human IFN alpha I alpha 17 Protein from R D Systems is derived from E coli The Recombinant Human IFN alpha I alpha 17 Protein has been validated for the following applications Bioactivity
    Catalog Number:
    11150-1
    Price:
    299
    Category:
    Proteins and Enzymes
    Source:
    E. coli-derived Recombinant Human IFN-alpha I (alpha 17) Protein
    Applications:
    Bioactivity
    Purity:
    >95%, by SDS-PAGE under reducing conditions and visualized by Colloidal Coomassie« Blue stain.
    Conjugate:
    Unconjugated
    Size:
    100000 UN
    Buy from Supplier


    Structured Review

    R&D Systems il 17
    Both, C5aR1 and C5aR2 knockout PT + HS mice show attenuated BAL IL-6 and <t>IL-17</t> but do not alter PMN recruitment. BAL samples were tested for ( A ) number of PMNs, ( B ) total protein content, ( C ) IL-6 and ( D ) IL-17. ( E ) Plasma CC16 levels. Kruskal–Wallis test was performed with Dunn’s post-hoc analysis, where *, denotes p
    The Recombinant Human IFN alpha I alpha 17 Protein from R D Systems is derived from E coli The Recombinant Human IFN alpha I alpha 17 Protein has been validated for the following applications Bioactivity
    https://www.bioz.com/result/il 17/product/R&D Systems
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 17 - by Bioz Stars, 2021-05
    94/100 stars

    Images

    1) Product Images from "Role of the C5a-C5a receptor axis in the inflammatory responses of the lungs after experimental polytrauma and hemorrhagic shock"

    Article Title: Role of the C5a-C5a receptor axis in the inflammatory responses of the lungs after experimental polytrauma and hemorrhagic shock

    Journal: Scientific Reports

    doi: 10.1038/s41598-020-79607-1

    Both, C5aR1 and C5aR2 knockout PT + HS mice show attenuated BAL IL-6 and IL-17 but do not alter PMN recruitment. BAL samples were tested for ( A ) number of PMNs, ( B ) total protein content, ( C ) IL-6 and ( D ) IL-17. ( E ) Plasma CC16 levels. Kruskal–Wallis test was performed with Dunn’s post-hoc analysis, where *, denotes p
    Figure Legend Snippet: Both, C5aR1 and C5aR2 knockout PT + HS mice show attenuated BAL IL-6 and IL-17 but do not alter PMN recruitment. BAL samples were tested for ( A ) number of PMNs, ( B ) total protein content, ( C ) IL-6 and ( D ) IL-17. ( E ) Plasma CC16 levels. Kruskal–Wallis test was performed with Dunn’s post-hoc analysis, where *, denotes p

    Techniques Used: Knock-Out, Mouse Assay

    2) Product Images from "Interleukin‐17/interleukin‐17 receptor axis elicits intestinal neutrophil migration, restrains gut dysbiosis and lipopolysaccharide translocation in high‐fat diet‐induced metabolic syndrome model"

    Article Title: Interleukin‐17/interleukin‐17 receptor axis elicits intestinal neutrophil migration, restrains gut dysbiosis and lipopolysaccharide translocation in high‐fat diet‐induced metabolic syndrome model

    Journal: Immunology

    doi: 10.1111/imm.13028

    Nutritional and metabolic parameters for wild‐type (WT) mice and mice lacking the interleukin‐17 (IL‐17) cytokine receptor (IL‐17RA −/− ) at 9 weeks of control diet (CD) or high‐fat diet (HFD). Time course of body weight (a), body weight gain (b), food intake (c) and fat content in feces (d) of WT or IL‐17RA −/− mice fed either a CD or an HFD. Blood glucose levels after fasting (e) and after the glucose tolerance test (GTT) (f); area under the curve for the GTT (g), insulin tolerance test (ITT) (h) and area under the curve for the ITT (i) in WT and IL‐17RA −/− mice fed a CD or an HFD. Concentrations of insulin (j), triglycerides (k) and cholesterol (l) were determined in the serum of these mice. Values are expressed as mean ± SEM. * P
    Figure Legend Snippet: Nutritional and metabolic parameters for wild‐type (WT) mice and mice lacking the interleukin‐17 (IL‐17) cytokine receptor (IL‐17RA −/− ) at 9 weeks of control diet (CD) or high‐fat diet (HFD). Time course of body weight (a), body weight gain (b), food intake (c) and fat content in feces (d) of WT or IL‐17RA −/− mice fed either a CD or an HFD. Blood glucose levels after fasting (e) and after the glucose tolerance test (GTT) (f); area under the curve for the GTT (g), insulin tolerance test (ITT) (h) and area under the curve for the ITT (i) in WT and IL‐17RA −/− mice fed a CD or an HFD. Concentrations of insulin (j), triglycerides (k) and cholesterol (l) were determined in the serum of these mice. Values are expressed as mean ± SEM. * P

    Techniques Used: Mouse Assay

    Expression of total and phosphorylated forms of phosphatidylinositol‐4,5‐bisphosphate 3‐kinase (PI3K) and serine/threonine‐specific protein kinase (AKT) in skeletal muscle and histopathological analysis of pancreatic tissues of wild‐type (WT) mice and mice lacking the interleukin‐17 (IL‐17) cytokine receptor (IL‐17RA −/− ) fed a control diet (CD) or a high‐fat diet (HFD) for 9 weeks. Representative images of total and phosphorylated PI3K and AKT expression (a, d). Quantification of phosphorylated and total PI3K (b, c) and AKT (e, f) by densitometry. The skeletal muscle was collected 5 min after administration of insulin in a concentration of 3·8 IU/kg body weight. Pancreatic histological sections were fixed and stained with hematoxylin eosin (g, top panels) or immunostained for insulin by immunohistochemistry (g, bottom panels). Values are expressed as mean ± SEM. * P
    Figure Legend Snippet: Expression of total and phosphorylated forms of phosphatidylinositol‐4,5‐bisphosphate 3‐kinase (PI3K) and serine/threonine‐specific protein kinase (AKT) in skeletal muscle and histopathological analysis of pancreatic tissues of wild‐type (WT) mice and mice lacking the interleukin‐17 (IL‐17) cytokine receptor (IL‐17RA −/− ) fed a control diet (CD) or a high‐fat diet (HFD) for 9 weeks. Representative images of total and phosphorylated PI3K and AKT expression (a, d). Quantification of phosphorylated and total PI3K (b, c) and AKT (e, f) by densitometry. The skeletal muscle was collected 5 min after administration of insulin in a concentration of 3·8 IU/kg body weight. Pancreatic histological sections were fixed and stained with hematoxylin eosin (g, top panels) or immunostained for insulin by immunohistochemistry (g, bottom panels). Values are expressed as mean ± SEM. * P

    Techniques Used: Expressing, Mouse Assay, Concentration Assay, Staining, Immunohistochemistry

    Histopathological analysis of the liver and small intestine (ileum) and gene expression of claudin‐2, occludin, mucin‐1 and mucin‐2 in the ileum of the wild‐type (WT) and mice lacking the interleukin‐17 (IL‐17) cytokine receptor (IL‐17RA −/− ) fed a control diet (CD) or a high‐fat diet (HFD) for 9 weeks. Histological sections of the livers (a, top panels) and the ileum (a, bottom panels) were fixed and stained with hematoxylin eosin. Gene expression of claudin‐2 (b), occludin (c), muc‐1 (d) and muc‐2 (e) in the ileum by RT‐PCR. Values are expressed as mean ± SEM. * P
    Figure Legend Snippet: Histopathological analysis of the liver and small intestine (ileum) and gene expression of claudin‐2, occludin, mucin‐1 and mucin‐2 in the ileum of the wild‐type (WT) and mice lacking the interleukin‐17 (IL‐17) cytokine receptor (IL‐17RA −/− ) fed a control diet (CD) or a high‐fat diet (HFD) for 9 weeks. Histological sections of the livers (a, top panels) and the ileum (a, bottom panels) were fixed and stained with hematoxylin eosin. Gene expression of claudin‐2 (b), occludin (c), muc‐1 (d) and muc‐2 (e) in the ileum by RT‐PCR. Values are expressed as mean ± SEM. * P

    Techniques Used: Expressing, Mouse Assay, Staining, Reverse Transcription Polymerase Chain Reaction

    Evaluation of intestinal dysbiosis, permeability, bacterial translocation and lipopolysaccharide (LPS) levels in blood and visceral adipose tissue (VAT) of wild‐type (WT) mice and mice lacking the interleukin‐17 (IL‐17) cytokine receptor (IL‐17RA −/− ) fed a control diet (CD) or a high‐fat diet (HFD) for 9 weeks. Relative abundance of fecal bacterial phylum (a) and genera (b) was evaluated by 16S rRNA gene sequencing. FITC‐Dextran concentration (c), number of colony forming units (CFU) (d), LPS levels in the serum or visceral adipose tissue (VAT) (e) A. muciniphila relative levels in the feces were determined by qPCR (f) were determined. Values are expressed as mean ± SEM. * P
    Figure Legend Snippet: Evaluation of intestinal dysbiosis, permeability, bacterial translocation and lipopolysaccharide (LPS) levels in blood and visceral adipose tissue (VAT) of wild‐type (WT) mice and mice lacking the interleukin‐17 (IL‐17) cytokine receptor (IL‐17RA −/− ) fed a control diet (CD) or a high‐fat diet (HFD) for 9 weeks. Relative abundance of fecal bacterial phylum (a) and genera (b) was evaluated by 16S rRNA gene sequencing. FITC‐Dextran concentration (c), number of colony forming units (CFU) (d), LPS levels in the serum or visceral adipose tissue (VAT) (e) A. muciniphila relative levels in the feces were determined by qPCR (f) were determined. Values are expressed as mean ± SEM. * P

    Techniques Used: Permeability, Translocation Assay, Mouse Assay, Sequencing, Concentration Assay, Real-time Polymerase Chain Reaction

    Gene and protein expression of the T helper type 17 (Th17) pattern‐related cytokines in the ileum and Th17 or interleukin‐17 (IL‐17) ‐producing γδ cell numbers in the mesenteric lymph nodes (MLN) of wild‐type (WT) mice at 9 weeks of control diet (CD) or high‐fat diet (HFD). Gene and protein expression of IL‐6 (a), tumor necrosis factor‐ α (TNF‐ α ) (b) IL‐17A (c) and IL‐22 (d) cytokines in the ileum, by RT‐PCR and ELISA, respectively. Percentage of Th17 (CD4 + CD3 + IL‐17 + ) and IL‐17‐producing γδ cells (CD3 + γδ + IL‐17 + ) in the MLN by FACS (e, g). Percentage of Th17 and IL‐17‐producing γδ cells is shown in representative dot plots (f, h). Values are expressed as mean ± SEM. * P
    Figure Legend Snippet: Gene and protein expression of the T helper type 17 (Th17) pattern‐related cytokines in the ileum and Th17 or interleukin‐17 (IL‐17) ‐producing γδ cell numbers in the mesenteric lymph nodes (MLN) of wild‐type (WT) mice at 9 weeks of control diet (CD) or high‐fat diet (HFD). Gene and protein expression of IL‐6 (a), tumor necrosis factor‐ α (TNF‐ α ) (b) IL‐17A (c) and IL‐22 (d) cytokines in the ileum, by RT‐PCR and ELISA, respectively. Percentage of Th17 (CD4 + CD3 + IL‐17 + ) and IL‐17‐producing γδ cells (CD3 + γδ + IL‐17 + ) in the MLN by FACS (e, g). Percentage of Th17 and IL‐17‐producing γδ cells is shown in representative dot plots (f, h). Values are expressed as mean ± SEM. * P

    Techniques Used: Expressing, Mouse Assay, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, FACS

    Percentage and absolute number of cells in mesenteric lymph nodes (MLN) and elastase protein levels, CXCR‐2 and CXCL‐1 gene expression in the ileum of mice lacking the interleukin‐17 (IL‐17) cytokine receptor (IL‐17RA −/− ) fed a control diet (CD) or a high‐fat diet (HFD) for 9 weeks. Percentage and absolute number of neutrophils (CD11b + Ly6G + ) (a, d), dendritic cells (CD11b + CD103 + ) (b, e) and macrophages (CD11b + CX3CR1 + ) (c, f) in MLN, determined by FACS. Percentages of neutrophils, dendritic cells or macrophages are shown in representative dot plots (g). Elastase concentration (h), CXCR‐2 (i) and CXCL‐1 (j) gene expression were quantified in the ileum by ELISA and RT‐PCR, respectively. Values are expressed as mean ± SEM. * P
    Figure Legend Snippet: Percentage and absolute number of cells in mesenteric lymph nodes (MLN) and elastase protein levels, CXCR‐2 and CXCL‐1 gene expression in the ileum of mice lacking the interleukin‐17 (IL‐17) cytokine receptor (IL‐17RA −/− ) fed a control diet (CD) or a high‐fat diet (HFD) for 9 weeks. Percentage and absolute number of neutrophils (CD11b + Ly6G + ) (a, d), dendritic cells (CD11b + CD103 + ) (b, e) and macrophages (CD11b + CX3CR1 + ) (c, f) in MLN, determined by FACS. Percentages of neutrophils, dendritic cells or macrophages are shown in representative dot plots (g). Elastase concentration (h), CXCR‐2 (i) and CXCL‐1 (j) gene expression were quantified in the ileum by ELISA and RT‐PCR, respectively. Values are expressed as mean ± SEM. * P

    Techniques Used: Expressing, Mouse Assay, FACS, Concentration Assay, Enzyme-linked Immunosorbent Assay, Reverse Transcription Polymerase Chain Reaction

    Gene expression of the interleukin‐17 receptor (IL‐17R) and CXCL‐1 or CXCL‐2 protein expression in epithelial cells (EC) and in intestinal lamina propria (ILP) cells stimulated with recombinant IL‐17 (rIL‐17). Cells were isolated from wild‐type (WT) mice fed the control diet (CD) or high‐fat diet (HFD). Relative expression of IL‐17RA in EC or ILP (a, d). After stimulation of cells for 24 hr with culture medium or recombinant IL‐17 (rIL‐17) at concentrations of 10 or 100 ng/ml, supernatants were collected from EC (b, c) or from ILP cells (e, f). Quantification of CXCL‐1 and CXCL‐2 chemokines was performed by ELISA. Values are expressed as mean ± SEM. * P
    Figure Legend Snippet: Gene expression of the interleukin‐17 receptor (IL‐17R) and CXCL‐1 or CXCL‐2 protein expression in epithelial cells (EC) and in intestinal lamina propria (ILP) cells stimulated with recombinant IL‐17 (rIL‐17). Cells were isolated from wild‐type (WT) mice fed the control diet (CD) or high‐fat diet (HFD). Relative expression of IL‐17RA in EC or ILP (a, d). After stimulation of cells for 24 hr with culture medium or recombinant IL‐17 (rIL‐17) at concentrations of 10 or 100 ng/ml, supernatants were collected from EC (b, c) or from ILP cells (e, f). Quantification of CXCL‐1 and CXCL‐2 chemokines was performed by ELISA. Values are expressed as mean ± SEM. * P

    Techniques Used: Expressing, Recombinant, Isolation, Mouse Assay, Enzyme-linked Immunosorbent Assay

    3) Product Images from "Ablation of RhoA impairs Th17 cell differentiation and alleviates house dust mite-triggered allergic airway inflammation"

    Article Title: Ablation of RhoA impairs Th17 cell differentiation and alleviates house dust mite-triggered allergic airway inflammation

    Journal: Journal of leukocyte biology

    doi: 10.1002/JLB.3A0119-025RRR

    RhoA specific inhibitor Y16 blocks Th17 differentiation. ( A ) Purified naïve CD4 + T cells (1 × 10 6 /mL) pooled from 8 WT mice were stimulated with plate-bound anti-CD3 plus free anti-CD28 for 2 days without or with Y16 (0~50 μM). IL-17 and IL-21 in the culture supernatants were determined by ELISA. ( B - D ) Naïve CD4 + T cells were differentiated under Th17 conditions for 4 days and restimulated with PMA plus ionomycin for 5 h, in the presence of vehicle (Veh) or Y16 (30 μM) throughout the culture. Cells were collected for IL-17/IFN-γ intracellular staining. Percentages of IL-17 + or IFN-γ + CD4 + T cells are shown in representative dot plots ( B ) and summarized in a bar graph ( C ). IL-17 and IL-21 in the culture supernatants were determined by ELISA ( D ). Data are representative of 2 independent experiments. ** P
    Figure Legend Snippet: RhoA specific inhibitor Y16 blocks Th17 differentiation. ( A ) Purified naïve CD4 + T cells (1 × 10 6 /mL) pooled from 8 WT mice were stimulated with plate-bound anti-CD3 plus free anti-CD28 for 2 days without or with Y16 (0~50 μM). IL-17 and IL-21 in the culture supernatants were determined by ELISA. ( B - D ) Naïve CD4 + T cells were differentiated under Th17 conditions for 4 days and restimulated with PMA plus ionomycin for 5 h, in the presence of vehicle (Veh) or Y16 (30 μM) throughout the culture. Cells were collected for IL-17/IFN-γ intracellular staining. Percentages of IL-17 + or IFN-γ + CD4 + T cells are shown in representative dot plots ( B ) and summarized in a bar graph ( C ). IL-17 and IL-21 in the culture supernatants were determined by ELISA ( D ). Data are representative of 2 independent experiments. ** P

    Techniques Used: Purification, Mouse Assay, Enzyme-linked Immunosorbent Assay, Staining

    RhoA deficiency dampens Th17 differentiation. ( A and B ) Purified CD4 + T cells were differentiated under Th17-polarizing conditions (TGF- β 1 + IL-6) for 4 days and restimulated with PMA plus ionomycin for 5 h with BD GolgiPlug in the last 2 h. Cells were collected for IL-17 intracellular staining. Percentages of IL-17 + cells are shown in representative dot plots ( A ) and summarized in a bar graph ( B ). ( C and D ) Supernatants were collected from CD4 + T cells stimulated with or without anti-CD3/CD28 mAbs ( C ) or differentiated under Th17-polarizing conditions and restimulated with PMA/ionomycin ( D )for ELISA assays of IL-17. ( E ) Total RNA was extracted from the cultured cells for real-time PCR analysis. The mRNA levels of Th17 effector cytokines as indicated are shown (arbitrary unit). The data are normalized to an 18S reference. Results ( B - E ) are expressed as mean + SD of triplicates, representative of 3 independent experiments. * P
    Figure Legend Snippet: RhoA deficiency dampens Th17 differentiation. ( A and B ) Purified CD4 + T cells were differentiated under Th17-polarizing conditions (TGF- β 1 + IL-6) for 4 days and restimulated with PMA plus ionomycin for 5 h with BD GolgiPlug in the last 2 h. Cells were collected for IL-17 intracellular staining. Percentages of IL-17 + cells are shown in representative dot plots ( A ) and summarized in a bar graph ( B ). ( C and D ) Supernatants were collected from CD4 + T cells stimulated with or without anti-CD3/CD28 mAbs ( C ) or differentiated under Th17-polarizing conditions and restimulated with PMA/ionomycin ( D )for ELISA assays of IL-17. ( E ) Total RNA was extracted from the cultured cells for real-time PCR analysis. The mRNA levels of Th17 effector cytokines as indicated are shown (arbitrary unit). The data are normalized to an 18S reference. Results ( B - E ) are expressed as mean + SD of triplicates, representative of 3 independent experiments. * P

    Techniques Used: Purification, Staining, Enzyme-linked Immunosorbent Assay, Cell Culture, Real-time Polymerase Chain Reaction

    4) Product Images from "Morphine Disrupts Interleukin-23 (IL-23)/IL-17-Mediated Pulmonary Mucosal Host Defense against Streptococcuspneumoniae Infection ▿"

    Article Title: Morphine Disrupts Interleukin-23 (IL-23)/IL-17-Mediated Pulmonary Mucosal Host Defense against Streptococcuspneumoniae Infection ▿

    Journal:

    doi: 10.1128/IAI.00914-09

    Effect of morphine treatment on IL-23/IL-17 production and bacterial clearance in TCRδ −/− and WT mice. IL-23 and IL-17 concentrations are shown at 4 h after intranasal infection with S. pneumoniae . Bacterial burden is shown at
    Figure Legend Snippet: Effect of morphine treatment on IL-23/IL-17 production and bacterial clearance in TCRδ −/− and WT mice. IL-23 and IL-17 concentrations are shown at 4 h after intranasal infection with S. pneumoniae . Bacterial burden is shown at

    Techniques Used: Mouse Assay, Infection

    Levels of IL-23 (A) and IL-17 (B), recruitment of neutrophils (C), and bacterial burden (D) in the lung tissues and BAL fluids in morphine-treated and placebo-treated control mice. Data are expressed as the mean ± SEM of the results for three
    Figure Legend Snippet: Levels of IL-23 (A) and IL-17 (B), recruitment of neutrophils (C), and bacterial burden (D) in the lung tissues and BAL fluids in morphine-treated and placebo-treated control mice. Data are expressed as the mean ± SEM of the results for three

    Techniques Used: Mouse Assay

    Protein production and mRNA expression of IL-23 and IL-17 in the lungs, BAL fluids, and cells after S. pneumoniae infection. Mice were intranasally infected (10 7 CFU per mouse) with S. pneumoniae (serotype 3). At various time points postinfection, lung
    Figure Legend Snippet: Protein production and mRNA expression of IL-23 and IL-17 in the lungs, BAL fluids, and cells after S. pneumoniae infection. Mice were intranasally infected (10 7 CFU per mouse) with S. pneumoniae (serotype 3). At various time points postinfection, lung

    Techniques Used: Expressing, Infection, Mouse Assay

    5) Product Images from "High plasma levels of pro-inflammatory factors interleukin-17 and interleukin-23 are associated with poor outcome of cardiac-arrest patients: a single center experience"

    Article Title: High plasma levels of pro-inflammatory factors interleukin-17 and interleukin-23 are associated with poor outcome of cardiac-arrest patients: a single center experience

    Journal: BMC Cardiovascular Disorders

    doi: 10.1186/s12872-020-01451-y

    Association between plasma levels of IL-17/IL-23 axis and APACHE II score or time to ROSC in PCAS patients. ( a-b ) Pearson linear regression analyses showed there were no associations between plasma IL-17 ( a ) and IL-23 ( b ) levels and APACHE II score at three time-points (1 h, 2 days and 7 days post ROSC). ( c-d ) Pearson linear regression analyses showed there were no associations between plasma IL-17 ( c ) and IL-23 ( d ) levels and time to ROSC at three time-points (1 h, 2 days and 7 days post ROSC)
    Figure Legend Snippet: Association between plasma levels of IL-17/IL-23 axis and APACHE II score or time to ROSC in PCAS patients. ( a-b ) Pearson linear regression analyses showed there were no associations between plasma IL-17 ( a ) and IL-23 ( b ) levels and APACHE II score at three time-points (1 h, 2 days and 7 days post ROSC). ( c-d ) Pearson linear regression analyses showed there were no associations between plasma IL-17 ( c ) and IL-23 ( d ) levels and time to ROSC at three time-points (1 h, 2 days and 7 days post ROSC)

    Techniques Used:

    Plasma levels of IL-17 and IL-23 are potential predictors of survival in PCAS patients. ROC curves for plasma levels of IL-17, IL-23, IL-22 and IL-33 at three time-points (1 h, 2 days and 7 days post ROSC) were assessed as possible predictors of survival in PCAS patients. The area under the curve (AUC), standard error of the mean (SEM), 95% confidence interval (95% CI) and P value were also illustrated
    Figure Legend Snippet: Plasma levels of IL-17 and IL-23 are potential predictors of survival in PCAS patients. ROC curves for plasma levels of IL-17, IL-23, IL-22 and IL-33 at three time-points (1 h, 2 days and 7 days post ROSC) were assessed as possible predictors of survival in PCAS patients. The area under the curve (AUC), standard error of the mean (SEM), 95% confidence interval (95% CI) and P value were also illustrated

    Techniques Used:

    The plasma levels of four kinds of pro-inflammatory factors in PCAS patients at three time-points. ( a ) Violin plot shows the plasma levels of IL-17, IL-23, IL-22 and IL-33 in PCAS patients at three time-points (1 h, 2 days and 7 days post ROSC). The thick dotted line in violin plot indicates the median, whereas the two solid thin lines indicate the upper and lower quartiles. ( b ) Scatter plot shows the comparison of plasma levels of IL-17, IL-23, IL-22 and IL-33 in survivors and non-survivors of PCAS patients at three time-points (1 h, 2 days and 7 days post ROSC). ** P
    Figure Legend Snippet: The plasma levels of four kinds of pro-inflammatory factors in PCAS patients at three time-points. ( a ) Violin plot shows the plasma levels of IL-17, IL-23, IL-22 and IL-33 in PCAS patients at three time-points (1 h, 2 days and 7 days post ROSC). The thick dotted line in violin plot indicates the median, whereas the two solid thin lines indicate the upper and lower quartiles. ( b ) Scatter plot shows the comparison of plasma levels of IL-17, IL-23, IL-22 and IL-33 in survivors and non-survivors of PCAS patients at three time-points (1 h, 2 days and 7 days post ROSC). ** P

    Techniques Used:

    6) Product Images from "Apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes mediated by SIRT1"

    Article Title: Apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes mediated by SIRT1

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm.2021.4845

    Knockdown of SIRT1 abolishes the protective effects of apremilast against IL-17-induced cellular senescence and the expression levels of p21 and PAI-1. Cells were transfected with SIRT1 siRNA, followed by stimulation with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) Cellular senescence. (B) mRNA levels of p21 and PAI-1. (C) Protein levels of p21 and PAI-1 as measured by western blotting. #### P
    Figure Legend Snippet: Knockdown of SIRT1 abolishes the protective effects of apremilast against IL-17-induced cellular senescence and the expression levels of p21 and PAI-1. Cells were transfected with SIRT1 siRNA, followed by stimulation with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) Cellular senescence. (B) mRNA levels of p21 and PAI-1. (C) Protein levels of p21 and PAI-1 as measured by western blotting. #### P

    Techniques Used: Expressing, Transfection, Western Blot

    Graphical representation of the underlying mechanism, whereby apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes. IL, interleukin; ROS, reactive oxygen species; SIRT1, sirtuin 1; MCP-1, monocyte chemoattractant protein-1; PAI-1, plasminogen activator inhibitor-1.
    Figure Legend Snippet: Graphical representation of the underlying mechanism, whereby apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes. IL, interleukin; ROS, reactive oxygen species; SIRT1, sirtuin 1; MCP-1, monocyte chemoattractant protein-1; PAI-1, plasminogen activator inhibitor-1.

    Techniques Used:

    Apremilast prevents IL-17-induced expression and secretions of pro-inflammatory cytokines in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. (A) Molecular structure of apremilast. (B) mRNA levels of IL-1β and MCP-1. (C) Secretions of IL-1β and MCP-1. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced expression and secretions of pro-inflammatory cytokines in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. (A) Molecular structure of apremilast. (B) mRNA levels of IL-1β and MCP-1. (C) Secretions of IL-1β and MCP-1. #### P

    Techniques Used: Expressing

    Apremilast prevents IL-17-induced cell cycle arrest in the G0/G1 phase in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. The cell cycle was assayed using flow cytometry. G0/G1 phase, G2/M phase, and S phase of cells were measured. ## P
    Figure Legend Snippet: Apremilast prevents IL-17-induced cell cycle arrest in the G0/G1 phase in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. The cell cycle was assayed using flow cytometry. G0/G1 phase, G2/M phase, and S phase of cells were measured. ## P

    Techniques Used: Flow Cytometry

    Apremilast prevents IL-17-induced reduction of SIRT1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of a Apremilast (1 µ M) for 24 h. (A) mRNA of SIRT1. (B) Protein level of SIRT1. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced reduction of SIRT1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of a Apremilast (1 µ M) for 24 h. (A) mRNA of SIRT1. (B) Protein level of SIRT1. #### P

    Techniques Used:

    Apremilast prevents IL-17-induced expression of p21 and PAI-1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) mRNA levels of p21 and PAI-1. (B) Protein levels of p21 and PAI-1 as measured by western blotting. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced expression of p21 and PAI-1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) mRNA levels of p21 and PAI-1. (B) Protein levels of p21 and PAI-1 as measured by western blotting. #### P

    Techniques Used: Expressing, Western Blot

    Apremilast prevents IL-17-induced cellular senescence in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. Cellular senescence was measured using SA-β-gal staining. ## P
    Figure Legend Snippet: Apremilast prevents IL-17-induced cellular senescence in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. Cellular senescence was measured using SA-β-gal staining. ## P

    Techniques Used: Staining

    Apremilast prevents IL-17-induced production of ROS in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. Production of ROS was measured using DCFH-DA staining (magnification, ×10). #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced production of ROS in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. Production of ROS was measured using DCFH-DA staining (magnification, ×10). #### P

    Techniques Used: Staining

    7) Product Images from "IL-17 is a potential biomarker for predicting the severity and outcomes of pulmonary contusion in trauma patients"

    Article Title: IL-17 is a potential biomarker for predicting the severity and outcomes of pulmonary contusion in trauma patients

    Journal: Biomedical Reports

    doi: 10.3892/br.2020.1381

    ROC curves of IL-17 for predicting the in-hospital outcomes of patients. (A) ROC curves for IL-17 (day 1) and ARDS. AUC, 0.770; standard error, 0.047; 95% CI, 0.679-0.862; P
    Figure Legend Snippet: ROC curves of IL-17 for predicting the in-hospital outcomes of patients. (A) ROC curves for IL-17 (day 1) and ARDS. AUC, 0.770; standard error, 0.047; 95% CI, 0.679-0.862; P

    Techniques Used:

    8) Product Images from "Development of Allergen-induced Airway Inflammation in the Absence of T-bet Regulation is Dependent on IL-17 1"

    Article Title: Development of Allergen-induced Airway Inflammation in the Absence of T-bet Regulation is Dependent on IL-17 1

    Journal:

    doi: 10.4049/jimmunol.0803109

    IL-17 production is increased in the lungs of T-bet −/− mice following OVA-induced allergic lung inflammation
    Figure Legend Snippet: IL-17 production is increased in the lungs of T-bet −/− mice following OVA-induced allergic lung inflammation

    Techniques Used: Mouse Assay

    IL-17 mediates allergen-induced airway inflammation in T-bet −/− mice
    Figure Legend Snippet: IL-17 mediates allergen-induced airway inflammation in T-bet −/− mice

    Techniques Used: Mouse Assay

    IL-17 receptor signaling is critical for antigen induced airway inflammation
    Figure Legend Snippet: IL-17 receptor signaling is critical for antigen induced airway inflammation

    Techniques Used:

    IL-25 (IL-17E) production in the lungs of OVA-sensitized and challenged mice
    Figure Legend Snippet: IL-25 (IL-17E) production in the lungs of OVA-sensitized and challenged mice

    Techniques Used: Mouse Assay

    9) Product Images from "IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes. IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes"

    Article Title: IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes. IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes

    Journal: Journal of Cellular Physiology

    doi: 10.1002/jcp.29323

    IL‐17 enhances the osteogenic differentiation of mMSCs but not MC3T3‐E1. (a,b) Increased mineralized nodule formation (red) in mesenchymal stem cells (MSCs) and MLO‐Y4 osteocytes after treatment with 0.5–50 ng/ml IL‐17 in osteogenic induction medium for 14 days. Mineralization of MC3T3‐E1 cells was inhibited, and there was no change in mineralization levels in MLO‐A5 cells. (c,d) Alkaline phosphatase (ALP) expression (purple) of MSCs was enhanced by IL‐17 (7 days). (e,f) mRNA expression of factors after IL‐17 treatment for 24 hr. Treatment with IL‐17 increased runt‐related transcription factor 2 (RUNX2), collagen‐1 (COL‐1) and osteocalcin (OCN) in MSCs, and only RUNX2 in MLO‐Y4 cells. All three factors were decreased in MC3T3‐E1 cells and no significant changes were measured in MLO‐A5 cells. (f) IL‐17 receptor A (RA) and IL‐6 were upregulated in MSCs and MLO‐Y4 cells, and IL‐β was significantly upregulated in MSCs. IL, interleukin; mMSC, mouse MSCs; mRNA, messenger RNA
    Figure Legend Snippet: IL‐17 enhances the osteogenic differentiation of mMSCs but not MC3T3‐E1. (a,b) Increased mineralized nodule formation (red) in mesenchymal stem cells (MSCs) and MLO‐Y4 osteocytes after treatment with 0.5–50 ng/ml IL‐17 in osteogenic induction medium for 14 days. Mineralization of MC3T3‐E1 cells was inhibited, and there was no change in mineralization levels in MLO‐A5 cells. (c,d) Alkaline phosphatase (ALP) expression (purple) of MSCs was enhanced by IL‐17 (7 days). (e,f) mRNA expression of factors after IL‐17 treatment for 24 hr. Treatment with IL‐17 increased runt‐related transcription factor 2 (RUNX2), collagen‐1 (COL‐1) and osteocalcin (OCN) in MSCs, and only RUNX2 in MLO‐Y4 cells. All three factors were decreased in MC3T3‐E1 cells and no significant changes were measured in MLO‐A5 cells. (f) IL‐17 receptor A (RA) and IL‐6 were upregulated in MSCs and MLO‐Y4 cells, and IL‐β was significantly upregulated in MSCs. IL, interleukin; mMSC, mouse MSCs; mRNA, messenger RNA

    Techniques Used: Expressing

    Osteogenic differentiation of mesenchymal stem cells (MSCs) after coculture (CC) with osteocytes is further enhanced by interleukin‐17 (IL‐17). (a) We used a transwell CC system, with MSCs seeded in the lower chamber and various osteogenic cells in the upper chambers. Cells were grown in osteoinductive media (OM) with or without IL‐17. MSCs in both the upper and lower chambers served as a control. (b,c) Alizarin red staining to detect mineralized nodule formation (red) in the lower chambers following CC with or without IL‐17 stimulation (50 ng/ml). IL‐17 enhanced mineralization in control‐MSCs (top row). No obvious change was found for MSCs in MC3T3‐E1 CC and MLO‐A5 CC (second and third rows). An increase in Alizarin red staining was found for MSCs in MLO‐Y4 CC, which was further increased with IL‐17. (d,e) ALP staining and quantification of ALP activity. IL‐17 induced ALP expression (purple) in MSCs under control CC condition (top row). ALP expression was also induced in MSC in CC with MLO‐Y4 cells (bottom row; Day 7). Each experiment was repeated at least three times independently and three different mMSC cell lines were used. ALP, alkaline phosphatase
    Figure Legend Snippet: Osteogenic differentiation of mesenchymal stem cells (MSCs) after coculture (CC) with osteocytes is further enhanced by interleukin‐17 (IL‐17). (a) We used a transwell CC system, with MSCs seeded in the lower chamber and various osteogenic cells in the upper chambers. Cells were grown in osteoinductive media (OM) with or without IL‐17. MSCs in both the upper and lower chambers served as a control. (b,c) Alizarin red staining to detect mineralized nodule formation (red) in the lower chambers following CC with or without IL‐17 stimulation (50 ng/ml). IL‐17 enhanced mineralization in control‐MSCs (top row). No obvious change was found for MSCs in MC3T3‐E1 CC and MLO‐A5 CC (second and third rows). An increase in Alizarin red staining was found for MSCs in MLO‐Y4 CC, which was further increased with IL‐17. (d,e) ALP staining and quantification of ALP activity. IL‐17 induced ALP expression (purple) in MSCs under control CC condition (top row). ALP expression was also induced in MSC in CC with MLO‐Y4 cells (bottom row; Day 7). Each experiment was repeated at least three times independently and three different mMSC cell lines were used. ALP, alkaline phosphatase

    Techniques Used: Staining, Activity Assay, Expressing

    Schematic of the findings of this study. Mesenchymal stem cells (MSCs) exposed to interleukin (IL)‐17 and osteocytes in coculture underwent differentiation along the osteogenic lineage, better than when exposed to either stimulus alone. IL‐17 induces the expression of inflammatory markers, IL‐6 and IL‐1β, which in turn, increase the expression of markers of osteoblastic differentiation in MSCs, such as alkaline phosphatase (ALP), runt‐related transcription factor 2 (RUNX2), osteocalcin (OCN) and collagen‐1 (COL‐1). The activation of extracellular signal‐regulated kinase 1/2 (ERK1/2), AKT, and signal transducer and activator of transcription 3 (STAT3) regulated IL‐17 induced osteogenesis in the MSC niche, which could be inhibited by antibodies of IL‐6 and IL‐1β
    Figure Legend Snippet: Schematic of the findings of this study. Mesenchymal stem cells (MSCs) exposed to interleukin (IL)‐17 and osteocytes in coculture underwent differentiation along the osteogenic lineage, better than when exposed to either stimulus alone. IL‐17 induces the expression of inflammatory markers, IL‐6 and IL‐1β, which in turn, increase the expression of markers of osteoblastic differentiation in MSCs, such as alkaline phosphatase (ALP), runt‐related transcription factor 2 (RUNX2), osteocalcin (OCN) and collagen‐1 (COL‐1). The activation of extracellular signal‐regulated kinase 1/2 (ERK1/2), AKT, and signal transducer and activator of transcription 3 (STAT3) regulated IL‐17 induced osteogenesis in the MSC niche, which could be inhibited by antibodies of IL‐6 and IL‐1β

    Techniques Used: Expressing, Activation Assay

    Three‐dimensional culture of mesenchymal stem cells (MSCs) on a polycaprolactone (PCL) scaffold enhances IL‐17‐stimulated osteogenesis when cocultured with MLO‐Y4 osteocytes. (a) Alizarin red staining shows mineralized nodule formation (red) in mouse MSCs (mMSCs) and human‐induced pluripotent stem cell‐derived MSCs (hMSCs) cultures on Day 10. Growth on the PCL scaffold promoted osteogenesis, and this could be further enhanced by coculture with MLO‐Y4 osteocytes and IL‐17 stimulation. (b) Quantification of mMSCs mineralazation. (c) Quantification of hMSCs mineralization. IL, interleukin
    Figure Legend Snippet: Three‐dimensional culture of mesenchymal stem cells (MSCs) on a polycaprolactone (PCL) scaffold enhances IL‐17‐stimulated osteogenesis when cocultured with MLO‐Y4 osteocytes. (a) Alizarin red staining shows mineralized nodule formation (red) in mouse MSCs (mMSCs) and human‐induced pluripotent stem cell‐derived MSCs (hMSCs) cultures on Day 10. Growth on the PCL scaffold promoted osteogenesis, and this could be further enhanced by coculture with MLO‐Y4 osteocytes and IL‐17 stimulation. (b) Quantification of mMSCs mineralazation. (c) Quantification of hMSCs mineralization. IL, interleukin

    Techniques Used: Staining, Derivative Assay

    Interleukin (IL)‐17 activates intercellular signaling of osteogenesis via IL‐6 and IL‐1β. Anti‐IL‐6 and anti‐IL‐1β antibodies were used in the IL‐17–induced coculture (CC) system. Both antibodies could effectively inhibit (a,b) the formation of mineral nodules, (c) the mRNA expression of ALP, RUNX2, OCN, and COL‐1 and (d) AKT, STAT3, and ERK1/2 phosphorylation in the control‐MSCs CC and MLO‐Y4 CC at Day 14 after IL‐17 treatment; albeit, the effects of IL‐1β neutralization were weaker than that of IL‐6. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3
    Figure Legend Snippet: Interleukin (IL)‐17 activates intercellular signaling of osteogenesis via IL‐6 and IL‐1β. Anti‐IL‐6 and anti‐IL‐1β antibodies were used in the IL‐17–induced coculture (CC) system. Both antibodies could effectively inhibit (a,b) the formation of mineral nodules, (c) the mRNA expression of ALP, RUNX2, OCN, and COL‐1 and (d) AKT, STAT3, and ERK1/2 phosphorylation in the control‐MSCs CC and MLO‐Y4 CC at Day 14 after IL‐17 treatment; albeit, the effects of IL‐1β neutralization were weaker than that of IL‐6. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3

    Techniques Used: Expressing, Neutralization

    Interleukin (IL)‐17 upregulates inflammatory factors, IL‐6 and IL‐1β, and activates ERK, AKT, and STAT3 signaling in mesenchymal stem cells (MSC)–MLO‐Y4 cocultures (CC). (a) The medium from CCs of MSCs and MLO‐Y4 osteocytes was analyzed by ELISA on days 7, 10, and 14. IL‐6 and IL‐1β were synergistically induced by IL‐17 (50 ng/ml) and osteocyte CC. (b) MLO‐Y4 osteocytes in the upper chamber of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1β after IL‐17 treatment. (c) MSCs in the lower chambers of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1 β after IL‐17 treatment. (d) Increased phosphorylation of signaling regulators ERK1/2, AKT, and STAT3 after IL‐17 stimulation in MLO‐Y4 CCs. Phosphorylated SARK/JNK and p38 were unchanged (24 hr). ELISA, enzyme‐linked immunosorbent assay; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; RA, receptor A; STAT3, signal transducer and activator of transcription 3. * p
    Figure Legend Snippet: Interleukin (IL)‐17 upregulates inflammatory factors, IL‐6 and IL‐1β, and activates ERK, AKT, and STAT3 signaling in mesenchymal stem cells (MSC)–MLO‐Y4 cocultures (CC). (a) The medium from CCs of MSCs and MLO‐Y4 osteocytes was analyzed by ELISA on days 7, 10, and 14. IL‐6 and IL‐1β were synergistically induced by IL‐17 (50 ng/ml) and osteocyte CC. (b) MLO‐Y4 osteocytes in the upper chamber of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1β after IL‐17 treatment. (c) MSCs in the lower chambers of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1 β after IL‐17 treatment. (d) Increased phosphorylation of signaling regulators ERK1/2, AKT, and STAT3 after IL‐17 stimulation in MLO‐Y4 CCs. Phosphorylated SARK/JNK and p38 were unchanged (24 hr). ELISA, enzyme‐linked immunosorbent assay; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; RA, receptor A; STAT3, signal transducer and activator of transcription 3. * p

    Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing

    AKT, STAT3, and ERK1/2 pathways are activated in IL‐17–mediated osteoblastic differentiation. (a) Ten micrometer of the AKT inhibitor Perifosine, the JAK1 and JAK2 inhibitor AZD1480 (to inhibit STAT3 signaling), and the MEK1/2 inhibitor U0126, solubilized in 0.1% DMSO in serum‐free medium efficiently suppressed AKT, STAT3, and ERK1/2 expression, respectively, in MSCs. (b,c) IL‐17–induced coculture systems with 10 μM of inhibitors inhibited mineralization (14 days). (d–g) Relative mRNA expression of ALP, RUNX2, OCN, and COL‐1 was significantly decreased by the suppression of AKT, STAT3, and ERK1/2 signaling pathways. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; IL, interleukin; mRNA, messenger RNA; MSC, mesenchymal stem cell; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3. (* p
    Figure Legend Snippet: AKT, STAT3, and ERK1/2 pathways are activated in IL‐17–mediated osteoblastic differentiation. (a) Ten micrometer of the AKT inhibitor Perifosine, the JAK1 and JAK2 inhibitor AZD1480 (to inhibit STAT3 signaling), and the MEK1/2 inhibitor U0126, solubilized in 0.1% DMSO in serum‐free medium efficiently suppressed AKT, STAT3, and ERK1/2 expression, respectively, in MSCs. (b,c) IL‐17–induced coculture systems with 10 μM of inhibitors inhibited mineralization (14 days). (d–g) Relative mRNA expression of ALP, RUNX2, OCN, and COL‐1 was significantly decreased by the suppression of AKT, STAT3, and ERK1/2 signaling pathways. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; IL, interleukin; mRNA, messenger RNA; MSC, mesenchymal stem cell; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3. (* p

    Techniques Used: Expressing

    10) Product Images from "Serum IL-9, IL-17, and TGF-β levels in subjects with diabetic kidney disease (CURES-134)"

    Article Title: Serum IL-9, IL-17, and TGF-β levels in subjects with diabetic kidney disease (CURES-134)

    Journal: Cytokine

    doi: 10.1016/j.cyto.2014.10.009

    Interleukin (IL)-9, IL-17, and TGF-β serum cytokine levels in subjects with NGT, DM, and DKD: (a) IL-17, (b) TGF-β, and (c) IL-9. The geometric mean is represented by the horizontal bars. The p -values were calculated by Kruskal–Wallis one-way analysis of variance. A p -value
    Figure Legend Snippet: Interleukin (IL)-9, IL-17, and TGF-β serum cytokine levels in subjects with NGT, DM, and DKD: (a) IL-17, (b) TGF-β, and (c) IL-9. The geometric mean is represented by the horizontal bars. The p -values were calculated by Kruskal–Wallis one-way analysis of variance. A p -value

    Techniques Used:

    11) Product Images from "IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes. IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes"

    Article Title: IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes. IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes

    Journal: Journal of Cellular Physiology

    doi: 10.1002/jcp.29323

    IL‐17 enhances the osteogenic differentiation of mMSCs but not MC3T3‐E1. (a,b) Increased mineralized nodule formation (red) in mesenchymal stem cells (MSCs) and MLO‐Y4 osteocytes after treatment with 0.5–50 ng/ml IL‐17 in osteogenic induction medium for 14 days. Mineralization of MC3T3‐E1 cells was inhibited, and there was no change in mineralization levels in MLO‐A5 cells. (c,d) Alkaline phosphatase (ALP) expression (purple) of MSCs was enhanced by IL‐17 (7 days). (e,f) mRNA expression of factors after IL‐17 treatment for 24 hr. Treatment with IL‐17 increased runt‐related transcription factor 2 (RUNX2), collagen‐1 (COL‐1) and osteocalcin (OCN) in MSCs, and only RUNX2 in MLO‐Y4 cells. All three factors were decreased in MC3T3‐E1 cells and no significant changes were measured in MLO‐A5 cells. (f) IL‐17 receptor A (RA) and IL‐6 were upregulated in MSCs and MLO‐Y4 cells, and IL‐β was significantly upregulated in MSCs. IL, interleukin; mMSC, mouse MSCs; mRNA, messenger RNA
    Figure Legend Snippet: IL‐17 enhances the osteogenic differentiation of mMSCs but not MC3T3‐E1. (a,b) Increased mineralized nodule formation (red) in mesenchymal stem cells (MSCs) and MLO‐Y4 osteocytes after treatment with 0.5–50 ng/ml IL‐17 in osteogenic induction medium for 14 days. Mineralization of MC3T3‐E1 cells was inhibited, and there was no change in mineralization levels in MLO‐A5 cells. (c,d) Alkaline phosphatase (ALP) expression (purple) of MSCs was enhanced by IL‐17 (7 days). (e,f) mRNA expression of factors after IL‐17 treatment for 24 hr. Treatment with IL‐17 increased runt‐related transcription factor 2 (RUNX2), collagen‐1 (COL‐1) and osteocalcin (OCN) in MSCs, and only RUNX2 in MLO‐Y4 cells. All three factors were decreased in MC3T3‐E1 cells and no significant changes were measured in MLO‐A5 cells. (f) IL‐17 receptor A (RA) and IL‐6 were upregulated in MSCs and MLO‐Y4 cells, and IL‐β was significantly upregulated in MSCs. IL, interleukin; mMSC, mouse MSCs; mRNA, messenger RNA

    Techniques Used: Expressing

    Osteogenic differentiation of mesenchymal stem cells (MSCs) after coculture (CC) with osteocytes is further enhanced by interleukin‐17 (IL‐17). (a) We used a transwell CC system, with MSCs seeded in the lower chamber and various osteogenic cells in the upper chambers. Cells were grown in osteoinductive media (OM) with or without IL‐17. MSCs in both the upper and lower chambers served as a control. (b,c) Alizarin red staining to detect mineralized nodule formation (red) in the lower chambers following CC with or without IL‐17 stimulation (50 ng/ml). IL‐17 enhanced mineralization in control‐MSCs (top row). No obvious change was found for MSCs in MC3T3‐E1 CC and MLO‐A5 CC (second and third rows). An increase in Alizarin red staining was found for MSCs in MLO‐Y4 CC, which was further increased with IL‐17. (d,e) ALP staining and quantification of ALP activity. IL‐17 induced ALP expression (purple) in MSCs under control CC condition (top row). ALP expression was also induced in MSC in CC with MLO‐Y4 cells (bottom row; Day 7). Each experiment was repeated at least three times independently and three different mMSC cell lines were used. ALP, alkaline phosphatase
    Figure Legend Snippet: Osteogenic differentiation of mesenchymal stem cells (MSCs) after coculture (CC) with osteocytes is further enhanced by interleukin‐17 (IL‐17). (a) We used a transwell CC system, with MSCs seeded in the lower chamber and various osteogenic cells in the upper chambers. Cells were grown in osteoinductive media (OM) with or without IL‐17. MSCs in both the upper and lower chambers served as a control. (b,c) Alizarin red staining to detect mineralized nodule formation (red) in the lower chambers following CC with or without IL‐17 stimulation (50 ng/ml). IL‐17 enhanced mineralization in control‐MSCs (top row). No obvious change was found for MSCs in MC3T3‐E1 CC and MLO‐A5 CC (second and third rows). An increase in Alizarin red staining was found for MSCs in MLO‐Y4 CC, which was further increased with IL‐17. (d,e) ALP staining and quantification of ALP activity. IL‐17 induced ALP expression (purple) in MSCs under control CC condition (top row). ALP expression was also induced in MSC in CC with MLO‐Y4 cells (bottom row; Day 7). Each experiment was repeated at least three times independently and three different mMSC cell lines were used. ALP, alkaline phosphatase

    Techniques Used: Staining, Activity Assay, Expressing

    Schematic of the findings of this study. Mesenchymal stem cells (MSCs) exposed to interleukin (IL)‐17 and osteocytes in coculture underwent differentiation along the osteogenic lineage, better than when exposed to either stimulus alone. IL‐17 induces the expression of inflammatory markers, IL‐6 and IL‐1β, which in turn, increase the expression of markers of osteoblastic differentiation in MSCs, such as alkaline phosphatase (ALP), runt‐related transcription factor 2 (RUNX2), osteocalcin (OCN) and collagen‐1 (COL‐1). The activation of extracellular signal‐regulated kinase 1/2 (ERK1/2), AKT, and signal transducer and activator of transcription 3 (STAT3) regulated IL‐17 induced osteogenesis in the MSC niche, which could be inhibited by antibodies of IL‐6 and IL‐1β
    Figure Legend Snippet: Schematic of the findings of this study. Mesenchymal stem cells (MSCs) exposed to interleukin (IL)‐17 and osteocytes in coculture underwent differentiation along the osteogenic lineage, better than when exposed to either stimulus alone. IL‐17 induces the expression of inflammatory markers, IL‐6 and IL‐1β, which in turn, increase the expression of markers of osteoblastic differentiation in MSCs, such as alkaline phosphatase (ALP), runt‐related transcription factor 2 (RUNX2), osteocalcin (OCN) and collagen‐1 (COL‐1). The activation of extracellular signal‐regulated kinase 1/2 (ERK1/2), AKT, and signal transducer and activator of transcription 3 (STAT3) regulated IL‐17 induced osteogenesis in the MSC niche, which could be inhibited by antibodies of IL‐6 and IL‐1β

    Techniques Used: Expressing, Activation Assay

    Three‐dimensional culture of mesenchymal stem cells (MSCs) on a polycaprolactone (PCL) scaffold enhances IL‐17‐stimulated osteogenesis when cocultured with MLO‐Y4 osteocytes. (a) Alizarin red staining shows mineralized nodule formation (red) in mouse MSCs (mMSCs) and human‐induced pluripotent stem cell‐derived MSCs (hMSCs) cultures on Day 10. Growth on the PCL scaffold promoted osteogenesis, and this could be further enhanced by coculture with MLO‐Y4 osteocytes and IL‐17 stimulation. (b) Quantification of mMSCs mineralazation. (c) Quantification of hMSCs mineralization. IL, interleukin
    Figure Legend Snippet: Three‐dimensional culture of mesenchymal stem cells (MSCs) on a polycaprolactone (PCL) scaffold enhances IL‐17‐stimulated osteogenesis when cocultured with MLO‐Y4 osteocytes. (a) Alizarin red staining shows mineralized nodule formation (red) in mouse MSCs (mMSCs) and human‐induced pluripotent stem cell‐derived MSCs (hMSCs) cultures on Day 10. Growth on the PCL scaffold promoted osteogenesis, and this could be further enhanced by coculture with MLO‐Y4 osteocytes and IL‐17 stimulation. (b) Quantification of mMSCs mineralazation. (c) Quantification of hMSCs mineralization. IL, interleukin

    Techniques Used: Staining, Derivative Assay

    Interleukin (IL)‐17 activates intercellular signaling of osteogenesis via IL‐6 and IL‐1β. Anti‐IL‐6 and anti‐IL‐1β antibodies were used in the IL‐17–induced coculture (CC) system. Both antibodies could effectively inhibit (a,b) the formation of mineral nodules, (c) the mRNA expression of ALP, RUNX2, OCN, and COL‐1 and (d) AKT, STAT3, and ERK1/2 phosphorylation in the control‐MSCs CC and MLO‐Y4 CC at Day 14 after IL‐17 treatment; albeit, the effects of IL‐1β neutralization were weaker than that of IL‐6. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3
    Figure Legend Snippet: Interleukin (IL)‐17 activates intercellular signaling of osteogenesis via IL‐6 and IL‐1β. Anti‐IL‐6 and anti‐IL‐1β antibodies were used in the IL‐17–induced coculture (CC) system. Both antibodies could effectively inhibit (a,b) the formation of mineral nodules, (c) the mRNA expression of ALP, RUNX2, OCN, and COL‐1 and (d) AKT, STAT3, and ERK1/2 phosphorylation in the control‐MSCs CC and MLO‐Y4 CC at Day 14 after IL‐17 treatment; albeit, the effects of IL‐1β neutralization were weaker than that of IL‐6. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3

    Techniques Used: Expressing, Neutralization

    Interleukin (IL)‐17 upregulates inflammatory factors, IL‐6 and IL‐1β, and activates ERK, AKT, and STAT3 signaling in mesenchymal stem cells (MSC)–MLO‐Y4 cocultures (CC). (a) The medium from CCs of MSCs and MLO‐Y4 osteocytes was analyzed by ELISA on days 7, 10, and 14. IL‐6 and IL‐1β were synergistically induced by IL‐17 (50 ng/ml) and osteocyte CC. (b) MLO‐Y4 osteocytes in the upper chamber of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1β after IL‐17 treatment. (c) MSCs in the lower chambers of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1 β after IL‐17 treatment. (d) Increased phosphorylation of signaling regulators ERK1/2, AKT, and STAT3 after IL‐17 stimulation in MLO‐Y4 CCs. Phosphorylated SARK/JNK and p38 were unchanged (24 hr). ELISA, enzyme‐linked immunosorbent assay; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; RA, receptor A; STAT3, signal transducer and activator of transcription 3. * p
    Figure Legend Snippet: Interleukin (IL)‐17 upregulates inflammatory factors, IL‐6 and IL‐1β, and activates ERK, AKT, and STAT3 signaling in mesenchymal stem cells (MSC)–MLO‐Y4 cocultures (CC). (a) The medium from CCs of MSCs and MLO‐Y4 osteocytes was analyzed by ELISA on days 7, 10, and 14. IL‐6 and IL‐1β were synergistically induced by IL‐17 (50 ng/ml) and osteocyte CC. (b) MLO‐Y4 osteocytes in the upper chamber of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1β after IL‐17 treatment. (c) MSCs in the lower chambers of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1 β after IL‐17 treatment. (d) Increased phosphorylation of signaling regulators ERK1/2, AKT, and STAT3 after IL‐17 stimulation in MLO‐Y4 CCs. Phosphorylated SARK/JNK and p38 were unchanged (24 hr). ELISA, enzyme‐linked immunosorbent assay; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; RA, receptor A; STAT3, signal transducer and activator of transcription 3. * p

    Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing

    AKT, STAT3, and ERK1/2 pathways are activated in IL‐17–mediated osteoblastic differentiation. (a) Ten micrometer of the AKT inhibitor Perifosine, the JAK1 and JAK2 inhibitor AZD1480 (to inhibit STAT3 signaling), and the MEK1/2 inhibitor U0126, solubilized in 0.1% DMSO in serum‐free medium efficiently suppressed AKT, STAT3, and ERK1/2 expression, respectively, in MSCs. (b,c) IL‐17–induced coculture systems with 10 μM of inhibitors inhibited mineralization (14 days). (d–g) Relative mRNA expression of ALP, RUNX2, OCN, and COL‐1 was significantly decreased by the suppression of AKT, STAT3, and ERK1/2 signaling pathways. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; IL, interleukin; mRNA, messenger RNA; MSC, mesenchymal stem cell; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3. (* p
    Figure Legend Snippet: AKT, STAT3, and ERK1/2 pathways are activated in IL‐17–mediated osteoblastic differentiation. (a) Ten micrometer of the AKT inhibitor Perifosine, the JAK1 and JAK2 inhibitor AZD1480 (to inhibit STAT3 signaling), and the MEK1/2 inhibitor U0126, solubilized in 0.1% DMSO in serum‐free medium efficiently suppressed AKT, STAT3, and ERK1/2 expression, respectively, in MSCs. (b,c) IL‐17–induced coculture systems with 10 μM of inhibitors inhibited mineralization (14 days). (d–g) Relative mRNA expression of ALP, RUNX2, OCN, and COL‐1 was significantly decreased by the suppression of AKT, STAT3, and ERK1/2 signaling pathways. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; IL, interleukin; mRNA, messenger RNA; MSC, mesenchymal stem cell; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3. (* p

    Techniques Used: Expressing

    12) Product Images from "Brown adipose tissue ameliorates autoimmune arthritis via inhibition of Th17 cells"

    Article Title: Brown adipose tissue ameliorates autoimmune arthritis via inhibition of Th17 cells

    Journal: Scientific Reports

    doi: 10.1038/s41598-020-68749-x

    BAT inhibits Th17 differentiation and induces IL-10 expression in vitro. ( A ) IL-17 and IL-10 levels were measured by ELISA in BAT and eWAT. ( B ) Levels of IL-17 and IL-10 in BAT and eWAT were detected by ELISA under Th17-inducing conditions for 72 h. ( C ) IL-17 and IL-10 levels of normal BAT and CIA BAT were measured by ELISA. ( D , E ) The population of Th17 cells and Treg cells in BAT co-culture condition were measured. *P
    Figure Legend Snippet: BAT inhibits Th17 differentiation and induces IL-10 expression in vitro. ( A ) IL-17 and IL-10 levels were measured by ELISA in BAT and eWAT. ( B ) Levels of IL-17 and IL-10 in BAT and eWAT were detected by ELISA under Th17-inducing conditions for 72 h. ( C ) IL-17 and IL-10 levels of normal BAT and CIA BAT were measured by ELISA. ( D , E ) The population of Th17 cells and Treg cells in BAT co-culture condition were measured. *P

    Techniques Used: Expressing, In Vitro, Enzyme-linked Immunosorbent Assay, Co-Culture Assay

    Transplantation of normal brown adipose tissue reduces secretion of proinflammatory cytokines. Immunohistochemistry images are shown with tissues stained by anti-IL-12, anti-IL-17, anti-IL-6, anti-TNF-α, and anti-IL-10 antibodies. *P
    Figure Legend Snippet: Transplantation of normal brown adipose tissue reduces secretion of proinflammatory cytokines. Immunohistochemistry images are shown with tissues stained by anti-IL-12, anti-IL-17, anti-IL-6, anti-TNF-α, and anti-IL-10 antibodies. *P

    Techniques Used: Transplantation Assay, Immunohistochemistry, Staining

    13) Product Images from "IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes. IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes"

    Article Title: IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes. IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes

    Journal: Journal of Cellular Physiology

    doi: 10.1002/jcp.29323

    IL‐17 enhances the osteogenic differentiation of mMSCs but not MC3T3‐E1. (a,b) Increased mineralized nodule formation (red) in mesenchymal stem cells (MSCs) and MLO‐Y4 osteocytes after treatment with 0.5–50 ng/ml IL‐17 in osteogenic induction medium for 14 days. Mineralization of MC3T3‐E1 cells was inhibited, and there was no change in mineralization levels in MLO‐A5 cells. (c,d) Alkaline phosphatase (ALP) expression (purple) of MSCs was enhanced by IL‐17 (7 days). (e,f) mRNA expression of factors after IL‐17 treatment for 24 hr. Treatment with IL‐17 increased runt‐related transcription factor 2 (RUNX2), collagen‐1 (COL‐1) and osteocalcin (OCN) in MSCs, and only RUNX2 in MLO‐Y4 cells. All three factors were decreased in MC3T3‐E1 cells and no significant changes were measured in MLO‐A5 cells. (f) IL‐17 receptor A (RA) and IL‐6 were upregulated in MSCs and MLO‐Y4 cells, and IL‐β was significantly upregulated in MSCs. IL, interleukin; mMSC, mouse MSCs; mRNA, messenger RNA
    Figure Legend Snippet: IL‐17 enhances the osteogenic differentiation of mMSCs but not MC3T3‐E1. (a,b) Increased mineralized nodule formation (red) in mesenchymal stem cells (MSCs) and MLO‐Y4 osteocytes after treatment with 0.5–50 ng/ml IL‐17 in osteogenic induction medium for 14 days. Mineralization of MC3T3‐E1 cells was inhibited, and there was no change in mineralization levels in MLO‐A5 cells. (c,d) Alkaline phosphatase (ALP) expression (purple) of MSCs was enhanced by IL‐17 (7 days). (e,f) mRNA expression of factors after IL‐17 treatment for 24 hr. Treatment with IL‐17 increased runt‐related transcription factor 2 (RUNX2), collagen‐1 (COL‐1) and osteocalcin (OCN) in MSCs, and only RUNX2 in MLO‐Y4 cells. All three factors were decreased in MC3T3‐E1 cells and no significant changes were measured in MLO‐A5 cells. (f) IL‐17 receptor A (RA) and IL‐6 were upregulated in MSCs and MLO‐Y4 cells, and IL‐β was significantly upregulated in MSCs. IL, interleukin; mMSC, mouse MSCs; mRNA, messenger RNA

    Techniques Used: Expressing

    Osteogenic differentiation of mesenchymal stem cells (MSCs) after coculture (CC) with osteocytes is further enhanced by interleukin‐17 (IL‐17). (a) We used a transwell CC system, with MSCs seeded in the lower chamber and various osteogenic cells in the upper chambers. Cells were grown in osteoinductive media (OM) with or without IL‐17. MSCs in both the upper and lower chambers served as a control. (b,c) Alizarin red staining to detect mineralized nodule formation (red) in the lower chambers following CC with or without IL‐17 stimulation (50 ng/ml). IL‐17 enhanced mineralization in control‐MSCs (top row). No obvious change was found for MSCs in MC3T3‐E1 CC and MLO‐A5 CC (second and third rows). An increase in Alizarin red staining was found for MSCs in MLO‐Y4 CC, which was further increased with IL‐17. (d,e) ALP staining and quantification of ALP activity. IL‐17 induced ALP expression (purple) in MSCs under control CC condition (top row). ALP expression was also induced in MSC in CC with MLO‐Y4 cells (bottom row; Day 7). Each experiment was repeated at least three times independently and three different mMSC cell lines were used. ALP, alkaline phosphatase
    Figure Legend Snippet: Osteogenic differentiation of mesenchymal stem cells (MSCs) after coculture (CC) with osteocytes is further enhanced by interleukin‐17 (IL‐17). (a) We used a transwell CC system, with MSCs seeded in the lower chamber and various osteogenic cells in the upper chambers. Cells were grown in osteoinductive media (OM) with or without IL‐17. MSCs in both the upper and lower chambers served as a control. (b,c) Alizarin red staining to detect mineralized nodule formation (red) in the lower chambers following CC with or without IL‐17 stimulation (50 ng/ml). IL‐17 enhanced mineralization in control‐MSCs (top row). No obvious change was found for MSCs in MC3T3‐E1 CC and MLO‐A5 CC (second and third rows). An increase in Alizarin red staining was found for MSCs in MLO‐Y4 CC, which was further increased with IL‐17. (d,e) ALP staining and quantification of ALP activity. IL‐17 induced ALP expression (purple) in MSCs under control CC condition (top row). ALP expression was also induced in MSC in CC with MLO‐Y4 cells (bottom row; Day 7). Each experiment was repeated at least three times independently and three different mMSC cell lines were used. ALP, alkaline phosphatase

    Techniques Used: Staining, Activity Assay, Expressing

    Schematic of the findings of this study. Mesenchymal stem cells (MSCs) exposed to interleukin (IL)‐17 and osteocytes in coculture underwent differentiation along the osteogenic lineage, better than when exposed to either stimulus alone. IL‐17 induces the expression of inflammatory markers, IL‐6 and IL‐1β, which in turn, increase the expression of markers of osteoblastic differentiation in MSCs, such as alkaline phosphatase (ALP), runt‐related transcription factor 2 (RUNX2), osteocalcin (OCN) and collagen‐1 (COL‐1). The activation of extracellular signal‐regulated kinase 1/2 (ERK1/2), AKT, and signal transducer and activator of transcription 3 (STAT3) regulated IL‐17 induced osteogenesis in the MSC niche, which could be inhibited by antibodies of IL‐6 and IL‐1β
    Figure Legend Snippet: Schematic of the findings of this study. Mesenchymal stem cells (MSCs) exposed to interleukin (IL)‐17 and osteocytes in coculture underwent differentiation along the osteogenic lineage, better than when exposed to either stimulus alone. IL‐17 induces the expression of inflammatory markers, IL‐6 and IL‐1β, which in turn, increase the expression of markers of osteoblastic differentiation in MSCs, such as alkaline phosphatase (ALP), runt‐related transcription factor 2 (RUNX2), osteocalcin (OCN) and collagen‐1 (COL‐1). The activation of extracellular signal‐regulated kinase 1/2 (ERK1/2), AKT, and signal transducer and activator of transcription 3 (STAT3) regulated IL‐17 induced osteogenesis in the MSC niche, which could be inhibited by antibodies of IL‐6 and IL‐1β

    Techniques Used: Expressing, Activation Assay

    Three‐dimensional culture of mesenchymal stem cells (MSCs) on a polycaprolactone (PCL) scaffold enhances IL‐17‐stimulated osteogenesis when cocultured with MLO‐Y4 osteocytes. (a) Alizarin red staining shows mineralized nodule formation (red) in mouse MSCs (mMSCs) and human‐induced pluripotent stem cell‐derived MSCs (hMSCs) cultures on Day 10. Growth on the PCL scaffold promoted osteogenesis, and this could be further enhanced by coculture with MLO‐Y4 osteocytes and IL‐17 stimulation. (b) Quantification of mMSCs mineralazation. (c) Quantification of hMSCs mineralization. IL, interleukin
    Figure Legend Snippet: Three‐dimensional culture of mesenchymal stem cells (MSCs) on a polycaprolactone (PCL) scaffold enhances IL‐17‐stimulated osteogenesis when cocultured with MLO‐Y4 osteocytes. (a) Alizarin red staining shows mineralized nodule formation (red) in mouse MSCs (mMSCs) and human‐induced pluripotent stem cell‐derived MSCs (hMSCs) cultures on Day 10. Growth on the PCL scaffold promoted osteogenesis, and this could be further enhanced by coculture with MLO‐Y4 osteocytes and IL‐17 stimulation. (b) Quantification of mMSCs mineralazation. (c) Quantification of hMSCs mineralization. IL, interleukin

    Techniques Used: Staining, Derivative Assay

    Interleukin (IL)‐17 activates intercellular signaling of osteogenesis via IL‐6 and IL‐1β. Anti‐IL‐6 and anti‐IL‐1β antibodies were used in the IL‐17–induced coculture (CC) system. Both antibodies could effectively inhibit (a,b) the formation of mineral nodules, (c) the mRNA expression of ALP, RUNX2, OCN, and COL‐1 and (d) AKT, STAT3, and ERK1/2 phosphorylation in the control‐MSCs CC and MLO‐Y4 CC at Day 14 after IL‐17 treatment; albeit, the effects of IL‐1β neutralization were weaker than that of IL‐6. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3
    Figure Legend Snippet: Interleukin (IL)‐17 activates intercellular signaling of osteogenesis via IL‐6 and IL‐1β. Anti‐IL‐6 and anti‐IL‐1β antibodies were used in the IL‐17–induced coculture (CC) system. Both antibodies could effectively inhibit (a,b) the formation of mineral nodules, (c) the mRNA expression of ALP, RUNX2, OCN, and COL‐1 and (d) AKT, STAT3, and ERK1/2 phosphorylation in the control‐MSCs CC and MLO‐Y4 CC at Day 14 after IL‐17 treatment; albeit, the effects of IL‐1β neutralization were weaker than that of IL‐6. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3

    Techniques Used: Expressing, Neutralization

    Interleukin (IL)‐17 upregulates inflammatory factors, IL‐6 and IL‐1β, and activates ERK, AKT, and STAT3 signaling in mesenchymal stem cells (MSC)–MLO‐Y4 cocultures (CC). (a) The medium from CCs of MSCs and MLO‐Y4 osteocytes was analyzed by ELISA on days 7, 10, and 14. IL‐6 and IL‐1β were synergistically induced by IL‐17 (50 ng/ml) and osteocyte CC. (b) MLO‐Y4 osteocytes in the upper chamber of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1β after IL‐17 treatment. (c) MSCs in the lower chambers of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1 β after IL‐17 treatment. (d) Increased phosphorylation of signaling regulators ERK1/2, AKT, and STAT3 after IL‐17 stimulation in MLO‐Y4 CCs. Phosphorylated SARK/JNK and p38 were unchanged (24 hr). ELISA, enzyme‐linked immunosorbent assay; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; RA, receptor A; STAT3, signal transducer and activator of transcription 3. * p
    Figure Legend Snippet: Interleukin (IL)‐17 upregulates inflammatory factors, IL‐6 and IL‐1β, and activates ERK, AKT, and STAT3 signaling in mesenchymal stem cells (MSC)–MLO‐Y4 cocultures (CC). (a) The medium from CCs of MSCs and MLO‐Y4 osteocytes was analyzed by ELISA on days 7, 10, and 14. IL‐6 and IL‐1β were synergistically induced by IL‐17 (50 ng/ml) and osteocyte CC. (b) MLO‐Y4 osteocytes in the upper chamber of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1β after IL‐17 treatment. (c) MSCs in the lower chambers of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1 β after IL‐17 treatment. (d) Increased phosphorylation of signaling regulators ERK1/2, AKT, and STAT3 after IL‐17 stimulation in MLO‐Y4 CCs. Phosphorylated SARK/JNK and p38 were unchanged (24 hr). ELISA, enzyme‐linked immunosorbent assay; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; RA, receptor A; STAT3, signal transducer and activator of transcription 3. * p

    Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing

    AKT, STAT3, and ERK1/2 pathways are activated in IL‐17–mediated osteoblastic differentiation. (a) Ten micrometer of the AKT inhibitor Perifosine, the JAK1 and JAK2 inhibitor AZD1480 (to inhibit STAT3 signaling), and the MEK1/2 inhibitor U0126, solubilized in 0.1% DMSO in serum‐free medium efficiently suppressed AKT, STAT3, and ERK1/2 expression, respectively, in MSCs. (b,c) IL‐17–induced coculture systems with 10 μM of inhibitors inhibited mineralization (14 days). (d–g) Relative mRNA expression of ALP, RUNX2, OCN, and COL‐1 was significantly decreased by the suppression of AKT, STAT3, and ERK1/2 signaling pathways. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; IL, interleukin; mRNA, messenger RNA; MSC, mesenchymal stem cell; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3. (* p
    Figure Legend Snippet: AKT, STAT3, and ERK1/2 pathways are activated in IL‐17–mediated osteoblastic differentiation. (a) Ten micrometer of the AKT inhibitor Perifosine, the JAK1 and JAK2 inhibitor AZD1480 (to inhibit STAT3 signaling), and the MEK1/2 inhibitor U0126, solubilized in 0.1% DMSO in serum‐free medium efficiently suppressed AKT, STAT3, and ERK1/2 expression, respectively, in MSCs. (b,c) IL‐17–induced coculture systems with 10 μM of inhibitors inhibited mineralization (14 days). (d–g) Relative mRNA expression of ALP, RUNX2, OCN, and COL‐1 was significantly decreased by the suppression of AKT, STAT3, and ERK1/2 signaling pathways. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; IL, interleukin; mRNA, messenger RNA; MSC, mesenchymal stem cell; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3. (* p

    Techniques Used: Expressing

    14) Product Images from "IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes. IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes"

    Article Title: IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes. IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes

    Journal: Journal of Cellular Physiology

    doi: 10.1002/jcp.29323

    IL‐17 enhances the osteogenic differentiation of mMSCs but not MC3T3‐E1. (a,b) Increased mineralized nodule formation (red) in mesenchymal stem cells (MSCs) and MLO‐Y4 osteocytes after treatment with 0.5–50 ng/ml IL‐17 in osteogenic induction medium for 14 days. Mineralization of MC3T3‐E1 cells was inhibited, and there was no change in mineralization levels in MLO‐A5 cells. (c,d) Alkaline phosphatase (ALP) expression (purple) of MSCs was enhanced by IL‐17 (7 days). (e,f) mRNA expression of factors after IL‐17 treatment for 24 hr. Treatment with IL‐17 increased runt‐related transcription factor 2 (RUNX2), collagen‐1 (COL‐1) and osteocalcin (OCN) in MSCs, and only RUNX2 in MLO‐Y4 cells. All three factors were decreased in MC3T3‐E1 cells and no significant changes were measured in MLO‐A5 cells. (f) IL‐17 receptor A (RA) and IL‐6 were upregulated in MSCs and MLO‐Y4 cells, and IL‐β was significantly upregulated in MSCs. IL, interleukin; mMSC, mouse MSCs; mRNA, messenger RNA
    Figure Legend Snippet: IL‐17 enhances the osteogenic differentiation of mMSCs but not MC3T3‐E1. (a,b) Increased mineralized nodule formation (red) in mesenchymal stem cells (MSCs) and MLO‐Y4 osteocytes after treatment with 0.5–50 ng/ml IL‐17 in osteogenic induction medium for 14 days. Mineralization of MC3T3‐E1 cells was inhibited, and there was no change in mineralization levels in MLO‐A5 cells. (c,d) Alkaline phosphatase (ALP) expression (purple) of MSCs was enhanced by IL‐17 (7 days). (e,f) mRNA expression of factors after IL‐17 treatment for 24 hr. Treatment with IL‐17 increased runt‐related transcription factor 2 (RUNX2), collagen‐1 (COL‐1) and osteocalcin (OCN) in MSCs, and only RUNX2 in MLO‐Y4 cells. All three factors were decreased in MC3T3‐E1 cells and no significant changes were measured in MLO‐A5 cells. (f) IL‐17 receptor A (RA) and IL‐6 were upregulated in MSCs and MLO‐Y4 cells, and IL‐β was significantly upregulated in MSCs. IL, interleukin; mMSC, mouse MSCs; mRNA, messenger RNA

    Techniques Used: Expressing

    Osteogenic differentiation of mesenchymal stem cells (MSCs) after coculture (CC) with osteocytes is further enhanced by interleukin‐17 (IL‐17). (a) We used a transwell CC system, with MSCs seeded in the lower chamber and various osteogenic cells in the upper chambers. Cells were grown in osteoinductive media (OM) with or without IL‐17. MSCs in both the upper and lower chambers served as a control. (b,c) Alizarin red staining to detect mineralized nodule formation (red) in the lower chambers following CC with or without IL‐17 stimulation (50 ng/ml). IL‐17 enhanced mineralization in control‐MSCs (top row). No obvious change was found for MSCs in MC3T3‐E1 CC and MLO‐A5 CC (second and third rows). An increase in Alizarin red staining was found for MSCs in MLO‐Y4 CC, which was further increased with IL‐17. (d,e) ALP staining and quantification of ALP activity. IL‐17 induced ALP expression (purple) in MSCs under control CC condition (top row). ALP expression was also induced in MSC in CC with MLO‐Y4 cells (bottom row; Day 7). Each experiment was repeated at least three times independently and three different mMSC cell lines were used. ALP, alkaline phosphatase
    Figure Legend Snippet: Osteogenic differentiation of mesenchymal stem cells (MSCs) after coculture (CC) with osteocytes is further enhanced by interleukin‐17 (IL‐17). (a) We used a transwell CC system, with MSCs seeded in the lower chamber and various osteogenic cells in the upper chambers. Cells were grown in osteoinductive media (OM) with or without IL‐17. MSCs in both the upper and lower chambers served as a control. (b,c) Alizarin red staining to detect mineralized nodule formation (red) in the lower chambers following CC with or without IL‐17 stimulation (50 ng/ml). IL‐17 enhanced mineralization in control‐MSCs (top row). No obvious change was found for MSCs in MC3T3‐E1 CC and MLO‐A5 CC (second and third rows). An increase in Alizarin red staining was found for MSCs in MLO‐Y4 CC, which was further increased with IL‐17. (d,e) ALP staining and quantification of ALP activity. IL‐17 induced ALP expression (purple) in MSCs under control CC condition (top row). ALP expression was also induced in MSC in CC with MLO‐Y4 cells (bottom row; Day 7). Each experiment was repeated at least three times independently and three different mMSC cell lines were used. ALP, alkaline phosphatase

    Techniques Used: Staining, Activity Assay, Expressing

    Schematic of the findings of this study. Mesenchymal stem cells (MSCs) exposed to interleukin (IL)‐17 and osteocytes in coculture underwent differentiation along the osteogenic lineage, better than when exposed to either stimulus alone. IL‐17 induces the expression of inflammatory markers, IL‐6 and IL‐1β, which in turn, increase the expression of markers of osteoblastic differentiation in MSCs, such as alkaline phosphatase (ALP), runt‐related transcription factor 2 (RUNX2), osteocalcin (OCN) and collagen‐1 (COL‐1). The activation of extracellular signal‐regulated kinase 1/2 (ERK1/2), AKT, and signal transducer and activator of transcription 3 (STAT3) regulated IL‐17 induced osteogenesis in the MSC niche, which could be inhibited by antibodies of IL‐6 and IL‐1β
    Figure Legend Snippet: Schematic of the findings of this study. Mesenchymal stem cells (MSCs) exposed to interleukin (IL)‐17 and osteocytes in coculture underwent differentiation along the osteogenic lineage, better than when exposed to either stimulus alone. IL‐17 induces the expression of inflammatory markers, IL‐6 and IL‐1β, which in turn, increase the expression of markers of osteoblastic differentiation in MSCs, such as alkaline phosphatase (ALP), runt‐related transcription factor 2 (RUNX2), osteocalcin (OCN) and collagen‐1 (COL‐1). The activation of extracellular signal‐regulated kinase 1/2 (ERK1/2), AKT, and signal transducer and activator of transcription 3 (STAT3) regulated IL‐17 induced osteogenesis in the MSC niche, which could be inhibited by antibodies of IL‐6 and IL‐1β

    Techniques Used: Expressing, Activation Assay

    Three‐dimensional culture of mesenchymal stem cells (MSCs) on a polycaprolactone (PCL) scaffold enhances IL‐17‐stimulated osteogenesis when cocultured with MLO‐Y4 osteocytes. (a) Alizarin red staining shows mineralized nodule formation (red) in mouse MSCs (mMSCs) and human‐induced pluripotent stem cell‐derived MSCs (hMSCs) cultures on Day 10. Growth on the PCL scaffold promoted osteogenesis, and this could be further enhanced by coculture with MLO‐Y4 osteocytes and IL‐17 stimulation. (b) Quantification of mMSCs mineralazation. (c) Quantification of hMSCs mineralization. IL, interleukin
    Figure Legend Snippet: Three‐dimensional culture of mesenchymal stem cells (MSCs) on a polycaprolactone (PCL) scaffold enhances IL‐17‐stimulated osteogenesis when cocultured with MLO‐Y4 osteocytes. (a) Alizarin red staining shows mineralized nodule formation (red) in mouse MSCs (mMSCs) and human‐induced pluripotent stem cell‐derived MSCs (hMSCs) cultures on Day 10. Growth on the PCL scaffold promoted osteogenesis, and this could be further enhanced by coculture with MLO‐Y4 osteocytes and IL‐17 stimulation. (b) Quantification of mMSCs mineralazation. (c) Quantification of hMSCs mineralization. IL, interleukin

    Techniques Used: Staining, Derivative Assay

    Interleukin (IL)‐17 activates intercellular signaling of osteogenesis via IL‐6 and IL‐1β. Anti‐IL‐6 and anti‐IL‐1β antibodies were used in the IL‐17–induced coculture (CC) system. Both antibodies could effectively inhibit (a,b) the formation of mineral nodules, (c) the mRNA expression of ALP, RUNX2, OCN, and COL‐1 and (d) AKT, STAT3, and ERK1/2 phosphorylation in the control‐MSCs CC and MLO‐Y4 CC at Day 14 after IL‐17 treatment; albeit, the effects of IL‐1β neutralization were weaker than that of IL‐6. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3
    Figure Legend Snippet: Interleukin (IL)‐17 activates intercellular signaling of osteogenesis via IL‐6 and IL‐1β. Anti‐IL‐6 and anti‐IL‐1β antibodies were used in the IL‐17–induced coculture (CC) system. Both antibodies could effectively inhibit (a,b) the formation of mineral nodules, (c) the mRNA expression of ALP, RUNX2, OCN, and COL‐1 and (d) AKT, STAT3, and ERK1/2 phosphorylation in the control‐MSCs CC and MLO‐Y4 CC at Day 14 after IL‐17 treatment; albeit, the effects of IL‐1β neutralization were weaker than that of IL‐6. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3

    Techniques Used: Expressing, Neutralization

    Interleukin (IL)‐17 upregulates inflammatory factors, IL‐6 and IL‐1β, and activates ERK, AKT, and STAT3 signaling in mesenchymal stem cells (MSC)–MLO‐Y4 cocultures (CC). (a) The medium from CCs of MSCs and MLO‐Y4 osteocytes was analyzed by ELISA on days 7, 10, and 14. IL‐6 and IL‐1β were synergistically induced by IL‐17 (50 ng/ml) and osteocyte CC. (b) MLO‐Y4 osteocytes in the upper chamber of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1β after IL‐17 treatment. (c) MSCs in the lower chambers of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1 β after IL‐17 treatment. (d) Increased phosphorylation of signaling regulators ERK1/2, AKT, and STAT3 after IL‐17 stimulation in MLO‐Y4 CCs. Phosphorylated SARK/JNK and p38 were unchanged (24 hr). ELISA, enzyme‐linked immunosorbent assay; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; RA, receptor A; STAT3, signal transducer and activator of transcription 3. * p
    Figure Legend Snippet: Interleukin (IL)‐17 upregulates inflammatory factors, IL‐6 and IL‐1β, and activates ERK, AKT, and STAT3 signaling in mesenchymal stem cells (MSC)–MLO‐Y4 cocultures (CC). (a) The medium from CCs of MSCs and MLO‐Y4 osteocytes was analyzed by ELISA on days 7, 10, and 14. IL‐6 and IL‐1β were synergistically induced by IL‐17 (50 ng/ml) and osteocyte CC. (b) MLO‐Y4 osteocytes in the upper chamber of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1β after IL‐17 treatment. (c) MSCs in the lower chambers of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1 β after IL‐17 treatment. (d) Increased phosphorylation of signaling regulators ERK1/2, AKT, and STAT3 after IL‐17 stimulation in MLO‐Y4 CCs. Phosphorylated SARK/JNK and p38 were unchanged (24 hr). ELISA, enzyme‐linked immunosorbent assay; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; RA, receptor A; STAT3, signal transducer and activator of transcription 3. * p

    Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing

    AKT, STAT3, and ERK1/2 pathways are activated in IL‐17–mediated osteoblastic differentiation. (a) Ten micrometer of the AKT inhibitor Perifosine, the JAK1 and JAK2 inhibitor AZD1480 (to inhibit STAT3 signaling), and the MEK1/2 inhibitor U0126, solubilized in 0.1% DMSO in serum‐free medium efficiently suppressed AKT, STAT3, and ERK1/2 expression, respectively, in MSCs. (b,c) IL‐17–induced coculture systems with 10 μM of inhibitors inhibited mineralization (14 days). (d–g) Relative mRNA expression of ALP, RUNX2, OCN, and COL‐1 was significantly decreased by the suppression of AKT, STAT3, and ERK1/2 signaling pathways. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; IL, interleukin; mRNA, messenger RNA; MSC, mesenchymal stem cell; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3. (* p
    Figure Legend Snippet: AKT, STAT3, and ERK1/2 pathways are activated in IL‐17–mediated osteoblastic differentiation. (a) Ten micrometer of the AKT inhibitor Perifosine, the JAK1 and JAK2 inhibitor AZD1480 (to inhibit STAT3 signaling), and the MEK1/2 inhibitor U0126, solubilized in 0.1% DMSO in serum‐free medium efficiently suppressed AKT, STAT3, and ERK1/2 expression, respectively, in MSCs. (b,c) IL‐17–induced coculture systems with 10 μM of inhibitors inhibited mineralization (14 days). (d–g) Relative mRNA expression of ALP, RUNX2, OCN, and COL‐1 was significantly decreased by the suppression of AKT, STAT3, and ERK1/2 signaling pathways. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; IL, interleukin; mRNA, messenger RNA; MSC, mesenchymal stem cell; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3. (* p

    Techniques Used: Expressing

    15) Product Images from "Inhibition of RIPK3 Pathway Attenuates Intestinal Inflammation and Cell Death of Inflammatory Bowel Disease and Suppresses Necroptosis in Peripheral Mononuclear Cells of Ulcerative Colitis Patients"

    Article Title: Inhibition of RIPK3 Pathway Attenuates Intestinal Inflammation and Cell Death of Inflammatory Bowel Disease and Suppresses Necroptosis in Peripheral Mononuclear Cells of Ulcerative Colitis Patients

    Journal: Immune Network

    doi: 10.4110/in.2020.20.e16

    RIPK3 inhibitor treatment downregulated the expression of necroptosis factors and IL-17 in CD4 + T cells from DSS-induced colitis. Confocal scanning of (A) RIPK3 and p-MLKL, (B) IL-17 expression in spleen tissue of DSS-induced colitis mice. Data are expressed as mean±SD. * p
    Figure Legend Snippet: RIPK3 inhibitor treatment downregulated the expression of necroptosis factors and IL-17 in CD4 + T cells from DSS-induced colitis. Confocal scanning of (A) RIPK3 and p-MLKL, (B) IL-17 expression in spleen tissue of DSS-induced colitis mice. Data are expressed as mean±SD. * p

    Techniques Used: Expressing, Mouse Assay

    RIPK3 inhibitor treatment reduced the expression of necroptosis factors and proinflammatory cytokines in DSS-induced colitis. Immunohistochemical visualization of (A) RIPK3 and p-MLKL, (B) IL-17 and TNF-α expression in colon tissue of DSS-induced colitis mice. Data are expressed as mean±SD. * p
    Figure Legend Snippet: RIPK3 inhibitor treatment reduced the expression of necroptosis factors and proinflammatory cytokines in DSS-induced colitis. Immunohistochemical visualization of (A) RIPK3 and p-MLKL, (B) IL-17 and TNF-α expression in colon tissue of DSS-induced colitis mice. Data are expressed as mean±SD. * p

    Techniques Used: Expressing, Immunohistochemistry, Mouse Assay

    Colitis induces the expression of necroptosis and IL-17 in CD4 + T cells. (A and B) Confocal scanning detection of RIPK3, MLKL, and IL-17 by staining in the colon tissue from UC patients. Images were obtained for each UC patients (n=3), and the representative images are shown (original magnification, ×200). * p
    Figure Legend Snippet: Colitis induces the expression of necroptosis and IL-17 in CD4 + T cells. (A and B) Confocal scanning detection of RIPK3, MLKL, and IL-17 by staining in the colon tissue from UC patients. Images were obtained for each UC patients (n=3), and the representative images are shown (original magnification, ×200). * p

    Techniques Used: Expressing, Staining

    RIPK3 inhibitor treatment suppresses necroptosis. (A) Positive cells differentiation of PI and annexin V in PBMCs from UC patients was induced by anti-CD3, and analyzed by flow cytometry. The cells were pretreated with vehicle (DMSO) or RIPK3 inhibitor (1 μM) for 2 h. (B) PBMCs from UC patients were treated with DMSO or RIPK3 inhibitor and stimulated with anti-CD3 for 72 hours. The expression of IL-6, IL-17 and TNF-α in culture supernatants was measured using ELISA. The data represent the mean±SD from three independent experiments. Statistical analyses were conducted using the nonparametric Mann-Whitney U test. (C) Positive cells differentiation of PI and annexin V in PBMCs from UC patients was induced by zVAD and TNF-α, and analyzed by flow cytometry. The cells were pretreated with vehicle or RIPK3 inhibitor (1 μM) for 2 h. *** p
    Figure Legend Snippet: RIPK3 inhibitor treatment suppresses necroptosis. (A) Positive cells differentiation of PI and annexin V in PBMCs from UC patients was induced by anti-CD3, and analyzed by flow cytometry. The cells were pretreated with vehicle (DMSO) or RIPK3 inhibitor (1 μM) for 2 h. (B) PBMCs from UC patients were treated with DMSO or RIPK3 inhibitor and stimulated with anti-CD3 for 72 hours. The expression of IL-6, IL-17 and TNF-α in culture supernatants was measured using ELISA. The data represent the mean±SD from three independent experiments. Statistical analyses were conducted using the nonparametric Mann-Whitney U test. (C) Positive cells differentiation of PI and annexin V in PBMCs from UC patients was induced by zVAD and TNF-α, and analyzed by flow cytometry. The cells were pretreated with vehicle or RIPK3 inhibitor (1 μM) for 2 h. *** p

    Techniques Used: Flow Cytometry, Expressing, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY

    RIPK3 inhibitor treatment downregulates Th17 cell differentiation and inflammatory response. (A) Normal splenocytes were treated with DMSO or RIPK3 inhibitor and stimulated with anti-CD3 for 72 h. The expression of IL-6, IL-17, and TNF-α in culture supernatants was measured using ELISA. Statistical analyses were conducted using the nonparametric Mann-Whitney U test. (B) Splenocytes from mice with collagen-induced arthritis were cultured under Th17 conditions for 72 h and then the population of CD4 + IL-17 + cells was quantified. (C) IL-17 and TNF-α expression in culture supernatants was measured using ELISA. The data represent the mean±SD from 3 independent experiments. SSC, side scatter. * p
    Figure Legend Snippet: RIPK3 inhibitor treatment downregulates Th17 cell differentiation and inflammatory response. (A) Normal splenocytes were treated with DMSO or RIPK3 inhibitor and stimulated with anti-CD3 for 72 h. The expression of IL-6, IL-17, and TNF-α in culture supernatants was measured using ELISA. Statistical analyses were conducted using the nonparametric Mann-Whitney U test. (B) Splenocytes from mice with collagen-induced arthritis were cultured under Th17 conditions for 72 h and then the population of CD4 + IL-17 + cells was quantified. (C) IL-17 and TNF-α expression in culture supernatants was measured using ELISA. The data represent the mean±SD from 3 independent experiments. SSC, side scatter. * p

    Techniques Used: Cell Differentiation, Expressing, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY, Mouse Assay, Cell Culture

    Colitis induces the expression of necroptosis and IL-17. (A) Colon tissues from UC patients were stained with H E (original magnification, ×200, n = 3). (B and C) Immunohistochemical visualization of RIPK3, MLKL, and IL-17 in the colon tissue of UC patients (n=3). * p
    Figure Legend Snippet: Colitis induces the expression of necroptosis and IL-17. (A) Colon tissues from UC patients were stained with H E (original magnification, ×200, n = 3). (B and C) Immunohistochemical visualization of RIPK3, MLKL, and IL-17 in the colon tissue of UC patients (n=3). * p

    Techniques Used: Expressing, Staining, Immunohistochemistry

    16) Product Images from "The DHODH Inhibitor PTC299 Arrests SARS-CoV-2 Replication and Suppresses Induction of Inflammatory Cytokines"

    Article Title: The DHODH Inhibitor PTC299 Arrests SARS-CoV-2 Replication and Suppresses Induction of Inflammatory Cytokines

    Journal: Virus Research

    doi: 10.1016/j.virusres.2020.198246

    PTC299 inhibits IL-17A and IL-17 F production in Th17 cells. (A-D) PMBCs were stimulated with T-cell activator CD3/CD28 Dynabeads and a combination of cytokines and antibodies to promote T-cell differentiation while blocking Th1 and Th2 differentiation. Cells were incubated with increasing concentrations of PTC299 and levels of (A) IL-17A and (B) IL-17 F in the medium were measured by ELISA. Following PMBC stimulation and incubation in the presence of 1 µM PTC299 and100 µM uridine, levels of (C) IL-17A and (D) IL-17 F in the medium were measured by ELISA. Vehicle (Medium plus 0.5%DMSO) was used as a negative control Secreted IL-17 F was reported as both pg/mL in the medium and as (pg/mL) normalized for cell number. Bars indicate standard deviation. Abbreviations: IL, interleukin; PBMC, peripheral blood mononuclear cell.
    Figure Legend Snippet: PTC299 inhibits IL-17A and IL-17 F production in Th17 cells. (A-D) PMBCs were stimulated with T-cell activator CD3/CD28 Dynabeads and a combination of cytokines and antibodies to promote T-cell differentiation while blocking Th1 and Th2 differentiation. Cells were incubated with increasing concentrations of PTC299 and levels of (A) IL-17A and (B) IL-17 F in the medium were measured by ELISA. Following PMBC stimulation and incubation in the presence of 1 µM PTC299 and100 µM uridine, levels of (C) IL-17A and (D) IL-17 F in the medium were measured by ELISA. Vehicle (Medium plus 0.5%DMSO) was used as a negative control Secreted IL-17 F was reported as both pg/mL in the medium and as (pg/mL) normalized for cell number. Bars indicate standard deviation. Abbreviations: IL, interleukin; PBMC, peripheral blood mononuclear cell.

    Techniques Used: Cell Differentiation, Blocking Assay, Incubation, Enzyme-linked Immunosorbent Assay, Negative Control, Standard Deviation

    17) Product Images from "The serum interleukin-26 level is a potential biomarker for chronical hepatitis B"

    Article Title: The serum interleukin-26 level is a potential biomarker for chronical hepatitis B

    Journal: Medicine

    doi: 10.1097/MD.0000000000018462

    The correlation of the serum IL-26 level with IL-17 level in CHB patients. A . The serum IL-17 level was measured at weeks 0 (baseline), 12, 24, 36, and 52 post LdT therapy in CHB patients. B. The correlation analysis was performed between the serum levels of IL-26 and IL-17 in CHB patients at baseline. Data are expressed as mean ± SD. ∗ P
    Figure Legend Snippet: The correlation of the serum IL-26 level with IL-17 level in CHB patients. A . The serum IL-17 level was measured at weeks 0 (baseline), 12, 24, 36, and 52 post LdT therapy in CHB patients. B. The correlation analysis was performed between the serum levels of IL-26 and IL-17 in CHB patients at baseline. Data are expressed as mean ± SD. ∗ P

    Techniques Used:

    18) Product Images from "Apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes mediated by SIRT1"

    Article Title: Apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes mediated by SIRT1

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm.2021.4845

    Knockdown of SIRT1 abolishes the protective effects of apremilast against IL-17-induced cellular senescence and the expression levels of p21 and PAI-1. Cells were transfected with SIRT1 siRNA, followed by stimulation with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) Cellular senescence. (B) mRNA levels of p21 and PAI-1. (C) Protein levels of p21 and PAI-1 as measured by western blotting. #### P
    Figure Legend Snippet: Knockdown of SIRT1 abolishes the protective effects of apremilast against IL-17-induced cellular senescence and the expression levels of p21 and PAI-1. Cells were transfected with SIRT1 siRNA, followed by stimulation with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) Cellular senescence. (B) mRNA levels of p21 and PAI-1. (C) Protein levels of p21 and PAI-1 as measured by western blotting. #### P

    Techniques Used: Expressing, Transfection, Western Blot

    Graphical representation of the underlying mechanism, whereby apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes. IL, interleukin; ROS, reactive oxygen species; SIRT1, sirtuin 1; MCP-1, monocyte chemoattractant protein-1; PAI-1, plasminogen activator inhibitor-1.
    Figure Legend Snippet: Graphical representation of the underlying mechanism, whereby apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes. IL, interleukin; ROS, reactive oxygen species; SIRT1, sirtuin 1; MCP-1, monocyte chemoattractant protein-1; PAI-1, plasminogen activator inhibitor-1.

    Techniques Used:

    Apremilast prevents IL-17-induced expression and secretions of pro-inflammatory cytokines in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. (A) Molecular structure of apremilast. (B) mRNA levels of IL-1β and MCP-1. (C) Secretions of IL-1β and MCP-1. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced expression and secretions of pro-inflammatory cytokines in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. (A) Molecular structure of apremilast. (B) mRNA levels of IL-1β and MCP-1. (C) Secretions of IL-1β and MCP-1. #### P

    Techniques Used: Expressing

    Apremilast prevents IL-17-induced cell cycle arrest in the G0/G1 phase in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. The cell cycle was assayed using flow cytometry. G0/G1 phase, G2/M phase, and S phase of cells were measured. ## P
    Figure Legend Snippet: Apremilast prevents IL-17-induced cell cycle arrest in the G0/G1 phase in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. The cell cycle was assayed using flow cytometry. G0/G1 phase, G2/M phase, and S phase of cells were measured. ## P

    Techniques Used: Flow Cytometry

    Apremilast prevents IL-17-induced reduction of SIRT1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of a Apremilast (1 µ M) for 24 h. (A) mRNA of SIRT1. (B) Protein level of SIRT1. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced reduction of SIRT1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of a Apremilast (1 µ M) for 24 h. (A) mRNA of SIRT1. (B) Protein level of SIRT1. #### P

    Techniques Used:

    Apremilast prevents IL-17-induced expression of p21 and PAI-1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) mRNA levels of p21 and PAI-1. (B) Protein levels of p21 and PAI-1 as measured by western blotting. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced expression of p21 and PAI-1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) mRNA levels of p21 and PAI-1. (B) Protein levels of p21 and PAI-1 as measured by western blotting. #### P

    Techniques Used: Expressing, Western Blot

    Apremilast prevents IL-17-induced cellular senescence in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. Cellular senescence was measured using SA-β-gal staining. ## P
    Figure Legend Snippet: Apremilast prevents IL-17-induced cellular senescence in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. Cellular senescence was measured using SA-β-gal staining. ## P

    Techniques Used: Staining

    Apremilast prevents IL-17-induced production of ROS in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. Production of ROS was measured using DCFH-DA staining (magnification, ×10). #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced production of ROS in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. Production of ROS was measured using DCFH-DA staining (magnification, ×10). #### P

    Techniques Used: Staining

    19) Product Images from "Apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes mediated by SIRT1"

    Article Title: Apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes mediated by SIRT1

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm.2021.4845

    Knockdown of SIRT1 abolishes the protective effects of apremilast against IL-17-induced cellular senescence and the expression levels of p21 and PAI-1. Cells were transfected with SIRT1 siRNA, followed by stimulation with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) Cellular senescence. (B) mRNA levels of p21 and PAI-1. (C) Protein levels of p21 and PAI-1 as measured by western blotting. #### P
    Figure Legend Snippet: Knockdown of SIRT1 abolishes the protective effects of apremilast against IL-17-induced cellular senescence and the expression levels of p21 and PAI-1. Cells were transfected with SIRT1 siRNA, followed by stimulation with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) Cellular senescence. (B) mRNA levels of p21 and PAI-1. (C) Protein levels of p21 and PAI-1 as measured by western blotting. #### P

    Techniques Used: Expressing, Transfection, Western Blot

    Graphical representation of the underlying mechanism, whereby apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes. IL, interleukin; ROS, reactive oxygen species; SIRT1, sirtuin 1; MCP-1, monocyte chemoattractant protein-1; PAI-1, plasminogen activator inhibitor-1.
    Figure Legend Snippet: Graphical representation of the underlying mechanism, whereby apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes. IL, interleukin; ROS, reactive oxygen species; SIRT1, sirtuin 1; MCP-1, monocyte chemoattractant protein-1; PAI-1, plasminogen activator inhibitor-1.

    Techniques Used:

    Apremilast prevents IL-17-induced expression and secretions of pro-inflammatory cytokines in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. (A) Molecular structure of apremilast. (B) mRNA levels of IL-1β and MCP-1. (C) Secretions of IL-1β and MCP-1. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced expression and secretions of pro-inflammatory cytokines in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. (A) Molecular structure of apremilast. (B) mRNA levels of IL-1β and MCP-1. (C) Secretions of IL-1β and MCP-1. #### P

    Techniques Used: Expressing

    Apremilast prevents IL-17-induced cell cycle arrest in the G0/G1 phase in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. The cell cycle was assayed using flow cytometry. G0/G1 phase, G2/M phase, and S phase of cells were measured. ## P
    Figure Legend Snippet: Apremilast prevents IL-17-induced cell cycle arrest in the G0/G1 phase in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. The cell cycle was assayed using flow cytometry. G0/G1 phase, G2/M phase, and S phase of cells were measured. ## P

    Techniques Used: Flow Cytometry

    Apremilast prevents IL-17-induced reduction of SIRT1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of a Apremilast (1 µ M) for 24 h. (A) mRNA of SIRT1. (B) Protein level of SIRT1. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced reduction of SIRT1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of a Apremilast (1 µ M) for 24 h. (A) mRNA of SIRT1. (B) Protein level of SIRT1. #### P

    Techniques Used:

    Apremilast prevents IL-17-induced expression of p21 and PAI-1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) mRNA levels of p21 and PAI-1. (B) Protein levels of p21 and PAI-1 as measured by western blotting. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced expression of p21 and PAI-1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) mRNA levels of p21 and PAI-1. (B) Protein levels of p21 and PAI-1 as measured by western blotting. #### P

    Techniques Used: Expressing, Western Blot

    Apremilast prevents IL-17-induced cellular senescence in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. Cellular senescence was measured using SA-β-gal staining. ## P
    Figure Legend Snippet: Apremilast prevents IL-17-induced cellular senescence in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. Cellular senescence was measured using SA-β-gal staining. ## P

    Techniques Used: Staining

    Apremilast prevents IL-17-induced production of ROS in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. Production of ROS was measured using DCFH-DA staining (magnification, ×10). #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced production of ROS in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. Production of ROS was measured using DCFH-DA staining (magnification, ×10). #### P

    Techniques Used: Staining

    20) Product Images from "Serum IL-9, IL-17, and TGF-β levels in subjects with diabetic kidney disease (CURES-134)"

    Article Title: Serum IL-9, IL-17, and TGF-β levels in subjects with diabetic kidney disease (CURES-134)

    Journal: Cytokine

    doi: 10.1016/j.cyto.2014.10.009

    Interleukin (IL)-9, IL-17, and TGF-β serum cytokine levels in subjects with NGT, DM, and DKD: (a) IL-17, (b) TGF-β, and (c) IL-9. The geometric mean is represented by the horizontal bars. The p -values were calculated by Kruskal–Wallis one-way analysis of variance. A p -value
    Figure Legend Snippet: Interleukin (IL)-9, IL-17, and TGF-β serum cytokine levels in subjects with NGT, DM, and DKD: (a) IL-17, (b) TGF-β, and (c) IL-9. The geometric mean is represented by the horizontal bars. The p -values were calculated by Kruskal–Wallis one-way analysis of variance. A p -value

    Techniques Used:

    21) Product Images from "Effects of a herbal formulation, KGC3P, and its individual component, nepetin, on coal fly dust-induced airway inflammation"

    Article Title: Effects of a herbal formulation, KGC3P, and its individual component, nepetin, on coal fly dust-induced airway inflammation

    Journal: Scientific Reports

    doi: 10.1038/s41598-020-68965-5

    The effects of KG3P and nepetin on pro-inflammatory cytokines in BALF and lung tissue. KG3P and nepetin reduced ( A ) IL-17A, ( B ) TNF-α, ( C ) MIP2, ( D ) and CXCL1 levels in the BALF obtained from serum collected from WT, CFD, Montelukast (10 mg/kg), KG3P (200 mg/kg, 100 mg/kg), and nepetin (20 mg/kg) treated mice; these levels were measured using ELISA. ( E ) Effects of KG3P and nepetin on the expression of cytokine mRNA in lung tissues. IL-17, ( F ) IL-1β, ( G ) IL-6 ( H ) TNF-α, ( I ) CCR3, ( J ) and MUC5AC expression was determined by Real-Time PCR. Expression is presented as relative quantitation (RQ). Data are from individual mice, with arithmetic mean points shown in histograms. Values in bar graphs are expressed as mean ± SEM (n = 8 mice). # p
    Figure Legend Snippet: The effects of KG3P and nepetin on pro-inflammatory cytokines in BALF and lung tissue. KG3P and nepetin reduced ( A ) IL-17A, ( B ) TNF-α, ( C ) MIP2, ( D ) and CXCL1 levels in the BALF obtained from serum collected from WT, CFD, Montelukast (10 mg/kg), KG3P (200 mg/kg, 100 mg/kg), and nepetin (20 mg/kg) treated mice; these levels were measured using ELISA. ( E ) Effects of KG3P and nepetin on the expression of cytokine mRNA in lung tissues. IL-17, ( F ) IL-1β, ( G ) IL-6 ( H ) TNF-α, ( I ) CCR3, ( J ) and MUC5AC expression was determined by Real-Time PCR. Expression is presented as relative quantitation (RQ). Data are from individual mice, with arithmetic mean points shown in histograms. Values in bar graphs are expressed as mean ± SEM (n = 8 mice). # p

    Techniques Used: Mouse Assay, Enzyme-linked Immunosorbent Assay, Expressing, Real-time Polymerase Chain Reaction, Quantitation Assay

    22) Product Images from "Serum DBI and biomarkers of neuroinflammation in Alzheimer’s disease and delirium"

    Article Title: Serum DBI and biomarkers of neuroinflammation in Alzheimer’s disease and delirium

    Journal: Neurological Sciences

    doi: 10.1007/s10072-020-04608-x

    Serum levels of a IL-17, p
    Figure Legend Snippet: Serum levels of a IL-17, p

    Techniques Used:

    23) Product Images from "Therapeutic Effects of Probiotic Minas Frescal Cheese on the Attenuation of Ulcerative Colitis in a Murine Model"

    Article Title: Therapeutic Effects of Probiotic Minas Frescal Cheese on the Attenuation of Ulcerative Colitis in a Murine Model

    Journal: Frontiers in Microbiology

    doi: 10.3389/fmicb.2021.623920

    Colonic expression of cytokines genes and immunomodulatory effect of probiotic cheese in dextran sodium sulfate (DSS) colitis mice. Colonic mRNA expression levels of (A) IL-10 , (B) IL-1β , and (C) IL-17 genes analyzed by qRT-PCR. Enzyme-linked immunosorbent assay (ELISA) of (D,G) IL-10, (E,H) IL-1β, and (F,I) IL-17 cytokines in spleen and lymph node cell culture supernatant, respectively. The data represent the mean ± SD ( n = 6). Asterisks represent statistically significant differences: * p
    Figure Legend Snippet: Colonic expression of cytokines genes and immunomodulatory effect of probiotic cheese in dextran sodium sulfate (DSS) colitis mice. Colonic mRNA expression levels of (A) IL-10 , (B) IL-1β , and (C) IL-17 genes analyzed by qRT-PCR. Enzyme-linked immunosorbent assay (ELISA) of (D,G) IL-10, (E,H) IL-1β, and (F,I) IL-17 cytokines in spleen and lymph node cell culture supernatant, respectively. The data represent the mean ± SD ( n = 6). Asterisks represent statistically significant differences: * p

    Techniques Used: Expressing, Mouse Assay, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Cell Culture

    24) Product Images from "Cancer-associated fibroblast-derived CXCL11 modulates hepatocellular carcinoma cell migration and tumor metastasis through the circUBAP2/miR-4756/IFIT1/3 axis"

    Article Title: Cancer-associated fibroblast-derived CXCL11 modulates hepatocellular carcinoma cell migration and tumor metastasis through the circUBAP2/miR-4756/IFIT1/3 axis

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-021-03545-7

    Effects of IFIT1/IFIT3 on HCC cell phenotype. A The mRNA expression of IFIT1 and IFIT3 was examined in 12 cases of nonmetastatic HCC tissues, metastatic HCC tissues, and para-carcinoma tissues by real-time PCR. B The protein contents and distribution of IFIT1 and IFIT3 were examined in nonmetastatic HCC tissues, metastatic HCC tissues, and para-carcinoma tissues by IHC staining. C MHCC-97H and Huh-7 cells were transfected with si-circUBAP2 and examined for the mRNA expression of IFIT1 and IFIT3 by real-time PCR. D IFIT1 or IFIT3 silencing was achieved in MHCC-97H and Huh-7 cells by transfecting small interfering RNA targeting IFIT1 or IFIT3 (si-IFIT1-1 or si-IFIT1-2; si-IFIT3-1 or si-IFIT3-2). Si-NC was transfected as a negative control. The transfection efficiency was confirmed by real-time PCR and si-IFIT3-1 and si-IFIT1-2 were chosen for further experiments due to better transfection efficiency. Next, MHCC-97H and Huh-7 cells were transfected with si-NC, si-IFIT1, or si-IFIT3, and examined for E Cell migration by Transwell assay; F Cell migration by wound healing assay; G Cellular protein content and distribution of Vimentin was examined by IF staining; H The protein levels of Vimentin and Twist was examined by Immunoblotting; I The concentrations of IL-1β and IL-17 in the culture medium by ELISA. * P
    Figure Legend Snippet: Effects of IFIT1/IFIT3 on HCC cell phenotype. A The mRNA expression of IFIT1 and IFIT3 was examined in 12 cases of nonmetastatic HCC tissues, metastatic HCC tissues, and para-carcinoma tissues by real-time PCR. B The protein contents and distribution of IFIT1 and IFIT3 were examined in nonmetastatic HCC tissues, metastatic HCC tissues, and para-carcinoma tissues by IHC staining. C MHCC-97H and Huh-7 cells were transfected with si-circUBAP2 and examined for the mRNA expression of IFIT1 and IFIT3 by real-time PCR. D IFIT1 or IFIT3 silencing was achieved in MHCC-97H and Huh-7 cells by transfecting small interfering RNA targeting IFIT1 or IFIT3 (si-IFIT1-1 or si-IFIT1-2; si-IFIT3-1 or si-IFIT3-2). Si-NC was transfected as a negative control. The transfection efficiency was confirmed by real-time PCR and si-IFIT3-1 and si-IFIT1-2 were chosen for further experiments due to better transfection efficiency. Next, MHCC-97H and Huh-7 cells were transfected with si-NC, si-IFIT1, or si-IFIT3, and examined for E Cell migration by Transwell assay; F Cell migration by wound healing assay; G Cellular protein content and distribution of Vimentin was examined by IF staining; H The protein levels of Vimentin and Twist was examined by Immunoblotting; I The concentrations of IL-1β and IL-17 in the culture medium by ELISA. * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Immunohistochemistry, Staining, Transfection, Small Interfering RNA, Negative Control, Migration, Transwell Assay, Wound Healing Assay, Enzyme-linked Immunosorbent Assay

    Combined effects—effects of circUBAP2 and miR-4756 on IFIT1/IFIT3 expression and HCC cell phenotype. MHCC-97H and Huh-7 cells were co-transfected with si-circUBAP2 and miR-4756 inhibitor and examined for A The protein levels of IFIT1 and IFIT3 by Immunoblotting; B The concentrations of IL-1β, and IL-17 in the culture medium by ELISA; C Cell migration by Transwell assay; D Cell migration by wound healing assay; E The cellular protein content and distribution of Vimentin was examined by IF staining; F The protein levels of Vimentin and Twist was examined by Immunoblotting. * P
    Figure Legend Snippet: Combined effects—effects of circUBAP2 and miR-4756 on IFIT1/IFIT3 expression and HCC cell phenotype. MHCC-97H and Huh-7 cells were co-transfected with si-circUBAP2 and miR-4756 inhibitor and examined for A The protein levels of IFIT1 and IFIT3 by Immunoblotting; B The concentrations of IL-1β, and IL-17 in the culture medium by ELISA; C Cell migration by Transwell assay; D Cell migration by wound healing assay; E The cellular protein content and distribution of Vimentin was examined by IF staining; F The protein levels of Vimentin and Twist was examined by Immunoblotting. * P

    Techniques Used: Expressing, Transfection, Enzyme-linked Immunosorbent Assay, Migration, Transwell Assay, Wound Healing Assay, Staining

    The function of circUBAP2 in the effects of CAFs-derived CXCL11 on HCC cells and the selection of mRNA related to the functions of circUBAP2. A Silencing of circUBAP2 was achieved in MHCC-97H and Huh-7 cells by transfecting small interfering RNA targeting circUBAP2 (si-circUBAP2-1 or si-circUBAP2-2). Si-NC was transfected as a negative control. The transfection efficiency was confirmed by real-time PCR and si-circUBAP2-1 was chosen for further experiments for its better transfection efficiency. Then, MHCC-97H and Huh-7 cells were transfected with si-circUBAP2 and examined for B Cell migration by Transwell assay; C Cell migration by wound healing assay; D The protein levels of Vimentin and Twist was examined by Immunoblotting; E The concentrations of IL-1β and IL-17 in the culture medium by ELISA. F , G The Volcano plot and hierarchical clustering heatmap showing differentially expressed mRNAs in CXCL11-treated MHCC-97H based on RNA sequencing. Upregulated genes were applied for H Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling enrichment analysis and I Gene Ontology (GO) of biological process enrichment analysis. J The expression of IFIT1/IFIT3 in CXCL11-treated and untreated HCC cells based on RNA sequencing data. * P
    Figure Legend Snippet: The function of circUBAP2 in the effects of CAFs-derived CXCL11 on HCC cells and the selection of mRNA related to the functions of circUBAP2. A Silencing of circUBAP2 was achieved in MHCC-97H and Huh-7 cells by transfecting small interfering RNA targeting circUBAP2 (si-circUBAP2-1 or si-circUBAP2-2). Si-NC was transfected as a negative control. The transfection efficiency was confirmed by real-time PCR and si-circUBAP2-1 was chosen for further experiments for its better transfection efficiency. Then, MHCC-97H and Huh-7 cells were transfected with si-circUBAP2 and examined for B Cell migration by Transwell assay; C Cell migration by wound healing assay; D The protein levels of Vimentin and Twist was examined by Immunoblotting; E The concentrations of IL-1β and IL-17 in the culture medium by ELISA. F , G The Volcano plot and hierarchical clustering heatmap showing differentially expressed mRNAs in CXCL11-treated MHCC-97H based on RNA sequencing. Upregulated genes were applied for H Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling enrichment analysis and I Gene Ontology (GO) of biological process enrichment analysis. J The expression of IFIT1/IFIT3 in CXCL11-treated and untreated HCC cells based on RNA sequencing data. * P

    Techniques Used: Derivative Assay, Selection, Small Interfering RNA, Transfection, Negative Control, Real-time Polymerase Chain Reaction, Migration, Transwell Assay, Wound Healing Assay, Enzyme-linked Immunosorbent Assay, RNA Sequencing Assay, Expressing

    25) Product Images from "Microenvironmental Th9 and Th17 lymphocytes induce metastatic spreading in lung cancer"

    Article Title: Microenvironmental Th9 and Th17 lymphocytes induce metastatic spreading in lung cancer

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI124037

    CD4 + T cell subtype–specific CM induces EMT and migration in mouse cancer cells. ( A ) Naive CD44 − CD62L + CD4 + T cells were isolated from C57BL/6 mice and treated with specific cytokines for 2–days to differentiate into Th9 (TGF-β and IL-4), Th17 (TGF-β and IL-6), or Th0 (without skewing cytokines) cells. Differentiation was confirmed by performing analysis for production of cell-specific cytokines, such as IL-2, IL-9, IL-17, and IFN-γ by flow cytometry. ( B ) Schematic experimental design showing CM from Th0, Th9, or Th17 cells or from their coculture with cancer cells used to stimulate LLC1 cells and evaluate EMT, proliferation, and migration. ( C ) Western blot analysis of EMT markers (N-cadherin, fibronectin, vimentin, ZO2, and cytokeratin 18) from LLC1 cell lysate after 48 hours of stimulation with Th0, Th9, or Th17 CM. ( D and E ) Proliferation and migration of LLC1 cells after 12-hour and 24-hour stimulation, respectively, with CM. ( F ) Western blot analysis of EMT markers (N-cadherin, fibronectin, vimentin, ZO2, and cytokeratin 18) from LLC1 cell lysate after 48-hour stimulation with respective coculture CMs. ( G and H ) Migration and proliferation of LLC1 cells after 12-hour and 24-hour stimulation, respectively, with coculture CMs. ( n = 3 donors) * P
    Figure Legend Snippet: CD4 + T cell subtype–specific CM induces EMT and migration in mouse cancer cells. ( A ) Naive CD44 − CD62L + CD4 + T cells were isolated from C57BL/6 mice and treated with specific cytokines for 2–days to differentiate into Th9 (TGF-β and IL-4), Th17 (TGF-β and IL-6), or Th0 (without skewing cytokines) cells. Differentiation was confirmed by performing analysis for production of cell-specific cytokines, such as IL-2, IL-9, IL-17, and IFN-γ by flow cytometry. ( B ) Schematic experimental design showing CM from Th0, Th9, or Th17 cells or from their coculture with cancer cells used to stimulate LLC1 cells and evaluate EMT, proliferation, and migration. ( C ) Western blot analysis of EMT markers (N-cadherin, fibronectin, vimentin, ZO2, and cytokeratin 18) from LLC1 cell lysate after 48 hours of stimulation with Th0, Th9, or Th17 CM. ( D and E ) Proliferation and migration of LLC1 cells after 12-hour and 24-hour stimulation, respectively, with CM. ( F ) Western blot analysis of EMT markers (N-cadherin, fibronectin, vimentin, ZO2, and cytokeratin 18) from LLC1 cell lysate after 48-hour stimulation with respective coculture CMs. ( G and H ) Migration and proliferation of LLC1 cells after 12-hour and 24-hour stimulation, respectively, with coculture CMs. ( n = 3 donors) * P

    Techniques Used: Migration, Isolation, Mouse Assay, Flow Cytometry, Western Blot

    Neutralization of IL-9 (anti–IL-9) and IL-17 (anti–IL-17) reduces tumor metastasis to the lung. ( A ) Schematic of experimental design. ( B ) Representative pictures of micro-CT scans, extracted lung images, H E-stained sections, and immunofluorescence of vimentin (red) in sections of lungs with metastatic nodules after treatment with neutralizing antibodies on day 20 after intravenous injection of LLC1 cells. Scale bars: 50 μm. ( C ) Quantification of average lung intensity in treated mice ( n = 5). ( D and E ) FACS analysis of CD4 + and CD8 + immune cells in lungs from treated mice after coinjection ( n = 3–4). ** P
    Figure Legend Snippet: Neutralization of IL-9 (anti–IL-9) and IL-17 (anti–IL-17) reduces tumor metastasis to the lung. ( A ) Schematic of experimental design. ( B ) Representative pictures of micro-CT scans, extracted lung images, H E-stained sections, and immunofluorescence of vimentin (red) in sections of lungs with metastatic nodules after treatment with neutralizing antibodies on day 20 after intravenous injection of LLC1 cells. Scale bars: 50 μm. ( C ) Quantification of average lung intensity in treated mice ( n = 5). ( D and E ) FACS analysis of CD4 + and CD8 + immune cells in lungs from treated mice after coinjection ( n = 3–4). ** P

    Techniques Used: Neutralization, Micro-CT, Staining, Immunofluorescence, Injection, Mouse Assay, FACS

    Coinjection of LLC1 cells with Th9 and/or Th17 in Il9r –/– or Il17ra –/– mice causes increased metastasis and EMT in the discordant ligand-receptor constellation (Th9 in Il17ra –/– mice and Th17 in Il9r –/– mice), with only limited efficacy in the concordant constellation. Naive CD44 − CD62L + CD4 + T cells were isolated from C57BL/6 mice and treated with specific cytokines for 2–3 days in order to differentiate into Th9 (TGF-β and IL-4), Th17 (TGF-β and IL-6) or Th0 (without cytokines) cells. Differentiation was confirmed by performing analysis for IL-9, IL-17, IL-2, and IFN-γ production by flow cytometry. Afterward, Th0, Th9 or Th17 cells were coinjected with LLC1 cells into Il17ra –/– ( A – E ) and Il9r –/– ( F – J ) mice intravenously. ( A ) Schematic of experimental design. ( B ) Representative images of micro-CT scans, extracted lung images, H E-stained sections, and immunofluorescence staining for vimentin (red) and DAPI (blue) in tumor sections. Scale bars: 50 μm. ( C ) Quantification of average lung intensity ( n = 5). ( D – G ) FACS analysis of immune cells in lungs from Il17ra –/– mice after coinjection ( n = 4). ( H ) Schematic of experimental design. ( I ) Representative images of micro-CT scans, extracted lungs, H E-stained sections and immunofluorescence staining for vimentin (red) and DAPI (blue) in tumor sections. Scale bars: 50 μm. ( J ) Quantification of average lung intensity ( n = 5). ( K – N ) FACS analysis of immune cells in lungs from Il9r –/– mice after coinjection ( n = 4). * P
    Figure Legend Snippet: Coinjection of LLC1 cells with Th9 and/or Th17 in Il9r –/– or Il17ra –/– mice causes increased metastasis and EMT in the discordant ligand-receptor constellation (Th9 in Il17ra –/– mice and Th17 in Il9r –/– mice), with only limited efficacy in the concordant constellation. Naive CD44 − CD62L + CD4 + T cells were isolated from C57BL/6 mice and treated with specific cytokines for 2–3 days in order to differentiate into Th9 (TGF-β and IL-4), Th17 (TGF-β and IL-6) or Th0 (without cytokines) cells. Differentiation was confirmed by performing analysis for IL-9, IL-17, IL-2, and IFN-γ production by flow cytometry. Afterward, Th0, Th9 or Th17 cells were coinjected with LLC1 cells into Il17ra –/– ( A – E ) and Il9r –/– ( F – J ) mice intravenously. ( A ) Schematic of experimental design. ( B ) Representative images of micro-CT scans, extracted lung images, H E-stained sections, and immunofluorescence staining for vimentin (red) and DAPI (blue) in tumor sections. Scale bars: 50 μm. ( C ) Quantification of average lung intensity ( n = 5). ( D – G ) FACS analysis of immune cells in lungs from Il17ra –/– mice after coinjection ( n = 4). ( H ) Schematic of experimental design. ( I ) Representative images of micro-CT scans, extracted lungs, H E-stained sections and immunofluorescence staining for vimentin (red) and DAPI (blue) in tumor sections. Scale bars: 50 μm. ( J ) Quantification of average lung intensity ( n = 5). ( K – N ) FACS analysis of immune cells in lungs from Il9r –/– mice after coinjection ( n = 4). * P

    Techniques Used: Mouse Assay, Isolation, Flow Cytometry, Micro-CT, Staining, Immunofluorescence, FACS

    Coinjection of LLC1 cells with Th9 and Th17 cells in immunodeficient mice leads to increased primary tumor growth and metastasis in vivo. ( A ) Schematic of experimental design. Naive CD44 − CD62L + CD4 + T cells were isolated from C57BL/6 mice and then treated with specific cytokines for 2–3 days in order to differentiate into Th9 (TGF-β and IL-4), Th17 (TGF-β and IL-6), or Th0 (without cytokines) cells. Differentiation was confirmed by performing analysis for IL-9, IL-17, IL-2, and IFN-γ production by flow cytometry. Afterward, Th0, Th9, or Th17 cells were coinjected with LLC1 cells into Rag1 –/– mice intravenously followed by anti–IL-9/anti–IL-17 treatment as indicated. ( B ) Representative images of micro-CT, extracted lungs, and H E-stained sections (scale bars: 1 mm), and immunofluorescence staining for vimentin (red) and DAPI (blue) in tumor sections (scale bars: 50 μm). ( C ) Quantification of average lung intensity ( n = 5). ( D – F ) FACS analysis of CD4 + and CD8 + immune cells in lungs from Rag1 –/– mice after Th9 and Th17 coinjection ( n = 3). * P
    Figure Legend Snippet: Coinjection of LLC1 cells with Th9 and Th17 cells in immunodeficient mice leads to increased primary tumor growth and metastasis in vivo. ( A ) Schematic of experimental design. Naive CD44 − CD62L + CD4 + T cells were isolated from C57BL/6 mice and then treated with specific cytokines for 2–3 days in order to differentiate into Th9 (TGF-β and IL-4), Th17 (TGF-β and IL-6), or Th0 (without cytokines) cells. Differentiation was confirmed by performing analysis for IL-9, IL-17, IL-2, and IFN-γ production by flow cytometry. Afterward, Th0, Th9, or Th17 cells were coinjected with LLC1 cells into Rag1 –/– mice intravenously followed by anti–IL-9/anti–IL-17 treatment as indicated. ( B ) Representative images of micro-CT, extracted lungs, and H E-stained sections (scale bars: 1 mm), and immunofluorescence staining for vimentin (red) and DAPI (blue) in tumor sections (scale bars: 50 μm). ( C ) Quantification of average lung intensity ( n = 5). ( D – F ) FACS analysis of CD4 + and CD8 + immune cells in lungs from Rag1 –/– mice after Th9 and Th17 coinjection ( n = 3). * P

    Techniques Used: Mouse Assay, In Vivo, Isolation, Flow Cytometry, Micro-CT, Staining, Immunofluorescence, FACS

    Stimulation with IL-9 and IL-17 results in an EMT-like phenotype in human tumor cells. ( A – I ) A549 were stimulated with ( A – C ) IL-9, ( D – F ) IL-17A, or ( G – I ) IL-17F. After 48-hour stimulation, ( A , D , and G ) Western blot analysis of EMT markers (E-cadherin, vimentin) and ( B , E , and H ) immunocytochemistry of E-cadherin (green) and vimentin (red) were performed. Scale bars: 50 μm. In addition, after 6-hour stimulation, ( C , F , and I ) migration assays were performed. ( J ) Migration of primary human NSCLC cells (PTCs), after 6-hour stimulation with cytokines IL-9, IL-17A, or IL-17F ( n = 9 replicates). * P
    Figure Legend Snippet: Stimulation with IL-9 and IL-17 results in an EMT-like phenotype in human tumor cells. ( A – I ) A549 were stimulated with ( A – C ) IL-9, ( D – F ) IL-17A, or ( G – I ) IL-17F. After 48-hour stimulation, ( A , D , and G ) Western blot analysis of EMT markers (E-cadherin, vimentin) and ( B , E , and H ) immunocytochemistry of E-cadherin (green) and vimentin (red) were performed. Scale bars: 50 μm. In addition, after 6-hour stimulation, ( C , F , and I ) migration assays were performed. ( J ) Migration of primary human NSCLC cells (PTCs), after 6-hour stimulation with cytokines IL-9, IL-17A, or IL-17F ( n = 9 replicates). * P

    Techniques Used: Western Blot, Immunocytochemistry, Migration

    Lymphocyte conditioned medium induces EMT and enhances the migratory potential of human lung cancer cells. Conditioned medium (CM) of A549 cells, primary human NSCLC cells (PTCs), Lymphocytes (Lymph), or coculture (A549/PTCs + Lymph) was used for stimulation of A549 cells and PTCs to assess epithelial-mesenchymal transition (EMT), migration, and proliferation. ( A ) Representative photomicrographs depicting the morphology of tumor cells (A549 and PTCs) after 48 hours of stimulation with CM. Scale bars: 50 μm. ( B and C ) Western blot analysis of EMT markers (E-cadherin, vimentin, N-cadherin, ZO2, and cytokeratin 18) from ( B ) A549 cells and ( C ) PTCs lysates after 48 hours stimulation with CM. ( D ) Immunofluorescence of E-cadherin (green) and vimentin (red) after 48 hours stimulation of A549 cells with CM. Scale bars: 50 μm. ( E ) mRNA profile expression of EMT markers after 24 hours stimulation of A549 cells ( n = 3 donors; 2 experimental replicates). ( F ) Migration and proliferation (as assessed by BrdU incorporation) of A549 cells after 6 hours and 24 hours of stimulation with CM, respectively. ( G ) Migration and proliferation (as assessed by BrdU incorporation) of PTCs after 12 hours and 48 hours of stimulation with CM, respectively ( n = 3 donors). ( H ) Quantitative analysis of IL-9 and IL-17A detected in CM with or without coculture by ELISA ( n = 4 donors 2 experimental replicates). * P
    Figure Legend Snippet: Lymphocyte conditioned medium induces EMT and enhances the migratory potential of human lung cancer cells. Conditioned medium (CM) of A549 cells, primary human NSCLC cells (PTCs), Lymphocytes (Lymph), or coculture (A549/PTCs + Lymph) was used for stimulation of A549 cells and PTCs to assess epithelial-mesenchymal transition (EMT), migration, and proliferation. ( A ) Representative photomicrographs depicting the morphology of tumor cells (A549 and PTCs) after 48 hours of stimulation with CM. Scale bars: 50 μm. ( B and C ) Western blot analysis of EMT markers (E-cadherin, vimentin, N-cadherin, ZO2, and cytokeratin 18) from ( B ) A549 cells and ( C ) PTCs lysates after 48 hours stimulation with CM. ( D ) Immunofluorescence of E-cadherin (green) and vimentin (red) after 48 hours stimulation of A549 cells with CM. Scale bars: 50 μm. ( E ) mRNA profile expression of EMT markers after 24 hours stimulation of A549 cells ( n = 3 donors; 2 experimental replicates). ( F ) Migration and proliferation (as assessed by BrdU incorporation) of A549 cells after 6 hours and 24 hours of stimulation with CM, respectively. ( G ) Migration and proliferation (as assessed by BrdU incorporation) of PTCs after 12 hours and 48 hours of stimulation with CM, respectively ( n = 3 donors). ( H ) Quantitative analysis of IL-9 and IL-17A detected in CM with or without coculture by ELISA ( n = 4 donors 2 experimental replicates). * P

    Techniques Used: Migration, Western Blot, Immunofluorescence, Expressing, BrdU Incorporation Assay, Enzyme-linked Immunosorbent Assay

    26) Product Images from "IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes. IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes"

    Article Title: IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes. IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes

    Journal: Journal of Cellular Physiology

    doi: 10.1002/jcp.29323

    IL‐17 enhances the osteogenic differentiation of mMSCs but not MC3T3‐E1. (a,b) Increased mineralized nodule formation (red) in mesenchymal stem cells (MSCs) and MLO‐Y4 osteocytes after treatment with 0.5–50 ng/ml IL‐17 in osteogenic induction medium for 14 days. Mineralization of MC3T3‐E1 cells was inhibited, and there was no change in mineralization levels in MLO‐A5 cells. (c,d) Alkaline phosphatase (ALP) expression (purple) of MSCs was enhanced by IL‐17 (7 days). (e,f) mRNA expression of factors after IL‐17 treatment for 24 hr. Treatment with IL‐17 increased runt‐related transcription factor 2 (RUNX2), collagen‐1 (COL‐1) and osteocalcin (OCN) in MSCs, and only RUNX2 in MLO‐Y4 cells. All three factors were decreased in MC3T3‐E1 cells and no significant changes were measured in MLO‐A5 cells. (f) IL‐17 receptor A (RA) and IL‐6 were upregulated in MSCs and MLO‐Y4 cells, and IL‐β was significantly upregulated in MSCs. IL, interleukin; mMSC, mouse MSCs; mRNA, messenger RNA
    Figure Legend Snippet: IL‐17 enhances the osteogenic differentiation of mMSCs but not MC3T3‐E1. (a,b) Increased mineralized nodule formation (red) in mesenchymal stem cells (MSCs) and MLO‐Y4 osteocytes after treatment with 0.5–50 ng/ml IL‐17 in osteogenic induction medium for 14 days. Mineralization of MC3T3‐E1 cells was inhibited, and there was no change in mineralization levels in MLO‐A5 cells. (c,d) Alkaline phosphatase (ALP) expression (purple) of MSCs was enhanced by IL‐17 (7 days). (e,f) mRNA expression of factors after IL‐17 treatment for 24 hr. Treatment with IL‐17 increased runt‐related transcription factor 2 (RUNX2), collagen‐1 (COL‐1) and osteocalcin (OCN) in MSCs, and only RUNX2 in MLO‐Y4 cells. All three factors were decreased in MC3T3‐E1 cells and no significant changes were measured in MLO‐A5 cells. (f) IL‐17 receptor A (RA) and IL‐6 were upregulated in MSCs and MLO‐Y4 cells, and IL‐β was significantly upregulated in MSCs. IL, interleukin; mMSC, mouse MSCs; mRNA, messenger RNA

    Techniques Used: Expressing

    Osteogenic differentiation of mesenchymal stem cells (MSCs) after coculture (CC) with osteocytes is further enhanced by interleukin‐17 (IL‐17). (a) We used a transwell CC system, with MSCs seeded in the lower chamber and various osteogenic cells in the upper chambers. Cells were grown in osteoinductive media (OM) with or without IL‐17. MSCs in both the upper and lower chambers served as a control. (b,c) Alizarin red staining to detect mineralized nodule formation (red) in the lower chambers following CC with or without IL‐17 stimulation (50 ng/ml). IL‐17 enhanced mineralization in control‐MSCs (top row). No obvious change was found for MSCs in MC3T3‐E1 CC and MLO‐A5 CC (second and third rows). An increase in Alizarin red staining was found for MSCs in MLO‐Y4 CC, which was further increased with IL‐17. (d,e) ALP staining and quantification of ALP activity. IL‐17 induced ALP expression (purple) in MSCs under control CC condition (top row). ALP expression was also induced in MSC in CC with MLO‐Y4 cells (bottom row; Day 7). Each experiment was repeated at least three times independently and three different mMSC cell lines were used. ALP, alkaline phosphatase
    Figure Legend Snippet: Osteogenic differentiation of mesenchymal stem cells (MSCs) after coculture (CC) with osteocytes is further enhanced by interleukin‐17 (IL‐17). (a) We used a transwell CC system, with MSCs seeded in the lower chamber and various osteogenic cells in the upper chambers. Cells were grown in osteoinductive media (OM) with or without IL‐17. MSCs in both the upper and lower chambers served as a control. (b,c) Alizarin red staining to detect mineralized nodule formation (red) in the lower chambers following CC with or without IL‐17 stimulation (50 ng/ml). IL‐17 enhanced mineralization in control‐MSCs (top row). No obvious change was found for MSCs in MC3T3‐E1 CC and MLO‐A5 CC (second and third rows). An increase in Alizarin red staining was found for MSCs in MLO‐Y4 CC, which was further increased with IL‐17. (d,e) ALP staining and quantification of ALP activity. IL‐17 induced ALP expression (purple) in MSCs under control CC condition (top row). ALP expression was also induced in MSC in CC with MLO‐Y4 cells (bottom row; Day 7). Each experiment was repeated at least three times independently and three different mMSC cell lines were used. ALP, alkaline phosphatase

    Techniques Used: Staining, Activity Assay, Expressing

    Schematic of the findings of this study. Mesenchymal stem cells (MSCs) exposed to interleukin (IL)‐17 and osteocytes in coculture underwent differentiation along the osteogenic lineage, better than when exposed to either stimulus alone. IL‐17 induces the expression of inflammatory markers, IL‐6 and IL‐1β, which in turn, increase the expression of markers of osteoblastic differentiation in MSCs, such as alkaline phosphatase (ALP), runt‐related transcription factor 2 (RUNX2), osteocalcin (OCN) and collagen‐1 (COL‐1). The activation of extracellular signal‐regulated kinase 1/2 (ERK1/2), AKT, and signal transducer and activator of transcription 3 (STAT3) regulated IL‐17 induced osteogenesis in the MSC niche, which could be inhibited by antibodies of IL‐6 and IL‐1β
    Figure Legend Snippet: Schematic of the findings of this study. Mesenchymal stem cells (MSCs) exposed to interleukin (IL)‐17 and osteocytes in coculture underwent differentiation along the osteogenic lineage, better than when exposed to either stimulus alone. IL‐17 induces the expression of inflammatory markers, IL‐6 and IL‐1β, which in turn, increase the expression of markers of osteoblastic differentiation in MSCs, such as alkaline phosphatase (ALP), runt‐related transcription factor 2 (RUNX2), osteocalcin (OCN) and collagen‐1 (COL‐1). The activation of extracellular signal‐regulated kinase 1/2 (ERK1/2), AKT, and signal transducer and activator of transcription 3 (STAT3) regulated IL‐17 induced osteogenesis in the MSC niche, which could be inhibited by antibodies of IL‐6 and IL‐1β

    Techniques Used: Expressing, Activation Assay

    Three‐dimensional culture of mesenchymal stem cells (MSCs) on a polycaprolactone (PCL) scaffold enhances IL‐17‐stimulated osteogenesis when cocultured with MLO‐Y4 osteocytes. (a) Alizarin red staining shows mineralized nodule formation (red) in mouse MSCs (mMSCs) and human‐induced pluripotent stem cell‐derived MSCs (hMSCs) cultures on Day 10. Growth on the PCL scaffold promoted osteogenesis, and this could be further enhanced by coculture with MLO‐Y4 osteocytes and IL‐17 stimulation. (b) Quantification of mMSCs mineralazation. (c) Quantification of hMSCs mineralization. IL, interleukin
    Figure Legend Snippet: Three‐dimensional culture of mesenchymal stem cells (MSCs) on a polycaprolactone (PCL) scaffold enhances IL‐17‐stimulated osteogenesis when cocultured with MLO‐Y4 osteocytes. (a) Alizarin red staining shows mineralized nodule formation (red) in mouse MSCs (mMSCs) and human‐induced pluripotent stem cell‐derived MSCs (hMSCs) cultures on Day 10. Growth on the PCL scaffold promoted osteogenesis, and this could be further enhanced by coculture with MLO‐Y4 osteocytes and IL‐17 stimulation. (b) Quantification of mMSCs mineralazation. (c) Quantification of hMSCs mineralization. IL, interleukin

    Techniques Used: Staining, Derivative Assay

    Interleukin (IL)‐17 activates intercellular signaling of osteogenesis via IL‐6 and IL‐1β. Anti‐IL‐6 and anti‐IL‐1β antibodies were used in the IL‐17–induced coculture (CC) system. Both antibodies could effectively inhibit (a,b) the formation of mineral nodules, (c) the mRNA expression of ALP, RUNX2, OCN, and COL‐1 and (d) AKT, STAT3, and ERK1/2 phosphorylation in the control‐MSCs CC and MLO‐Y4 CC at Day 14 after IL‐17 treatment; albeit, the effects of IL‐1β neutralization were weaker than that of IL‐6. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3
    Figure Legend Snippet: Interleukin (IL)‐17 activates intercellular signaling of osteogenesis via IL‐6 and IL‐1β. Anti‐IL‐6 and anti‐IL‐1β antibodies were used in the IL‐17–induced coculture (CC) system. Both antibodies could effectively inhibit (a,b) the formation of mineral nodules, (c) the mRNA expression of ALP, RUNX2, OCN, and COL‐1 and (d) AKT, STAT3, and ERK1/2 phosphorylation in the control‐MSCs CC and MLO‐Y4 CC at Day 14 after IL‐17 treatment; albeit, the effects of IL‐1β neutralization were weaker than that of IL‐6. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3

    Techniques Used: Expressing, Neutralization

    Interleukin (IL)‐17 upregulates inflammatory factors, IL‐6 and IL‐1β, and activates ERK, AKT, and STAT3 signaling in mesenchymal stem cells (MSC)–MLO‐Y4 cocultures (CC). (a) The medium from CCs of MSCs and MLO‐Y4 osteocytes was analyzed by ELISA on days 7, 10, and 14. IL‐6 and IL‐1β were synergistically induced by IL‐17 (50 ng/ml) and osteocyte CC. (b) MLO‐Y4 osteocytes in the upper chamber of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1β after IL‐17 treatment. (c) MSCs in the lower chambers of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1 β after IL‐17 treatment. (d) Increased phosphorylation of signaling regulators ERK1/2, AKT, and STAT3 after IL‐17 stimulation in MLO‐Y4 CCs. Phosphorylated SARK/JNK and p38 were unchanged (24 hr). ELISA, enzyme‐linked immunosorbent assay; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; RA, receptor A; STAT3, signal transducer and activator of transcription 3. * p
    Figure Legend Snippet: Interleukin (IL)‐17 upregulates inflammatory factors, IL‐6 and IL‐1β, and activates ERK, AKT, and STAT3 signaling in mesenchymal stem cells (MSC)–MLO‐Y4 cocultures (CC). (a) The medium from CCs of MSCs and MLO‐Y4 osteocytes was analyzed by ELISA on days 7, 10, and 14. IL‐6 and IL‐1β were synergistically induced by IL‐17 (50 ng/ml) and osteocyte CC. (b) MLO‐Y4 osteocytes in the upper chamber of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1β after IL‐17 treatment. (c) MSCs in the lower chambers of the transwell CC were tested for changes in the mRNA expression levels of IL‐17RA, IL‐6, and IL‐1 β after IL‐17 treatment. (d) Increased phosphorylation of signaling regulators ERK1/2, AKT, and STAT3 after IL‐17 stimulation in MLO‐Y4 CCs. Phosphorylated SARK/JNK and p38 were unchanged (24 hr). ELISA, enzyme‐linked immunosorbent assay; ERK1/2, extracellular signal‐regulated kinase 1/2; mRNA, messenger RNA; RA, receptor A; STAT3, signal transducer and activator of transcription 3. * p

    Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing

    AKT, STAT3, and ERK1/2 pathways are activated in IL‐17–mediated osteoblastic differentiation. (a) Ten micrometer of the AKT inhibitor Perifosine, the JAK1 and JAK2 inhibitor AZD1480 (to inhibit STAT3 signaling), and the MEK1/2 inhibitor U0126, solubilized in 0.1% DMSO in serum‐free medium efficiently suppressed AKT, STAT3, and ERK1/2 expression, respectively, in MSCs. (b,c) IL‐17–induced coculture systems with 10 μM of inhibitors inhibited mineralization (14 days). (d–g) Relative mRNA expression of ALP, RUNX2, OCN, and COL‐1 was significantly decreased by the suppression of AKT, STAT3, and ERK1/2 signaling pathways. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; IL, interleukin; mRNA, messenger RNA; MSC, mesenchymal stem cell; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3. (* p
    Figure Legend Snippet: AKT, STAT3, and ERK1/2 pathways are activated in IL‐17–mediated osteoblastic differentiation. (a) Ten micrometer of the AKT inhibitor Perifosine, the JAK1 and JAK2 inhibitor AZD1480 (to inhibit STAT3 signaling), and the MEK1/2 inhibitor U0126, solubilized in 0.1% DMSO in serum‐free medium efficiently suppressed AKT, STAT3, and ERK1/2 expression, respectively, in MSCs. (b,c) IL‐17–induced coculture systems with 10 μM of inhibitors inhibited mineralization (14 days). (d–g) Relative mRNA expression of ALP, RUNX2, OCN, and COL‐1 was significantly decreased by the suppression of AKT, STAT3, and ERK1/2 signaling pathways. ALP, alkaline phosphatase; COL‐1, collagen‐1; ERK1/2, extracellular signal‐regulated kinase 1/2; IL, interleukin; mRNA, messenger RNA; MSC, mesenchymal stem cell; OCN, osteocalcin; RUNX2, runt‐related transcription factor 2; STAT3, signal transducer and activator of transcription 3. (* p

    Techniques Used: Expressing

    27) Product Images from "Interleukin‐38 alleviates cardiac remodelling after myocardial infarction, et al. Interleukin‐38 alleviates cardiac remodelling after myocardial infarction"

    Article Title: Interleukin‐38 alleviates cardiac remodelling after myocardial infarction, et al. Interleukin‐38 alleviates cardiac remodelling after myocardial infarction

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.14741

    IL‐38 plus TNI treated DCs augment the percentage of regulatory T cells in vitro. We used small doses of LPS (10 ng/mL) and TNI (1 μg/mL) to induce the tolerance of DCs. A‐B, IL‐10 and IDO mRNA expression levels in cultured DCs. C‐E, IL‐23, TNF‐α, and IFN‐γ expression levels were assessed by ELISA in cultured supernatants of different DCs. F, Splenic CD4 + T cells (1 × 10 6 cells/mL) were cultured for 3 d in the presence of medium alone or combined with imDCs, mDCs, or tDCs (2 × 10 5 cells/mL). The cells were stained with anti‐CD4, anti‐CD25, and anti‐Foxp3 and analyzed by flow cytometry. G‐J, Analysis of the expression levels of IFN‐γ, IL‐17A, IL‐22 and IL‐10 in culture supernatants of CD4 + T cells using ELISA in different groups. (each group n=4 and repeat at least three times). * P
    Figure Legend Snippet: IL‐38 plus TNI treated DCs augment the percentage of regulatory T cells in vitro. We used small doses of LPS (10 ng/mL) and TNI (1 μg/mL) to induce the tolerance of DCs. A‐B, IL‐10 and IDO mRNA expression levels in cultured DCs. C‐E, IL‐23, TNF‐α, and IFN‐γ expression levels were assessed by ELISA in cultured supernatants of different DCs. F, Splenic CD4 + T cells (1 × 10 6 cells/mL) were cultured for 3 d in the presence of medium alone or combined with imDCs, mDCs, or tDCs (2 × 10 5 cells/mL). The cells were stained with anti‐CD4, anti‐CD25, and anti‐Foxp3 and analyzed by flow cytometry. G‐J, Analysis of the expression levels of IFN‐γ, IL‐17A, IL‐22 and IL‐10 in culture supernatants of CD4 + T cells using ELISA in different groups. (each group n=4 and repeat at least three times). * P

    Techniques Used: In Vitro, Expressing, Cell Culture, Enzyme-linked Immunosorbent Assay, Staining, Flow Cytometry, Cytometry

    IL‐38 inhibits inflammatory response in the infarcted heart. A, Representative images of haematoxylin and eosin (HE) staining, infiltration of myeloperoxidase (MPO + ) neutrophils and mouse CD68 + macrophages in the border area of infarcted hearts. Images for HE staining and neutrophils are from day 3 after MI, and images for macrophages are from day7 post‐MI. B, Infiltration of neutrophils and macrophages were compared between the different groups at set time points (each group n = 6). C–F, Analysis of mRNA levels of IL‐6, IL‐1β, TNF‐α and IL‐17A on day 3 and 7 after MI. Data are depicted as fold changes vs sham and shown as the mean ± SEM of 3‐6 independent experiments. ** P
    Figure Legend Snippet: IL‐38 inhibits inflammatory response in the infarcted heart. A, Representative images of haematoxylin and eosin (HE) staining, infiltration of myeloperoxidase (MPO + ) neutrophils and mouse CD68 + macrophages in the border area of infarcted hearts. Images for HE staining and neutrophils are from day 3 after MI, and images for macrophages are from day7 post‐MI. B, Infiltration of neutrophils and macrophages were compared between the different groups at set time points (each group n = 6). C–F, Analysis of mRNA levels of IL‐6, IL‐1β, TNF‐α and IL‐17A on day 3 and 7 after MI. Data are depicted as fold changes vs sham and shown as the mean ± SEM of 3‐6 independent experiments. ** P

    Techniques Used: Staining

    28) Product Images from "Apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes mediated by SIRT1"

    Article Title: Apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes mediated by SIRT1

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm.2021.4845

    Knockdown of SIRT1 abolishes the protective effects of apremilast against IL-17-induced cellular senescence and the expression levels of p21 and PAI-1. Cells were transfected with SIRT1 siRNA, followed by stimulation with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) Cellular senescence. (B) mRNA levels of p21 and PAI-1. (C) Protein levels of p21 and PAI-1 as measured by western blotting. #### P
    Figure Legend Snippet: Knockdown of SIRT1 abolishes the protective effects of apremilast against IL-17-induced cellular senescence and the expression levels of p21 and PAI-1. Cells were transfected with SIRT1 siRNA, followed by stimulation with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) Cellular senescence. (B) mRNA levels of p21 and PAI-1. (C) Protein levels of p21 and PAI-1 as measured by western blotting. #### P

    Techniques Used: Expressing, Transfection, Western Blot

    Graphical representation of the underlying mechanism, whereby apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes. IL, interleukin; ROS, reactive oxygen species; SIRT1, sirtuin 1; MCP-1, monocyte chemoattractant protein-1; PAI-1, plasminogen activator inhibitor-1.
    Figure Legend Snippet: Graphical representation of the underlying mechanism, whereby apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes. IL, interleukin; ROS, reactive oxygen species; SIRT1, sirtuin 1; MCP-1, monocyte chemoattractant protein-1; PAI-1, plasminogen activator inhibitor-1.

    Techniques Used:

    Apremilast prevents IL-17-induced expression and secretions of pro-inflammatory cytokines in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. (A) Molecular structure of apremilast. (B) mRNA levels of IL-1β and MCP-1. (C) Secretions of IL-1β and MCP-1. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced expression and secretions of pro-inflammatory cytokines in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. (A) Molecular structure of apremilast. (B) mRNA levels of IL-1β and MCP-1. (C) Secretions of IL-1β and MCP-1. #### P

    Techniques Used: Expressing

    Apremilast prevents IL-17-induced cell cycle arrest in the G0/G1 phase in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. The cell cycle was assayed using flow cytometry. G0/G1 phase, G2/M phase, and S phase of cells were measured. ## P
    Figure Legend Snippet: Apremilast prevents IL-17-induced cell cycle arrest in the G0/G1 phase in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. The cell cycle was assayed using flow cytometry. G0/G1 phase, G2/M phase, and S phase of cells were measured. ## P

    Techniques Used: Flow Cytometry

    Apremilast prevents IL-17-induced reduction of SIRT1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of a Apremilast (1 µ M) for 24 h. (A) mRNA of SIRT1. (B) Protein level of SIRT1. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced reduction of SIRT1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of a Apremilast (1 µ M) for 24 h. (A) mRNA of SIRT1. (B) Protein level of SIRT1. #### P

    Techniques Used:

    Apremilast prevents IL-17-induced expression of p21 and PAI-1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) mRNA levels of p21 and PAI-1. (B) Protein levels of p21 and PAI-1 as measured by western blotting. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced expression of p21 and PAI-1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) mRNA levels of p21 and PAI-1. (B) Protein levels of p21 and PAI-1 as measured by western blotting. #### P

    Techniques Used: Expressing, Western Blot

    Apremilast prevents IL-17-induced cellular senescence in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. Cellular senescence was measured using SA-β-gal staining. ## P
    Figure Legend Snippet: Apremilast prevents IL-17-induced cellular senescence in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. Cellular senescence was measured using SA-β-gal staining. ## P

    Techniques Used: Staining

    Apremilast prevents IL-17-induced production of ROS in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. Production of ROS was measured using DCFH-DA staining (magnification, ×10). #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced production of ROS in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. Production of ROS was measured using DCFH-DA staining (magnification, ×10). #### P

    Techniques Used: Staining

    29) Product Images from "Apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes mediated by SIRT1"

    Article Title: Apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes mediated by SIRT1

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm.2021.4845

    Knockdown of SIRT1 abolishes the protective effects of apremilast against IL-17-induced cellular senescence and the expression levels of p21 and PAI-1. Cells were transfected with SIRT1 siRNA, followed by stimulation with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) Cellular senescence. (B) mRNA levels of p21 and PAI-1. (C) Protein levels of p21 and PAI-1 as measured by western blotting. #### P
    Figure Legend Snippet: Knockdown of SIRT1 abolishes the protective effects of apremilast against IL-17-induced cellular senescence and the expression levels of p21 and PAI-1. Cells were transfected with SIRT1 siRNA, followed by stimulation with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) Cellular senescence. (B) mRNA levels of p21 and PAI-1. (C) Protein levels of p21 and PAI-1 as measured by western blotting. #### P

    Techniques Used: Expressing, Transfection, Western Blot

    Graphical representation of the underlying mechanism, whereby apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes. IL, interleukin; ROS, reactive oxygen species; SIRT1, sirtuin 1; MCP-1, monocyte chemoattractant protein-1; PAI-1, plasminogen activator inhibitor-1.
    Figure Legend Snippet: Graphical representation of the underlying mechanism, whereby apremilast prevents IL-17-induced cellular senescence in ATDC5 chondrocytes. IL, interleukin; ROS, reactive oxygen species; SIRT1, sirtuin 1; MCP-1, monocyte chemoattractant protein-1; PAI-1, plasminogen activator inhibitor-1.

    Techniques Used:

    Apremilast prevents IL-17-induced expression and secretions of pro-inflammatory cytokines in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. (A) Molecular structure of apremilast. (B) mRNA levels of IL-1β and MCP-1. (C) Secretions of IL-1β and MCP-1. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced expression and secretions of pro-inflammatory cytokines in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. (A) Molecular structure of apremilast. (B) mRNA levels of IL-1β and MCP-1. (C) Secretions of IL-1β and MCP-1. #### P

    Techniques Used: Expressing

    Apremilast prevents IL-17-induced cell cycle arrest in the G0/G1 phase in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. The cell cycle was assayed using flow cytometry. G0/G1 phase, G2/M phase, and S phase of cells were measured. ## P
    Figure Legend Snippet: Apremilast prevents IL-17-induced cell cycle arrest in the G0/G1 phase in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. The cell cycle was assayed using flow cytometry. G0/G1 phase, G2/M phase, and S phase of cells were measured. ## P

    Techniques Used: Flow Cytometry

    Apremilast prevents IL-17-induced reduction of SIRT1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of a Apremilast (1 µ M) for 24 h. (A) mRNA of SIRT1. (B) Protein level of SIRT1. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced reduction of SIRT1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of a Apremilast (1 µ M) for 24 h. (A) mRNA of SIRT1. (B) Protein level of SIRT1. #### P

    Techniques Used:

    Apremilast prevents IL-17-induced expression of p21 and PAI-1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) mRNA levels of p21 and PAI-1. (B) Protein levels of p21 and PAI-1 as measured by western blotting. #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced expression of p21 and PAI-1 in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 24 h. (A) mRNA levels of p21 and PAI-1. (B) Protein levels of p21 and PAI-1 as measured by western blotting. #### P

    Techniques Used: Expressing, Western Blot

    Apremilast prevents IL-17-induced cellular senescence in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. Cellular senescence was measured using SA-β-gal staining. ## P
    Figure Legend Snippet: Apremilast prevents IL-17-induced cellular senescence in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (1 µ M) for 7 days. Cellular senescence was measured using SA-β-gal staining. ## P

    Techniques Used: Staining

    Apremilast prevents IL-17-induced production of ROS in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. Production of ROS was measured using DCFH-DA staining (magnification, ×10). #### P
    Figure Legend Snippet: Apremilast prevents IL-17-induced production of ROS in mouse ATDC5 chondrocytes. Cells were treated with IL-17 (10 ng/ml) in the presence or absence of apremilast (0.5 and 1 µ M) for 24 h. Production of ROS was measured using DCFH-DA staining (magnification, ×10). #### P

    Techniques Used: Staining

    30) Product Images from "The role of the msaABCR operon in implant-associated chronic osteomyelitis in Staphylococcus aureus USA300 LAC"

    Article Title: The role of the msaABCR operon in implant-associated chronic osteomyelitis in Staphylococcus aureus USA300 LAC

    Journal: BMC Microbiology

    doi: 10.1186/s12866-020-01964-8

    Immune response against staphylococcal bone infection. Blood samples were collected after each infection period (on days 4, 8 and 15) and were processed to obtain serum. Quantitative measurements of IL-1 ( a ), IL-17 ( b ), and IL-6 ( c ) were performed. All values were analyzed using one-way ANOVA followed by a post-hoc Tukey test. Error bars indicate standard errors of the means. A P -value of
    Figure Legend Snippet: Immune response against staphylococcal bone infection. Blood samples were collected after each infection period (on days 4, 8 and 15) and were processed to obtain serum. Quantitative measurements of IL-1 ( a ), IL-17 ( b ), and IL-6 ( c ) were performed. All values were analyzed using one-way ANOVA followed by a post-hoc Tukey test. Error bars indicate standard errors of the means. A P -value of

    Techniques Used: Infection

    31) Product Images from "Alcohol-induced interleukin-17 expression causes murine lung fibroblast-to-myofibroblast transdifferentiation via Thy-1 downregulation"

    Article Title: Alcohol-induced interleukin-17 expression causes murine lung fibroblast-to-myofibroblast transdifferentiation via Thy-1 downregulation

    Journal: Alcoholism, clinical and experimental research

    doi: 10.1111/acer.14110

    Bleomycin-induced acute lung injury augments IL-17 expression in alcohol-fed mice. Three-month-old wild-type mice were treated ± alcohol (20% v/v in drinking water for 8 weeks) before intratracheal administration of bleomycin (2.5 units/kg) or saline vehicle. Lungs were collected at 7 and 14 days following induction of injury and analyzed for IL-17 protein expression by Western blot. *p
    Figure Legend Snippet: Bleomycin-induced acute lung injury augments IL-17 expression in alcohol-fed mice. Three-month-old wild-type mice were treated ± alcohol (20% v/v in drinking water for 8 weeks) before intratracheal administration of bleomycin (2.5 units/kg) or saline vehicle. Lungs were collected at 7 and 14 days following induction of injury and analyzed for IL-17 protein expression by Western blot. *p

    Techniques Used: Expressing, Mouse Assay, Western Blot

    Chronic alcohol ingestion increases the systemic Th17 immune response. CD4 + T cells were harvested from the spleen and lymph nodes of three-month-old control-fed and alcohol-fed wild-type mice (20% v/v in drinking water for 8 weeks). ( A ) Cells were analyzed for IL-17 gene expression by quantitative PCR. CD4 + T cells harvested from control-fed and alcohol-fed animals were activated ex vivo with anti-CD3 (5 μg/ml) and anti-CD28 (1 μg/ml) for 72 hours. ( B ) Cell culture supernatant was analyzed for IL-17 protein expression by ELISA. ( C ) Lastly, FACS analysis was performed on freshly isolated peripheral CD4 + T cells to determine the percentage of Th17 cells (CD4 + IL-17 + ). The right panel shows representative scattered dot plots. *p
    Figure Legend Snippet: Chronic alcohol ingestion increases the systemic Th17 immune response. CD4 + T cells were harvested from the spleen and lymph nodes of three-month-old control-fed and alcohol-fed wild-type mice (20% v/v in drinking water for 8 weeks). ( A ) Cells were analyzed for IL-17 gene expression by quantitative PCR. CD4 + T cells harvested from control-fed and alcohol-fed animals were activated ex vivo with anti-CD3 (5 μg/ml) and anti-CD28 (1 μg/ml) for 72 hours. ( B ) Cell culture supernatant was analyzed for IL-17 protein expression by ELISA. ( C ) Lastly, FACS analysis was performed on freshly isolated peripheral CD4 + T cells to determine the percentage of Th17 cells (CD4 + IL-17 + ). The right panel shows representative scattered dot plots. *p

    Techniques Used: Mouse Assay, Expressing, Real-time Polymerase Chain Reaction, Ex Vivo, Cell Culture, Enzyme-linked Immunosorbent Assay, FACS, Isolation

    Chronic alcohol ingestion did not alter the CD4 + Th17 population in the lung. CD4 + T cells were isolated from the lung of three-month-old control-fed and alcohol-fed wild-type mice. FACS analysis was performed on freshly isolated peripheral CD4 + T cells to determine the percentage of Th17 cells (CD4 + IL-17 + ). The right panel shows representative scattered dot plots. N = 3 per group. Data are presented as mean ± SEM.
    Figure Legend Snippet: Chronic alcohol ingestion did not alter the CD4 + Th17 population in the lung. CD4 + T cells were isolated from the lung of three-month-old control-fed and alcohol-fed wild-type mice. FACS analysis was performed on freshly isolated peripheral CD4 + T cells to determine the percentage of Th17 cells (CD4 + IL-17 + ). The right panel shows representative scattered dot plots. N = 3 per group. Data are presented as mean ± SEM.

    Techniques Used: Isolation, Mouse Assay, FACS

    Alcohol exposure induces Th17 differentiation and enhances IL-17 production in both naïve CD4 + T helper cells (Th0) and Th17 cells in vitro . CD4 + T cells were harvested from the spleen and lymph nodes of three-month-old wild-type mice. Naïve CD4 + T helper cells were activated ex vivo with anti-CD3 (5 μg/ml) and anti-CD28 (1 μg/ml) for 72 hours (Th0). A subgroup of Th0 cells were activated and polarized with recombinant IL-6 (20 ng/ml) and recombinant TGFβ1 (5 ng/ml) for 72 hours to generate Th17 cells. Th0 and Th17 CD4 + T cells were cultured ± alcohol (60 mM) for 72 hours. The cell culture supernatant was collected and analyzed for IL-17 production by ELISA. *p
    Figure Legend Snippet: Alcohol exposure induces Th17 differentiation and enhances IL-17 production in both naïve CD4 + T helper cells (Th0) and Th17 cells in vitro . CD4 + T cells were harvested from the spleen and lymph nodes of three-month-old wild-type mice. Naïve CD4 + T helper cells were activated ex vivo with anti-CD3 (5 μg/ml) and anti-CD28 (1 μg/ml) for 72 hours (Th0). A subgroup of Th0 cells were activated and polarized with recombinant IL-6 (20 ng/ml) and recombinant TGFβ1 (5 ng/ml) for 72 hours to generate Th17 cells. Th0 and Th17 CD4 + T cells were cultured ± alcohol (60 mM) for 72 hours. The cell culture supernatant was collected and analyzed for IL-17 production by ELISA. *p

    Techniques Used: In Vitro, Mouse Assay, Ex Vivo, Recombinant, Cell Culture, Enzyme-linked Immunosorbent Assay

    IL-17 and TGFβ1 independently and additively inhibit lung fibroblast Thy-1 expression. Primary lung fibroblasts (PLFs from passage 3–8) were isolated from wild-type mice and cultured ± IL-17 (10 ng/ml) ± TGFβ1 (2 ng/ml) for 72 hours prior to analysis for Thy-1 by FACS. *p
    Figure Legend Snippet: IL-17 and TGFβ1 independently and additively inhibit lung fibroblast Thy-1 expression. Primary lung fibroblasts (PLFs from passage 3–8) were isolated from wild-type mice and cultured ± IL-17 (10 ng/ml) ± TGFβ1 (2 ng/ml) for 72 hours prior to analysis for Thy-1 by FACS. *p

    Techniques Used: Expressing, Isolation, Mouse Assay, Cell Culture, FACS

    Thy-1 mediates the effects of IL-17 on α-SMA. Thy-1 subpopulations were enriched by immunomagnetic separation using the Miltenyi magnetic bead system. Thy-1 + and Thy-1 − PLFs were exposed to IL-17 (10 ng/ml) for 72 hours. Thy1 − PLFs (white bar (untreated) and dark gray bar (treated)) and Thy-1 + PLFs (black bar (untreated) and light gray bar (treated)) were harvested and then analyzed for α-SMA protein expression by Western blot. The top panel shows representative immunoblots. *p
    Figure Legend Snippet: Thy-1 mediates the effects of IL-17 on α-SMA. Thy-1 subpopulations were enriched by immunomagnetic separation using the Miltenyi magnetic bead system. Thy-1 + and Thy-1 − PLFs were exposed to IL-17 (10 ng/ml) for 72 hours. Thy1 − PLFs (white bar (untreated) and dark gray bar (treated)) and Thy-1 + PLFs (black bar (untreated) and light gray bar (treated)) were harvested and then analyzed for α-SMA protein expression by Western blot. The top panel shows representative immunoblots. *p

    Techniques Used: Immunomagnetic Separation, Expressing, Western Blot

    IL-17 selectively induces myofibroblast stress fiber development in Thy-1 negative (Thy-1 − ) lung fibroblasts. Thy-1 + and Thy-1 − mouse PLFs were separately treated with IL-17 (10 ng/ml) or TGFβ1 (5 ng/ml) for 96 hours. Myofibroblast transdifferentiation was evaluated using immunofluorescent staining for α-SMA (green). DAPI (blue) was used for nuclear staining. Panels ( A - B ) show untreated Thy-1 + and Thy-1 − cells, respectively, ( C - D ) show Thy-1 + and Thy-1 − cells treated with IL-17, respectively, and ( E and F ) show Thy-1 + and Thy-1 − cells treated with TGFβ1, respectively. ( G ) Four random high-power fields from each sample were analyzed for stress fiber formation. Scale bar = 100 μm. *p
    Figure Legend Snippet: IL-17 selectively induces myofibroblast stress fiber development in Thy-1 negative (Thy-1 − ) lung fibroblasts. Thy-1 + and Thy-1 − mouse PLFs were separately treated with IL-17 (10 ng/ml) or TGFβ1 (5 ng/ml) for 96 hours. Myofibroblast transdifferentiation was evaluated using immunofluorescent staining for α-SMA (green). DAPI (blue) was used for nuclear staining. Panels ( A - B ) show untreated Thy-1 + and Thy-1 − cells, respectively, ( C - D ) show Thy-1 + and Thy-1 − cells treated with IL-17, respectively, and ( E and F ) show Thy-1 + and Thy-1 − cells treated with TGFβ1, respectively. ( G ) Four random high-power fields from each sample were analyzed for stress fiber formation. Scale bar = 100 μm. *p

    Techniques Used: Staining

    IL-17 and alcohol upregulate α-SMA in lung fibroblasts. Total lung fibroblasts (Thy-1 + and Thy-1 − subpopulations) were exposed to either alcohol (60 mM) or IL-17 (10 ng/ml) for 72 hours. PLFs were harvested and then analyzed for α-SMA protein expression by Western blot. Untreated cells are represented by the white bar, alcohol-treated cells by the black bar, and IL-17-treated cells by the gray bar. The top panel shows a representative immunoblot. *p
    Figure Legend Snippet: IL-17 and alcohol upregulate α-SMA in lung fibroblasts. Total lung fibroblasts (Thy-1 + and Thy-1 − subpopulations) were exposed to either alcohol (60 mM) or IL-17 (10 ng/ml) for 72 hours. PLFs were harvested and then analyzed for α-SMA protein expression by Western blot. Untreated cells are represented by the white bar, alcohol-treated cells by the black bar, and IL-17-treated cells by the gray bar. The top panel shows a representative immunoblot. *p

    Techniques Used: Expressing, Western Blot

    Hypothesis schematic showing the effects of IL-17 on myofibroblast development in chronic alcohol ingestion. In the current study, we showed that in the otherwise healthy animals, chronic alcohol ingestion increased systemic Th17 immune response. Acute injury caused a persistent increase in IL-17 in the lung. Alcohol, IL-17, and TGFβ1 independently inhibited Thy-1 expression by lung fibroblasts and IL-17 and TGFβ1 additively decreased Thy-1 expression leading to myofibroblast differentiation. We believe this sequence of events is one of the mechanisms by which alcohol induces fibroproliferative disrepair following acute lung injury.
    Figure Legend Snippet: Hypothesis schematic showing the effects of IL-17 on myofibroblast development in chronic alcohol ingestion. In the current study, we showed that in the otherwise healthy animals, chronic alcohol ingestion increased systemic Th17 immune response. Acute injury caused a persistent increase in IL-17 in the lung. Alcohol, IL-17, and TGFβ1 independently inhibited Thy-1 expression by lung fibroblasts and IL-17 and TGFβ1 additively decreased Thy-1 expression leading to myofibroblast differentiation. We believe this sequence of events is one of the mechanisms by which alcohol induces fibroproliferative disrepair following acute lung injury.

    Techniques Used: Expressing, Sequencing

    Related Articles

    Activation Assay:

    Article Title: Contribution of Herpesvirus Specific CD8 T Cells to Anti-Viral T Cell Response in Humans
    Article Snippet: Finally, cells were stained with anti-IFN-γ and anti-IL-2 for 30 min on ice, washed, and fixed with 1% formaldehyde before acquisition on a FACS Canto flow cytometer. .. For analysis of anti-virus-specific CD8 T activation in vitro , freshly isolated PBMC or purified CD8+ T cells were incubated in vitro at 2×106 /ml with or without cytokines (IL-7, IL-2, IL-15, IFN-γ, IFN- α, TNF- α, purchased from RnD Systems, Minneapolis, MN). .. The cells were collected at indicated time points, and the intracellular cytokine staining was performed as described above.

    In Vitro:

    Article Title: Contribution of Herpesvirus Specific CD8 T Cells to Anti-Viral T Cell Response in Humans
    Article Snippet: Finally, cells were stained with anti-IFN-γ and anti-IL-2 for 30 min on ice, washed, and fixed with 1% formaldehyde before acquisition on a FACS Canto flow cytometer. .. For analysis of anti-virus-specific CD8 T activation in vitro , freshly isolated PBMC or purified CD8+ T cells were incubated in vitro at 2×106 /ml with or without cytokines (IL-7, IL-2, IL-15, IFN-γ, IFN- α, TNF- α, purchased from RnD Systems, Minneapolis, MN). .. The cells were collected at indicated time points, and the intracellular cytokine staining was performed as described above.

    Isolation:

    Article Title: Contribution of Herpesvirus Specific CD8 T Cells to Anti-Viral T Cell Response in Humans
    Article Snippet: Finally, cells were stained with anti-IFN-γ and anti-IL-2 for 30 min on ice, washed, and fixed with 1% formaldehyde before acquisition on a FACS Canto flow cytometer. .. For analysis of anti-virus-specific CD8 T activation in vitro , freshly isolated PBMC or purified CD8+ T cells were incubated in vitro at 2×106 /ml with or without cytokines (IL-7, IL-2, IL-15, IFN-γ, IFN- α, TNF- α, purchased from RnD Systems, Minneapolis, MN). .. The cells were collected at indicated time points, and the intracellular cytokine staining was performed as described above.

    Purification:

    Article Title: Contribution of Herpesvirus Specific CD8 T Cells to Anti-Viral T Cell Response in Humans
    Article Snippet: Finally, cells were stained with anti-IFN-γ and anti-IL-2 for 30 min on ice, washed, and fixed with 1% formaldehyde before acquisition on a FACS Canto flow cytometer. .. For analysis of anti-virus-specific CD8 T activation in vitro , freshly isolated PBMC or purified CD8+ T cells were incubated in vitro at 2×106 /ml with or without cytokines (IL-7, IL-2, IL-15, IFN-γ, IFN- α, TNF- α, purchased from RnD Systems, Minneapolis, MN). .. The cells were collected at indicated time points, and the intracellular cytokine staining was performed as described above.

    Incubation:

    Article Title: Contribution of Herpesvirus Specific CD8 T Cells to Anti-Viral T Cell Response in Humans
    Article Snippet: Finally, cells were stained with anti-IFN-γ and anti-IL-2 for 30 min on ice, washed, and fixed with 1% formaldehyde before acquisition on a FACS Canto flow cytometer. .. For analysis of anti-virus-specific CD8 T activation in vitro , freshly isolated PBMC or purified CD8+ T cells were incubated in vitro at 2×106 /ml with or without cytokines (IL-7, IL-2, IL-15, IFN-γ, IFN- α, TNF- α, purchased from RnD Systems, Minneapolis, MN). .. The cells were collected at indicated time points, and the intracellular cytokine staining was performed as described above.

    Article Title: miR-155 in the progression of lung fibrosis in systemic sclerosis
    Article Snippet: Lung fibroblasts were cultured in DMEM supplemented with 10 % fetal bovine serum and penicillin/streptomycin and utilized at passages 2–4. .. Fibroblasts (100 % confluent) were incubated in serum-free DMEM overnight prior to stimulation with TGFß (R & D System; 2.5 ng/ml), recombinant human IL-13 (R & D Systems, 20 ng/ml), or interferon-alpha (IFN) (R & D Systems; 500 U/ml) for 18 hours. .. Total RNA from fibroblasts was transferred in Qiazol buffer and purified using the miRNease mini kit protocol (Qiagen).

    Recombinant:

    Article Title: Molecular Signatures Associated with Mx1-Mediated Resistance to Highly Pathogenic Influenza Virus Infection: Mechanisms of Survival
    Article Snippet: .. In addition, half of the animals were intranasally treated with 10,000 units of recombinant human alpha interferon (IFN-α) A/D (R & D Systems, Minneapolis, MN) before infection with the reconstructed 1918 virus and euthanized 12, 24, and 72 h posttreatment. ..

    Article Title: HIV envelope gp120 activates human arterial smooth muscle cells
    Article Snippet: These results provide evidence for direct viral activation of human SMC and may provide insight into the mechanism underlying the increased incidence of acute coronary syndromes and prothrombotic states in patients with HIV. .. Recombinant human macrophage inflammatory protein-1β (MIP-1), platelet-derived growth factor, recombinant human IL-16, recombinant human stromal cell-derived growth factor 1-α (SDF-1), and monoclonal antibodies to human CXCR4 and CCR5 were from R & D Systems. .. FBS, 8-bromoadenosine 3′:5′-cyclic monophosphate sodium (Tiron), actinomycin D, phorbol 12,13-dibutyrate, a monoclonal anti-human CD4 antibody, clone Q4120, and its isotype-matched IgG control were from Sigma.

    Article Title: miR-155 in the progression of lung fibrosis in systemic sclerosis
    Article Snippet: Lung fibroblasts were cultured in DMEM supplemented with 10 % fetal bovine serum and penicillin/streptomycin and utilized at passages 2–4. .. Fibroblasts (100 % confluent) were incubated in serum-free DMEM overnight prior to stimulation with TGFß (R & D System; 2.5 ng/ml), recombinant human IL-13 (R & D Systems, 20 ng/ml), or interferon-alpha (IFN) (R & D Systems; 500 U/ml) for 18 hours. .. Total RNA from fibroblasts was transferred in Qiazol buffer and purified using the miRNease mini kit protocol (Qiagen).

    Infection:

    Article Title: Molecular Signatures Associated with Mx1-Mediated Resistance to Highly Pathogenic Influenza Virus Infection: Mechanisms of Survival
    Article Snippet: .. In addition, half of the animals were intranasally treated with 10,000 units of recombinant human alpha interferon (IFN-α) A/D (R & D Systems, Minneapolis, MN) before infection with the reconstructed 1918 virus and euthanized 12, 24, and 72 h posttreatment. ..

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    R&D Systems il 17f
    IL-17A Promotes Inflammatory Cytokine Expression in Endothelial Cells (A) IL-17 receptor A ( Il17ra ) and auxiliary subunits Il17rc and Il17re mRNA expression was determined by using quantitative polymerase chain reaction (qPCR). Il17rb messenger ribonucleic acid (mRNA) was below detection limit (n = 4, 2 exp.). (B to I) Endothelial cells were stimulated for 2 h with 50 ng/ml IL-17A (B to E) or <t>IL-17F</t> (F to I) . CCL2 (B and F) , CXCL1 (C and G) , IL-6 (D and H) , and granulocyte-macrophage colony-stimulating factor (GM-CSF) (E and I) cytokine expression quantified by using qPCR (n = 8 from 4 independent experiments for each cytokine).
    Il 17f, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    R&D Systems il 17 ifn γ
    Expression of surface markers on monocytes stimulated with <t>IL-17.</t> Human CD14 ++ CD16 − and CD14 ++ CD16 + /CD14 + CD16 ++ monocytes were treated with IL-17, IFN- γ , which was used as a positive control, IL-17/IFN- γ , or culture medium alone, which was used as a negative control, for 24 hours. Human CD14 ++ CD16 − in STEMI: (a) TLR4, (e) CD86, and (i) HLA-DR. Human CD14 ++ CD16 − in post-STEMI: (b) TLR4, (f) CD86, and (j) HLA-DR. Human CD14 ++ CD16 + /CD14 + CD16 ++ monocytes in STEMI: (c) TLR4, (g) CD86, and (k) HLA-DR. CD14 ++ CD16 + /CD14 + CD16 ++ monocytes post-STEMI: (d) TLR4, (h) CD86, and (l) HLA-DR. Expression levels of TLR4, CD86, and HLA-DR are expressed as MFI. White column: STEMI; black column: post-STEMI; n = 11. ∗ p
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    R&D Systems human il 7
    Membrane γ c regulation after IL-2, <t>IL-7,</t> and IL-15 treatment in vitro. A , B ) Regulation of surface γ c expression on CD4 + ( A ) or CD8 + ( B ) T cells by IL-2, IL-7, IL-15 alone or combination treatments, as indicated on the x axis. C ) Representative
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    R&D Systems il 17a
    Neutrophils are reduced in the joints of Il17ra −/− mice and are unresponsive to direct stimulation with <t>IL-17A.</t> A, Number of neutrophils in the ankle joints of WT and Il17ra −/− mice on day 12 was determined by FACS analysis counting Ly6G + cells in relation to counting beads. Data are presented as mean ± SEM (n = 3 mice per group). One of three independent experiments is shown. B, Chemotaxis of freshly isolated murine bone marrow-derived neutrophils towards 100 nM LTB 4 and IL-17A (10 and 100 ng/ml) assessed using 24-well transwell assays. Data represent numbers of migrated neutrophils (n = 3 independently performed experiments). C, Chemotaxis of freshly isolated murine bone marrow-derived neutrophils towards LTB 4 (100 nM) MIP-2 (100 nM) and IL-17A (1, 10, 100, 1000 ng/ml) as well as their corresponding chemokinesis controls assessed using 96-well ChemoTx assays. Data are presented as chemotactic index (number of cells migrating to chemoattractant/number of cell migrating to medium control). Data shown are mean ± SEM (n = 4 independently performed experiments). D, Levels of IL-17RA and IL-17RC mRNA determined by qPCR on RNA isolated from murine FLS and freshly isolated bone marrow-derived neutrophils (n = 3 independently performed experiments). Data were compared by unpaired two-tailed Student's t test, ** = p
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    IL-17A Promotes Inflammatory Cytokine Expression in Endothelial Cells (A) IL-17 receptor A ( Il17ra ) and auxiliary subunits Il17rc and Il17re mRNA expression was determined by using quantitative polymerase chain reaction (qPCR). Il17rb messenger ribonucleic acid (mRNA) was below detection limit (n = 4, 2 exp.). (B to I) Endothelial cells were stimulated for 2 h with 50 ng/ml IL-17A (B to E) or IL-17F (F to I) . CCL2 (B and F) , CXCL1 (C and G) , IL-6 (D and H) , and granulocyte-macrophage colony-stimulating factor (GM-CSF) (E and I) cytokine expression quantified by using qPCR (n = 8 from 4 independent experiments for each cytokine).

    Journal: JACC: Basic to Translational Science

    Article Title: Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibition of Interleukin-17A

    doi: 10.1016/j.jacbts.2017.08.005

    Figure Lengend Snippet: IL-17A Promotes Inflammatory Cytokine Expression in Endothelial Cells (A) IL-17 receptor A ( Il17ra ) and auxiliary subunits Il17rc and Il17re mRNA expression was determined by using quantitative polymerase chain reaction (qPCR). Il17rb messenger ribonucleic acid (mRNA) was below detection limit (n = 4, 2 exp.). (B to I) Endothelial cells were stimulated for 2 h with 50 ng/ml IL-17A (B to E) or IL-17F (F to I) . CCL2 (B and F) , CXCL1 (C and G) , IL-6 (D and H) , and granulocyte-macrophage colony-stimulating factor (GM-CSF) (E and I) cytokine expression quantified by using qPCR (n = 8 from 4 independent experiments for each cytokine).

    Article Snippet: In addition, IL-17F, which was above mRNA detection limits in atherosclerotic aortas, was lower in Il17ra –/– LDLr –/– mice than in LDLr –/– mice.

    Techniques: Expressing, Real-time Polymerase Chain Reaction

    Expression of surface markers on monocytes stimulated with IL-17. Human CD14 ++ CD16 − and CD14 ++ CD16 + /CD14 + CD16 ++ monocytes were treated with IL-17, IFN- γ , which was used as a positive control, IL-17/IFN- γ , or culture medium alone, which was used as a negative control, for 24 hours. Human CD14 ++ CD16 − in STEMI: (a) TLR4, (e) CD86, and (i) HLA-DR. Human CD14 ++ CD16 − in post-STEMI: (b) TLR4, (f) CD86, and (j) HLA-DR. Human CD14 ++ CD16 + /CD14 + CD16 ++ monocytes in STEMI: (c) TLR4, (g) CD86, and (k) HLA-DR. CD14 ++ CD16 + /CD14 + CD16 ++ monocytes post-STEMI: (d) TLR4, (h) CD86, and (l) HLA-DR. Expression levels of TLR4, CD86, and HLA-DR are expressed as MFI. White column: STEMI; black column: post-STEMI; n = 11. ∗ p

    Journal: Journal of Immunology Research

    Article Title: Effect of Interleukin-17 in the Activation of Monocyte Subsets in Patients with ST-Segment Elevation Myocardial Infarction

    doi: 10.1155/2020/5692829

    Figure Lengend Snippet: Expression of surface markers on monocytes stimulated with IL-17. Human CD14 ++ CD16 − and CD14 ++ CD16 + /CD14 + CD16 ++ monocytes were treated with IL-17, IFN- γ , which was used as a positive control, IL-17/IFN- γ , or culture medium alone, which was used as a negative control, for 24 hours. Human CD14 ++ CD16 − in STEMI: (a) TLR4, (e) CD86, and (i) HLA-DR. Human CD14 ++ CD16 − in post-STEMI: (b) TLR4, (f) CD86, and (j) HLA-DR. Human CD14 ++ CD16 + /CD14 + CD16 ++ monocytes in STEMI: (c) TLR4, (g) CD86, and (k) HLA-DR. CD14 ++ CD16 + /CD14 + CD16 ++ monocytes post-STEMI: (d) TLR4, (h) CD86, and (l) HLA-DR. Expression levels of TLR4, CD86, and HLA-DR are expressed as MFI. White column: STEMI; black column: post-STEMI; n = 11. ∗ p

    Article Snippet: The HUVECs were activated for 1 day with IL-17 (60 ng/ml), interferon- (IFN-) γ (25 ng/ml), which was used as an inhibitory control for monocyte migration, or IL-17/IFN-γ (R & D Systems, Minnesota, USA), and culture medium alone was used as a negative control.

    Techniques: Expressing, Positive Control, Negative Control

    IL-17 induces the secretion of proinflammatory cytokines in monocyte subsets. Human CD14 ++ CD16 − or CD14 ++ CD16 + /CD14 + CD16 ++ monocytes were treated with IL-17, IFN- γ , which was used as a positive control, IL-17/IFN- γ , or culture medium alone, which was used as a negative control, for 24 hours. Human CD14 ++ CD16 − in STEMI: (a) TNF- α and (c) IL-6. Human CD14 ++ CD16 − in post-STEMI: (b) TNF- α and (d) IL-6. Human CD14 ++ CD16 + /CD14 + CD16 ++ monocytes in STEMI: (e) TNF- α and (g) IL-6. CD14 ++ CD16 + /CD14 + CD16 ++ monocytes post-STEMI: (f) TNF- α and (h) IL-6. Concentrations of TNF- α and IL-6 in the culture supernatants were determined by ELISA. White column: STEMI; black column: post-STEMI; n = 11. ∗ p

    Journal: Journal of Immunology Research

    Article Title: Effect of Interleukin-17 in the Activation of Monocyte Subsets in Patients with ST-Segment Elevation Myocardial Infarction

    doi: 10.1155/2020/5692829

    Figure Lengend Snippet: IL-17 induces the secretion of proinflammatory cytokines in monocyte subsets. Human CD14 ++ CD16 − or CD14 ++ CD16 + /CD14 + CD16 ++ monocytes were treated with IL-17, IFN- γ , which was used as a positive control, IL-17/IFN- γ , or culture medium alone, which was used as a negative control, for 24 hours. Human CD14 ++ CD16 − in STEMI: (a) TNF- α and (c) IL-6. Human CD14 ++ CD16 − in post-STEMI: (b) TNF- α and (d) IL-6. Human CD14 ++ CD16 + /CD14 + CD16 ++ monocytes in STEMI: (e) TNF- α and (g) IL-6. CD14 ++ CD16 + /CD14 + CD16 ++ monocytes post-STEMI: (f) TNF- α and (h) IL-6. Concentrations of TNF- α and IL-6 in the culture supernatants were determined by ELISA. White column: STEMI; black column: post-STEMI; n = 11. ∗ p

    Article Snippet: The HUVECs were activated for 1 day with IL-17 (60 ng/ml), interferon- (IFN-) γ (25 ng/ml), which was used as an inhibitory control for monocyte migration, or IL-17/IFN-γ (R & D Systems, Minnesota, USA), and culture medium alone was used as a negative control.

    Techniques: Positive Control, Negative Control, Enzyme-linked Immunosorbent Assay

    Monocytes transmigrate across a human umbilical vein endothelial cell monolayer in response to IL-17. A sample of 3 × 10 5 (a–c) CD14 ++ CD16 − or (d–f) CD14 ++ CD16 + /CD14 + CD16 ++ monocytes was added to the upper surface of monolayers of human umbilical vein endothelial cells (HUVECs) previously treated with IL-17, IFN- γ , or IL-17/IFN- γ ; culture medium alone was used as a negative control. The monocytes were allowed to transmigrate across the HUVEC monolayers in the presence of CCL2, CX3CL1, or culture medium for 3 hours. All data are presented as the migration index, which relates the number of cells that migrated in response to the indicated stimulus to the number of cells that migrated in response to the negative control. White column: STEMI: black column: post-STEMI; n = 11. ∗ p

    Journal: Journal of Immunology Research

    Article Title: Effect of Interleukin-17 in the Activation of Monocyte Subsets in Patients with ST-Segment Elevation Myocardial Infarction

    doi: 10.1155/2020/5692829

    Figure Lengend Snippet: Monocytes transmigrate across a human umbilical vein endothelial cell monolayer in response to IL-17. A sample of 3 × 10 5 (a–c) CD14 ++ CD16 − or (d–f) CD14 ++ CD16 + /CD14 + CD16 ++ monocytes was added to the upper surface of monolayers of human umbilical vein endothelial cells (HUVECs) previously treated with IL-17, IFN- γ , or IL-17/IFN- γ ; culture medium alone was used as a negative control. The monocytes were allowed to transmigrate across the HUVEC monolayers in the presence of CCL2, CX3CL1, or culture medium for 3 hours. All data are presented as the migration index, which relates the number of cells that migrated in response to the indicated stimulus to the number of cells that migrated in response to the negative control. White column: STEMI: black column: post-STEMI; n = 11. ∗ p

    Article Snippet: The HUVECs were activated for 1 day with IL-17 (60 ng/ml), interferon- (IFN-) γ (25 ng/ml), which was used as an inhibitory control for monocyte migration, or IL-17/IFN-γ (R & D Systems, Minnesota, USA), and culture medium alone was used as a negative control.

    Techniques: Negative Control, Migration

    Membrane γ c regulation after IL-2, IL-7, and IL-15 treatment in vitro. A , B ) Regulation of surface γ c expression on CD4 + ( A ) or CD8 + ( B ) T cells by IL-2, IL-7, IL-15 alone or combination treatments, as indicated on the x axis. C ) Representative

    Journal: The FASEB Journal

    Article Title: Rapid down-regulation of ?c on T cells in early SIV infection correlates with impairment of T-cell function

    doi: 10.1096/fj.11-195180

    Figure Lengend Snippet: Membrane γ c regulation after IL-2, IL-7, and IL-15 treatment in vitro. A , B ) Regulation of surface γ c expression on CD4 + ( A ) or CD8 + ( B ) T cells by IL-2, IL-7, IL-15 alone or combination treatments, as indicated on the x axis. C ) Representative

    Article Snippet: Purified PBMCs from normal and uninfected animals were isolated from heparinized blood, and 1 × 106 /ml PBMCs in R10 medium were treated with human IL-2 (final concentration 20 U/ml; BD Biosciences), human IL-7 (20 ng/ml; R & D Systems, Minneapolis, MN, USA), human IL-15 (20 ng/ml; R & D Systems) alone or combined at 37°C in a 5% CO2 incubator for 30 min.

    Techniques: In Vitro, Expressing

    γ c cytokine levels in plasma in SIV-infected macaques and effects of SIV infection on γ c expression on T cells in vitro. A ) Dynamics of γ c cytokine (IL-2, IL-7, and IL-15) levels in plasma of SHIV162p3- or SIV-infected macaques.

    Journal: The FASEB Journal

    Article Title: Rapid down-regulation of ?c on T cells in early SIV infection correlates with impairment of T-cell function

    doi: 10.1096/fj.11-195180

    Figure Lengend Snippet: γ c cytokine levels in plasma in SIV-infected macaques and effects of SIV infection on γ c expression on T cells in vitro. A ) Dynamics of γ c cytokine (IL-2, IL-7, and IL-15) levels in plasma of SHIV162p3- or SIV-infected macaques.

    Article Snippet: Purified PBMCs from normal and uninfected animals were isolated from heparinized blood, and 1 × 106 /ml PBMCs in R10 medium were treated with human IL-2 (final concentration 20 U/ml; BD Biosciences), human IL-7 (20 ng/ml; R & D Systems, Minneapolis, MN, USA), human IL-15 (20 ng/ml; R & D Systems) alone or combined at 37°C in a 5% CO2 incubator for 30 min.

    Techniques: Infection, Expressing, In Vitro

    Neutrophils are reduced in the joints of Il17ra −/− mice and are unresponsive to direct stimulation with IL-17A. A, Number of neutrophils in the ankle joints of WT and Il17ra −/− mice on day 12 was determined by FACS analysis counting Ly6G + cells in relation to counting beads. Data are presented as mean ± SEM (n = 3 mice per group). One of three independent experiments is shown. B, Chemotaxis of freshly isolated murine bone marrow-derived neutrophils towards 100 nM LTB 4 and IL-17A (10 and 100 ng/ml) assessed using 24-well transwell assays. Data represent numbers of migrated neutrophils (n = 3 independently performed experiments). C, Chemotaxis of freshly isolated murine bone marrow-derived neutrophils towards LTB 4 (100 nM) MIP-2 (100 nM) and IL-17A (1, 10, 100, 1000 ng/ml) as well as their corresponding chemokinesis controls assessed using 96-well ChemoTx assays. Data are presented as chemotactic index (number of cells migrating to chemoattractant/number of cell migrating to medium control). Data shown are mean ± SEM (n = 4 independently performed experiments). D, Levels of IL-17RA and IL-17RC mRNA determined by qPCR on RNA isolated from murine FLS and freshly isolated bone marrow-derived neutrophils (n = 3 independently performed experiments). Data were compared by unpaired two-tailed Student's t test, ** = p

    Journal: PLoS ONE

    Article Title: IL-17RA Signaling Amplifies Antibody-Induced Arthritis

    doi: 10.1371/journal.pone.0026342

    Figure Lengend Snippet: Neutrophils are reduced in the joints of Il17ra −/− mice and are unresponsive to direct stimulation with IL-17A. A, Number of neutrophils in the ankle joints of WT and Il17ra −/− mice on day 12 was determined by FACS analysis counting Ly6G + cells in relation to counting beads. Data are presented as mean ± SEM (n = 3 mice per group). One of three independent experiments is shown. B, Chemotaxis of freshly isolated murine bone marrow-derived neutrophils towards 100 nM LTB 4 and IL-17A (10 and 100 ng/ml) assessed using 24-well transwell assays. Data represent numbers of migrated neutrophils (n = 3 independently performed experiments). C, Chemotaxis of freshly isolated murine bone marrow-derived neutrophils towards LTB 4 (100 nM) MIP-2 (100 nM) and IL-17A (1, 10, 100, 1000 ng/ml) as well as their corresponding chemokinesis controls assessed using 96-well ChemoTx assays. Data are presented as chemotactic index (number of cells migrating to chemoattractant/number of cell migrating to medium control). Data shown are mean ± SEM (n = 4 independently performed experiments). D, Levels of IL-17RA and IL-17RC mRNA determined by qPCR on RNA isolated from murine FLS and freshly isolated bone marrow-derived neutrophils (n = 3 independently performed experiments). Data were compared by unpaired two-tailed Student's t test, ** = p

    Article Snippet: In order to determine which of the genes downregulated in the ankles of Il17ra−/− mice might be directly regulated by IL-17RA signaling, murine fibroblast-like synoviocytes (FLS) were either left unstimulated or stimulated with 100 ng/ml IL-17A for 16 h. RNA was then isolated and gene expression assessed by qPCR.

    Techniques: Mouse Assay, FACS, Chemotaxis Assay, Isolation, Derivative Assay, Real-time Polymerase Chain Reaction, Two Tailed Test