Journal:

Article Title: Porphyromonas gingivalis lipopolysaccharide induces tumor necrosis factor-α and interleukin-6 (IL-6) secretion and CCL25 gene expression in mouse primary gingival cell lines: IL-6-driven activation of CCL2

doi:

Figure Lengend Snippet: (A-C) CCL2 and TNFα levels in cell-free supernatants 24 hr after stimulation with rIL-6, rIL-6 plus sIL-6R, rIL-6 plus sIL-6R plus sgp130, sgp130, or PBS; data from 3 independent sets of experiments showing an increase in CCL2 secretion from gingival cells stimulated with rIL-6 plus sIL-6R; rIL-6 plus sIL-6R plus sgp130; or sgp130 compared to PBS control cultures. (D) Neutralization of sgp130 by anti-gp130 antibody causes an increase in CCL2 secretion. (E) A gingival cell line stained with sgp130 indicated that about one-fifth of the cells express gp130. (F) Cell supernatants used for CCL2 assays had no detectable TNFα production.

Article Snippet: Reagents used in this study included ultrapure P. gingivalis LPS (Invitrogen; San Diego; CA) and E. coli LPS (Sigma); recombinant IL-6 (rIL-6) (<0.01 ng endotoxin per μg cytokine (eBioscience; San Diego, CA); sIL-6R (<0.0 EU endotoxin per 1 μg cytokine receptor) (R&D Systems; Minneapolis, MN); two preparations of sgp130: recombinant human sgp130 (<1.0 EU endotoxin per 1 μg receptor) (R&D Systems), and recombinant mouse sgp130/Fc chimera (<1.0 ng endotoxin per 1 μg receptor) (R&D systems).

Techniques: Control, Neutralization, Staining

Journal:

Article Title: Porphyromonas gingivalis lipopolysaccharide induces tumor necrosis factor-α and interleukin-6 (IL-6) secretion and CCL25 gene expression in mouse primary gingival cell lines: IL-6-driven activation of CCL2

doi:

Figure Lengend Snippet: Stimulatory effects on CCL2 secretion from gingival cell lines

Article Snippet: Reagents used in this study included ultrapure P. gingivalis LPS (Invitrogen; San Diego; CA) and E. coli LPS (Sigma); recombinant IL-6 (rIL-6) (<0.01 ng endotoxin per μg cytokine (eBioscience; San Diego, CA); sIL-6R (<0.0 EU endotoxin per 1 μg cytokine receptor) (R&D Systems; Minneapolis, MN); two preparations of sgp130: recombinant human sgp130 (<1.0 EU endotoxin per 1 μg receptor) (R&D Systems), and recombinant mouse sgp130/Fc chimera (<1.0 ng endotoxin per 1 μg receptor) (R&D systems).

Techniques:

Journal: Oncology Reports

Article Title: Increased interleukin-6 expression is associated with poor prognosis and acquired cisplatin resistance in head and neck squamous cell carcinoma

doi: 10.3892/or.2016.4765

Figure Lengend Snippet: Cisplatin resistance in HNSCC cell lines was independent of IL-6/gp130/STAT3 signaling pathway. (A and B) Neither exogenous IL-6 nor IL-6 pathway inhibitors affected cisplatin resistance in HNSCC cell lines. Cells were grown in the presence (+) or absence (−) of human IL-6 receptor neutralizing antibody (40 µ g/ml; A), human gp130 neutralizing antibody (60 µ g/ml; A) or human recombinant IL-6 (100 ng/ml; B), for 24 h and then treated with (+) or without (−) 5 µ M cisplatin. Cells without any treatment were set as control. NS, not significant (p>0.05; n=5, paired Student's t-test). (C and D) Effect of cisplatin (C and D), exogenous IL-6 (D), anti-IL-6 antibody (C and D) and anti-gp130 antibody (C) on the acquired cisplatin resistant C12cis (C) cell line and sensitive C12 cell line (D). Whereas IL-6 induced p-STAT3 Tyr705 in C12 cell line through IL-6R, unstimulated C12cis cells had p-STAT3 Tyr705 that was unchanged after IL-6 receptor inhibition. (E) IL-6/STAT3 pathway was reduced in the acquired cisplatin-resistant cell lines. (F and G) Acquired cisplatin-resistant cell lines had decreased IL-6R mRNA and protein levels. The mRNA expression levels were normalized to housekeeping gene TBP ( * p<0.05, ** p<0.01 and *** p<0.001; n=4, paired Student's t-test).

Article Snippet: Cells were also cultured in the presence of human recombinant IL-6 or human IL-6R/gp130 neutralizing antibody (all from R&D Systems, Minneapolis, MN, USA) for 24 h, followed by 5 μ M cisplatin treatment to examine changes in drug resistance.

Techniques: Recombinant, Control, Inhibition, Expressing