• Tuberculosis and Respiratory Diseases
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• v.48 no.4
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• pp.464-470
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• 2000

Background : The recognition of bronchial asthma as an inflammatory disease led to the search for soluble markers that would be useful in assessing airway inflammation. Interleukin-6 (IL-6) is a representative proinflammatory cytokine that has been shown to be connected with various inflammatory diseases. IL-6 acts via specific receptors that consist of the IL-6 binding glycoprotein gp80 and the signal transducer gp130. In the search for markers of airway inflammation, delete the role of soluble interleukin-6 receptor (sIL-6R) and IL-6 in acute asthma were investigated. Methods : Serum levels of sIL-6R and IL-6 were measured in 78 acute asthmatics, in 15 patients with asymptomatic asthma and in 10 healthy control subjects by a specific ELISA using a murine antihuman IL-6R, IL-6 mAb ($Quantikine^{(R)}sIL$-6R, IL-6). Results : Serum levels of IL-6 in acute asthmatics significantly exceeded those of control subjects. The levels of sIL-6R in acute asthmatics were also significantly increased compared to those of control subjects. The serum concentrations of IL-6 obtained in acute asthmatics were elevated compared with those in asymptomatic asthmatics. However, association between eosinophilic count/IgE and IL-6/sIL-6R in acute asthma could not be found. Conclusion : Our results suggest that IL-6 may be involved in the pathogenesis of acute asthma, and serum levels of IL-6 and sIL-6R may reflect the severity of airway inflammation.

• Korean Journal of Microbiology
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• v.50 no.3
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• pp.261-263
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• 2014

Chronic inflammation is involved in cancers, rheumatoid arthritis, and Crohn's disease. Inerleukin-6 (IL-6) plays major roles in inflammation. Chungkookjang, fermented soybean contains diverse peptides produced by cleavage of soybean proteins. The peptides can be bioactive compounds. Peptide (Gly-Val-Tyr-Tyr-Met-Tyr was purified from Chungkookjang, and modified to be 6mer H, Glu-Val-Tyr-Tyr-Met-Tyr (EVYYMY). Peptide H's activity to suppress IL-6 expression in a human breast cancer cell, MDA-MB-231 was determined. IL-6 Expression was reduced in the cell treated with peptide H 25 times less than controls which were not treated with peptide H. Proliferation of MDA-MB-231 cells was inhibited by peptide H, which is concentration-dependent. Blocking of IL-6 signals is known to be effective in reducing inflammation in rheumatoid arthritis, Crohn's disease, and cancers. Since peptide H can reduce inflammatory IL-6 expression, application of this study will contribute to drug development for diseases which are caused by excessive IL-6.

• Childhood Kidney Diseases
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• v.1 no.2
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• pp.130-135
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• 1997

Purpose : Interleukin-6(IL-6), a multifunctional cytokine, has been found to have growth and differentiation activities on a wide variety of tissues and cells, including mesangial cells. It has been known that IL-6 is an autocrine growth factor for the proliferation of mesangial cells. Several studies have been performed for revealing the clinical significance of IL-6 in mesangial proliferative glomerulonephritis. Methods : The author measured serum and urinary IL-6 in 30 patients with $Henoch-Sch\"{o}nlein$ purpura (HSP), 18 patients with HSP nephritis, and 10 normal children as a control group. Results : The serum level of IL-6 was increased significantly in the patients with HSP and HSP nephritis compared to normal control. The level of urinary IL-6 was increased significantly in the patients with HSP nephritis compared to both HSP and normal control groups. The level of urinary IL-6 was not correlated with the level of serum. Conclusion : IL-6 was correlated with the amount of proteinuria. These data suggest that IL-6 may be involved in the pathological proliferation of mesangial cell in HSP nephritis.

• The Korean Journal of Food And Nutrition
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• v.28 no.4
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• pp.695-701
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• 2015

Previous reports revealed that DMfree (green tea extract) inhibited expression of the IL-6 gene in Mycobacterium lepraeinfected MSCs (mesenchymal stem cells). This study aimed to measure IL-6, $IL-1{\beta}$, $TNF-{\alpha}$ and PGE2 production in M. leprae-infected MSCs using ELISA. To confirm the effect of DMfree on IL-6 and signal transduction, a western blotting test was performed. DMfree inhibited the expression of IL-6 in the MSCs and the heterodimer of STAT3, which also affects the expression of multiple genes. Though DMfree pre-treatment of control MSCs produced a baseline level of IL-6, it significantly inhibited the production of IL-6 in M. leprae-infected MSCs. There was no significant difference in IL-6 production between 1 and 7 day treatment groups. M. leprae-infected MSCs produced more $IL-1{\beta}$, $TNF-{\alpha}$ and PGE2, but DMfree could not inhibit their production at a physiological concentration. This is different from other reports that used higher concentration of EGCG treatment, resulting in significant inhibition of the cytokines. The inhibition appears to be related to the concentration of EGCG. These results indicate that DMfree can alleviate inflammation involving IL-6.

• Microbiology and Biotechnology Letters
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• v.21 no.5
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• pp.421-427
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• 1993

Some interleukin 6 (IL-60 transcription control factors were resported as the regulator of IL-6 expression. A nuclear protein bound to interleukin 1 (IL-1) responsive element in the IL-6 promoter region was named NF-IL6 (nuclear factor for IL-6). This NF-IL6 was known to be very imporant as a transcription factor for various immuno-protein as well as for IL-6. The human NF-IL6 genes were transfected into the mouse L cells under the metallothionein promoter (MT promoter) to establish a model system for the expression of foreign gene in the mammalian cell line.

• Journal of Periodontal and Implant Science
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• v.29 no.3
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• pp.645-654
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• 1999

Interleukin-6(IL-6) stimulate osteoclast differentiation. $17{\beta}$-estradiol, 1,25-dihydroxyvitamin $D_3$(1,25-$(OH)_2D_3$) and interleukin-$1{\beta}$ inhibit or stimulate osteoclast differentiation by decreasing or increasing the synthesis of interleukin-6(IL-6) from stromal/osteoblastic cells, respectively. Periodontal ligament(PDL) cells reside between the alveolar bone and the cementum and have osteoblastic characteristics. To estimate the effect of $17{\beta}$-estradiol and 1,25$(OH)_2D_3$ on IL-6 production of PDL cells, PDL cells were treated with $17{\beta}$-estradiol or 1,25-$(OH)_2D_3$ in the absence or the presence of IL-$1{\beta}$. The concentration of IL-6 produced form PDL cells was determined by enzym linked immunosorbent assay(ELISA). In unstimulated PDL cells, we detected constitutive production of IL-6 at 1st and 2nd day. IL-$1{\beta}$ increased IL-6 synthesis at 1st day and 2nd day. $17{\beta}$-estradiol had no significant effect on the secretion of this cytokine, either constitutively or after stimulation with IL- $1{\beta}$(0.05 ng/ml). 1,25-$(OH)_2D_3$($10^{-8}M$) decreased not only constitutive IL-6 production but also IL-$1{\beta}$-induced IL-6 production at 2nd day. These results suggest that 1,25-$(OH)_2D_3$ may control IL-$1{\beta}$-induced osteoclast differentiation by decreasing IL-$1{\beta}$-induced IL-6 secretion of PDL cells.

• BMB Reports
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• v.40 no.4
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• pp.562-570
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• 2007

Soluble or cell-bound IL-1 receptor accessory protein (IL-1RAcP) does not bind IL-1 but rather forms a complex with IL-1 and IL-1 receptor type I (IL-1RI) resulting in signal transduction. Synthetic peptides to various regions in the Ig-like domains of IL-1RAcP were used to produce antibodies and these antibodies were affinity-purified using the respective antigens. An anti-peptide-4 antibody which targets domain III inhibited 70% of IL-$1\beta$-induced productions of IL-6 and PGE2 from 3T3-L1 cells. Anti-peptide-2 or 3 also inhibited IL-1-induced IL-6 production by 30%. However, antipeptide-1 which is directed against domain I had no effect. The antibody was more effective against IL-$1\beta$ compared to IL-$1\alpha$. IL-1-induced IL-6 production was augmented by coincubation with PGE2. The COX inhibitor ibuprofen blocked IL-1-induced IL-6 and PGE2 production. These results confirm that IL-1RAcP is essential for IL-1 signaling and that increased production of IL-6 by IL-1 needs the co-induction of PGE2. However, the effect of PGE2 is independent of expressions of IL-1RI and IL-1RAcP. Our data suggest that domain III of IL-1RAcP may be involved in the formation or stabilization of the IL-1RI/IL-1 complex by binding to epitopes on domain III of the IL-1RI created following IL-1 binding to the IL-1RI.

• Food Science of Animal Resources
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• v.23 no.1
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• pp.75-79
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• 2003

This study was carried out to detect the pro-inflammatory cytokines(IL-1, IL-6, TNF-a, IL-18) and IL-1 receptor accessory in mongolia mare's milk by western blotting. IL-1 and TNF-a were detected in 4 samples of mare's milk Proteins of 6 kD and 7 kD were bound to specific antibody against hIL-18. But, IL-l and TNF-a were not detectable in Difco skim milk IL-6 like factor of 60 kD was detected in both Difco skim milk and mare's milk. Also, IL-1 receptor accessory of 55 kD was detected in the mongolia mare's milk.

• Natural Product Sciences
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• v.18 no.4
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• pp.221-226
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• 2012

Hesperidin (HES) is a bioflavonoid with antioxidant, anti-inflammatory and anti-diabetic properties. IL-6 is well known as a primary proinflammatory cytokine that contributes to impaired insulin signaling in liver. This study was to investigate whether HES improves IL-6-mediated impairment of insulin sensitivity in liver. Hepa-1c1c7 cells were pre-treated with 50 and $100{\mu}M$ HES in complete media for 1 h and then cultured in the presence or absence of IL-6 (20 ng/ml). These results demonstrated that HES restored IL-6-suppressed expression of IRS-1 protein, downregulated IL-6-increased expression of CRP and SOCS-3 mRNA, and inhibited LPS-induced production of IL-6 in Hepa-1c1c7 cells. These findings indicate that HES may ameliorate hepatic insulin resistance via improvement of IL-6-mediated impaired insulin signaling in hepatocytes.

• Natural Product Sciences
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• v.19 no.4
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• pp.360-365
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• 2013

Baicalin has antioxidant, anti-inflammatory and anti-diabetic properties. IL-6 is a primary proinflammatory cytokine that contributes to impaired insulin signaling in liver. This study was carried out to investigate whether baicalin improves IL-6-mediated insulin resistance in liver. Hepa-1c1c7 cells were pre-treated with 50 and 100 ${\mu}M$ baicalin in complete media for 1 h and then cultured in the presence or absence of IL-6 (20 ng/ml). These results demonstrated that baicalin restored IL-6-suppressed expression of insulin receptor substrate (IRS)-1 protein, downregulated IL-6-increased gene expression of C-reactive protein (CRP) and suppressor of cytokine signaling (SOCS)-3, and inhibited LPS-induced production of IL-6 in Hepa-1c1c7 cells. These findings indicate that baicalin may ameliorate hepatic insulin resistance via improvement of IL-6-mediated impaired insulin signaling in hepatocytes.