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IL-6 Treatment (il-6 + treatment)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Interleukin 6 alleviates hepatic steatosis and ischemia/reperfusion injury in mice with fatty liver disease

HEPATOLOGY, Issue 4 2004
Feng Hong
Fatty liver, formerly associated predominantly with excessive alcohol intake, is now also recognized as a complication of obesity and an important precursor state to more severe forms of liver pathology including ischemia/reperfusion injury. No standard protocol for treating fatty liver exists at this time. We therefore examined the effects of 10 days of interleukin 6 (IL-6) injection in 3 murine models of fatty liver: leptin deficient ob/ob mice, ethanol-fed mice, and mice fed a high-fat diet. In all 3 models, IL-6 injection decreased steatosis and normalized serum aminotransferase. The beneficial effects of IL-6 treatment in vivo resulted in part from an increase in mitochondrial , oxidation of fatty acid and an increase in hepatic export of triglyceride and cholesterol. However, administration of IL-6 to isolated cultured steatotic hepatocytes failed to decrease lipid contents, suggesting that the beneficial effects of IL-6 in vivo do not result from its effects on hepatocytes alone. IL-6 treatment increased hepatic peroxisome proliferator-activated receptor (PPAR) , and decreased liver and serum tumor necrosis factor (TNF) ,. Finally, 10 days of treatment with IL-6 prevented the susceptibility of fatty livers to warm ischemia/reperfusion injury. In conclusion, long-term IL-6 administration ameliorates fatty livers and protects against warm ischemia/reperfusion fatty liver injury, suggesting the therapeutic potential of IL-6 in treating human fatty liver disease. Supplementary material for this article can be found on the Hepatology website (http://interscience.wiley.com/jpages/0270-9139/suppmat/index.html). (HEPATOLOGY 2004;40:933,941.) [source]

ORIGINAL ARTICLE: IL-6 as a Regulatory Factor of the Humoral Response During Pregnancy

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2008
Valeria Dubinsky
Problem, Regulatory factors seem to be essential to achieve transition from implantation window to placental vascularization. A novel function of interleukin (IL)-6 in the promotion of Th2 differentiation and inhibition of Th1 polarization has been demonstrated. Considering that Th2 response promotes antibody synthesis, we postulate that IL-6 could be modulating the quality of this response during pregnancy by increasing the proportion of blocking asymmetric antibodies. Method of study, We investigated expression of blocking-asymmetric-IgG during pregnancy of CBA/J × DBA/2 abortion model treated with IL-6, with regards to CBA/J × BALB/c. We also determined asymmetric-IgG production in IL-6-deficient pregnant mice. Results, We found that IL-6 treatment increased asymmetric-IgG in multiparous placentas from abortion combination whereas diminished abortion rate. Moreover, asymmetric-IgG proportion was diminished in sera from IL-6-deficient pregnant mice. Conclusion, Modulation of asymmetric antibody synthesis could be another mechanism implicated in the beneficial effect of IL-6 in prevention of murine recurrent abortion. [source]

C/EBP, is a downstream mediator of IL-6 induced growth inhibition of prostate cancer cells

THE PROSTATE, Issue 2 2005
Daniel C. Sanford
Abstract BACKGROUND Although a number of reports have investigated the effects of IL-6 family cytokines on prostate cell growth, there is limited information available identifying IL-6 inducible downstream effector genes and their function in growth control. Previous studies have demonstrated that IL-6 treatment results in the activation of signal transducer and activator of transcription3 (STAT3) in prostate cancer cells. The goal of this study was to investigate the influence of IL-6 treatment and activation of the Jak/STAT signal transduction pathway on C/EBP, gene expression and growth inhibition of human prostate cancer cells. METHODS Expression of C/EBP, and STAT3 activation were assayed using Northern and Western blotting techniques. Proliferation was assessed by [3H] thymidine incorporation, flow cytometry, and colony formation analyses. The analysis of the transcriptional regulation of C/EBP, was performed using luciferase-reporter constructs. RESULTS In this report, we demonstrate that IL-6 treatment induces STAT3 activation (pSTAT3), pSTAT3 binds to the human C/EBP, gene promoter and induces its expression. We also demonstrate that C/EBP, over-expression is capable of suppressing prostate cancer cell growth. CONCLUSIONS These results demonstrate that C/EBP, gene expression is increased in IL-6 treated LNCaP cells. Increased C/EBP, gene expression plays an important role in IL-6/STAT3 mediated growth arrest of LNCaP prostate cancer cells. Ongoing studies are investigating the mechanism by which C/EBP, controls prostate cancer cell growth and the potential role of C/EBP, in the survival and chemo resistance of prostate cancer metastasis. © 2004 Wiley-Liss, Inc. [source]

Cytokines alter the expression and activity of the multidrug resistance transporters in human hepatoma cell lines; analysis using RT-PCR and cDNA microarrays

JOURNAL OF PHARMACEUTICAL SCIENCES, Issue 11 2003
Gigi Lee
Abstract Pro-inflammatory cytokines suppress the hepatic expression of the multidrug resistance transporters in rodents, indicating potential usefulness in chemotherapy. Our objective was to investigate their impact in human hepatoma cells. HuH 7 and HepG2 cells were treated with IL-1,, IL-6, or TNF-, for 0,72 h. Expression and activity of MDR1 and the MRP (MRP1, 2, 3, and 6) transporters were examined by RT-PCR, efflux assays, and microarrays. Significant reductions in the MDR1-mediated efflux of Rhodamine 123 and MDR1 mRNA levels were observed in HuH 7 cells treated with IL-6, TNF-,, or IL-1, and in TNF-,,treated HepG2 cells. However, cytokine-treated HuH7 cells also demonstrated 1.6- to 2.6-fold greater efflux of the MRP substrate, 5-carboxyfluorescein (5-CF) and higher MRP3 mRNA levels (p,<,0.05). IL-1, and IL-6 treatments increased MRP activity and MRP1 mRNA levels in HepG2 cells (p,<,0.05). Microarrays studies performed in IL-6 and TNF-,,treated HepG2 cells detected similar changes in the expression of the MDR1 and MRP transporters, but this did not reach significance. However, the microarrays confirmed cytokine-mediated induction of several acute phase proteins. Our data suggests that although cytokine-mediated suppression of PGP may alter drug resistance in malignant cells, these cytokines may also impose an induction in other multidrug resistance genes. © 2003 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 92:2152,2163, 2003 [source]