• 제목/요약/키워드: interleukin-10(IL-10)

검색결과 1,825건 처리시간 0.027초

Induction of IL-6 and IL-8 Expression by Leptin Treatment in Periodontal Ligament Cells and Gingival Fibroblasts

  • Park, Hong-Gyu;Kim, Ji-Hye;Cha, Jeong-Heon;Bak, Eun-Jung;Yoo, Yun-Jung
    • International Journal of Oral Biology
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    • 제38권2호
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    • pp.73-80
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    • 2013
  • Leptin is one of the adipocytokines produced from adipose tissue but its functions in periodontal tissue have not previously been investigated. In our current study, we examined the effects of leptin on the expression of interleukin (IL)-6 and IL-8 in periodontal ligament (PDL) cells and gingival fibroblasts. Leptin receptor expression was evaluated by RT-PCR and the production of cytokines was measured by ELISA. The phosphorylation of Akt and Erk1/2 was assessed by western blotting. mRNA of long and short form leptin receptors were detected in both PDL cells and gingival fibroblasts. Leptin was found to increase the production of IL-6 and IL-8 in both of these cell types, an effect which was not blocked by polymyxin B, an inhibitor of lipopolysaccharide (LPS). Leptin did not alter the production of IL-6 and IL-8 induced by LPS in PDL cells but increased Akt and Erk1/2 phosphorylation in these cells. These results suggest that leptin acts as an inducer of IL-6 and IL-8 in PDL cells and gingival fibroblasts.

Interleukin-32: Frenemy in cancer?

  • Han, Sora;Yang, Young
    • BMB Reports
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    • 제52권3호
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    • pp.165-174
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    • 2019
  • Interleukin-32 (IL-32) was originally identified in natural killer (NK) cells activated by IL-2 in 1992. Thus, it was named NK cell transcript 4 (NK4) because of its unknown function at that time. The function of IL-32 has been elucidated over the last decade. IL-32 is primarily considered to be a booster of inflammatory reactions because it is induced by pro-inflammatory cytokines and stimulates the production of those cytokines and vice versa. Therefore, many studies have been devoted to studying the roles of IL-32 in inflammation-associated cancers, including gastric, colon cancer, and hepatocellular carcinoma. At the same time, roles of IL-32 have also been discovered in other cancers. Collectively, IL-32 fosters the tumor progression by nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$)-mediated cytokines and metalloproteinase production, as well as stimulation of differentiation into immunosuppressive cell types in some cancer types. However, it is also able to induce tumor cell apoptosis and enhance NK and cytotoxic T cell sensitivity in other cancer types. In this review, we will address the function of each IL-32 isoform in different cancer types studied to date, and suggest further strategies to comprehensively elucidate the roles of IL-32 in a context-dependent manner.

A novel IL-10-producing innate lymphoid cells (ILC10) in a contact hypersensitivity mouse model

  • Kim, Hyuk Soon;Jang, Jong-Hwa;Lee, Min Bum;Jung, In Duk;Park, Yeong-Min;Kim, Young Mi;Choi, Wahn Soo
    • BMB Reports
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    • 제49권5호
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    • pp.293-296
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    • 2016
  • The immunoregulatory cytokine Interleukin 10 (IL-10) protein is produced by various cells during the course of inflammatory disorders. Mainly, it downregulates pro-inflammatory cytokines, antigen presentation, and helper T cell activation. In this study, we show that the ratio of IL-10-producing cells was significantly increased in lineage negative (i.e., not T, B, or leukocyte cell lineages) cells than in lineage positive cells in lymphoid and peripheral tissues. We further observed that IL-10-producing innate lymphoid cells (ILCs), here called firstly ILC10, were increased in number in oxazolone-induced contact hypersensitivity (CHS) mice. In detail, IL-10-producing lineage negative cells were elevated in the axillary, inguinal lymph node, and ear tissues of CHS mice. Notably, the cells expressed classical ILC marker proteins such as CD45, CD127, and Sca-1. Altogether, our findings suggest for the first time that ILC10s are present in various physiological settings and could be involved in numerous immune responses as regulatory cells.

주요 우울증에서 Interleukin-10 유전자의 제한효소 절편길이 다형성 (Restriction Fragment Length Polymorphism of Interleukin-10 Gene in Major Depression)

  • 전태연;배치운;이정태;박원명;김광수
    • 생물정신의학
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    • 제7권2호
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    • pp.147-151
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    • 2000
  • Objective : Major depression is known to have immunologic dysfunctions, the recent studies revealed that cytokines including IL-6 and IL-$1{\beta}$ were increased in patients with major depression. Since molecular genetic methods have been progressed, this study was to investigate the relationship between major depression and immunologic aspects by analyzing polymorphism of IL-10 gene. Method : 92 patients with major depression were included and data of 146 normal controls obtained from the Catholic Hemopoietic Stem Cell Information Bank of Korea were used in this study. DNA was extracted from whole blood, thereafter amplified by polymerase chain reaction, and digested by Mae III After that procedure, we obtained and assessed RFLP of two alleles, IL-10T and IL-10C. All data were analyzed by ${\chi}^2$ test. Results : 1) There were no significant difference in genotype frequencies of $IL-10^*T/T$, $IL-10^*T/C$, and $IL-10^*C/C$ between major depression patients group and control group. 2) There were no significant difference in allelic frequencies of $IL-10^*T$ and $IL-10^*C$ between major depression patients group and control group. Conclusion : We did not verified the differences in frequencies of $IL-10^*T/^*IL-10^*C$ gene between the major depression patients group and control group, respectively. But the results of this study do not declare that the IL-10 gene has no association with major depression. We do suggest that further systematic studies including various clinical variables should be conducted.

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Suppressive Effects of a Truncated Inhibitor K562 Protein-Derived Peptide on Two Pro-inflammatory Cytokines, IL-17 and TNF-α

  • Hwang, Jong Tae;Yu, Ji Won;Nam, Hee Jin;Song, Sun Kwang;Sung, Woo Yong;Kim, Yongae;Cho, Jang-Hee
    • Journal of Microbiology and Biotechnology
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    • 제30권12호
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    • pp.1810-1818
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    • 2020
  • Inhibitor K562 (IK) protein was first isolated from the culture medium of K562 cells, a leukemia cell line, and is an inhibitory regulator of interferon-γ-induced major histocompatibility complex class II expression. Recently, exogenous truncated IK (tIK) protein showed potential as a therapeutic agent for inflammation-related diseases. In this study, we designed a novel putative anti-inflammatory peptide derived from tIK protein based on homology modeling of the human interleukin-10 (hIL-10) structure, and investigated whether the peptide exerted inhibitory effects against pro-inflammatory cytokines such as IL-17 and tumor necrosis factor-α (TNF-α). The peptide contains key residues involved in binding hIL-10 to the IL-10 receptor, and exerted strong inhibitory effects on IL-17 (43.8%) and TNF-α (50.7%). In addition, we used circular dichroism spectroscopy to confirm that the peptide is usually present in a random coil configuration in aqueous solution. In terms of toxicity, the peptide was found to be biologically safe. The mechanisms by which the short peptide derived from human tIK protein exerts inhibitory effects against IL-17 and TNF-α should be explored further. We also evaluated the feasibility of using this novel peptide in skincare products.

Interleukin-8 (IL-8) 분비에 미치는 neuropeptides의 영향에 관한 연구 (The effect of neuropeptides on secretion of Interleukin-8(IL-8))

  • 김경준;박상혁;최경규;박상진
    • Restorative Dentistry and Endodontics
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    • 제31권3호
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    • pp.153-160
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    • 2006
  • 본 연구는 치수조직, 치은, 치주인대로부터 배양된 조직을 SP (Substance P)로 4시간 SP, CGRP (Calcitonin Gene-related Peptide) , Tumor necrosis factor-$\alpha$ (TNF-$\alpha$)로 8시간 자극 후 RNase Protection Assay를 시행하고, IL-8의 분비량을 측정해 다음 결과를 얻었다. 1. IL-8 mRNA는 모든세포에서 발현됐다. 2. IL-8 mRNA 발현은 SP ($10^{-5}M$)와 SP ($10^{-8}M$)로 4시간 자극 시 증가되지 않았다. 3. IL-8 mRNA 발현은 SP ($10^{-4}M$)와 CGRP ($10^{-6}M$)로 8시간 자극 시 증가되지 않았다. 4. TNF-$\alpha$ (2 ng/ml) 자극 시, IL-8 mRNA 발현이 증가됐다. 5. 치은 세포를 CGRP ($10^{-6}M$)로 8시간 자극 시, IL-8 분비량이 증가했다 (p<0.05). 6. 치주인대 세포를 SP ($10^{-4}M$)로 8시간 자극 시 IL-8 분비량이 증가했다 (p<0.05).

Interleukin-32 in Inflammatory Autoimmune Diseases

  • Kim, Soohyun
    • IMMUNE NETWORK
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    • 제14권3호
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    • pp.123-127
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    • 2014
  • Interleukin-32 (IL-32) is a cytokine inducing crucial inflammatory cytokines such as tumor necrosis factor-${\alpha}(TNF{\alpha})$ and IL-6 and its expression is elevated in various inflammatory autoimmune diseases, certain cancers, as well as viral infections. IL-32 gene was first cloned from activated T cells, however IL-32 expression was also found in other immune cells and non-immune cells. IL-32 gene was identified in most mammals except rodents. It is transcribed as multiple-spliced variants in the absence of a specific activity of each isoform. IL-32 has been studied mostly in clinical fields such as infection, autoimmune, cancer, vascular disease, and pulmonary diseases. It is difficult to investigate the precise role of IL-32 in vivo due to the absence of IL-32 gene in mouse. The lack of mouse IL-32 gene restricts in vivo studies and restrains further development of IL-32 research in clinical applications although IL-32 new cytokine getting a spotlight as an immune regulatory molecule processing important roles in autoimmune, infection, and cancer. In this review, we discuss the regulation and function of IL-32 in inflammatory bowel diseases and rheumatoid arthritis.

Generation of Antagonistic RNA Aptamers Specific to Proinflammatory Cytokine Interleukin-32

  • Kim, Se-Ho;Kim, Jung-Hee;Yoon, Su-Jin;Kim, Keun-Sik;Yoon, Moon-Young;Yoon, Do-Young;Kim, Dong-Eun
    • Bulletin of the Korean Chemical Society
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    • 제31권12호
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    • pp.3561-3566
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    • 2010
  • Interleukin 32 (IL-32) is a recently identified cytokine that induces major proinflammatory cytokines such as $TNF{\alpha}$ and IL-$1{\beta}$, which play an important role in chronic inflammatory diseases. To antagonize the biological function of IL-32 in cells, we generated RNA aptamers that could bind specifically to IL-32 protein. The highest affinity aptamer, AC3-3, successfully antagonized IL-32 by abolishing the induction of $TNF{\alpha}$ in the human lung carcinoma cells expressing IL-32. This aptamer could be used as a potent and selective antagonist against IL-32 to further elucidate the roles of IL-32 in chronic inflammatory diseases, as well as a therapeutic agent.

Effects of Cardiovascular Training on Interleukin-6 in Stroke Patients: a Systematic Review and Meta-analysis of Randomized Controlled Trials

  • Jeong Keun Song;Ju Hui Moon
    • Physical Therapy Rehabilitation Science
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    • 제12권2호
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    • pp.115-122
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    • 2023
  • Objective: A previous study reported that cardiovascular training (CT) decreased interleukin-6 (IL-6), a pro-inflammatory cytokine with bidirectional effects. However, because of conflicting results of increasing and decreasing IL-6 levels in stroke patients, it is essential to clarify the effects of CT on IL-6 levels in this population. Therefore, this review aimed to investigate the effects of CT on IL-6 levels in stroke patients through a meta-analysis of randomized controlled trials (RCTs), synthesizing and analyzing the effects qualitatively and quantitatively. Design: A systematic review and meta-analysis of randomized controlled trials. Methods: In this review, conducted in April 2023, electronic databases (Web of Science, CINAHL, Embase, MEDLINE, Google Scholar) were searched to ascertain the effects of CT on IL-6 levels in stroke patients. For qualitative evaluation, ReVMan, provided by the Cochrane Group, was used, and for quantitative evaluation, a random-effects model and SMD (Standardized Mean Difference) were used. Results: Three RCTs measured IL-6 in 117 patients with stroke. The experimental group to which CT was applied showed no significant change compared to the control group.The result of analysis using the random effect model is SMD=-0.23; 95% confidence interval, -0.66 to 0.20. Conclusions: CT does not affect IL-6 levels in stroke patients. These results suggest that CT can be applied regardless of its positive or negative effect on IL-6 levels in stroke patients.

The Effect of Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) on The Expression of IL-1 System mRNA in Mouse Embryos

  • Kim, D. H.;S. S. Ko;Lee, H. C.;Lee, H. H.;Kim, S. S.;Lee, H. J.;B. C. Yang;Park, S. B.;W. K. Chang
    • 한국동물번식학회:학술대회논문집
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    • 한국동물번식학회 2003년도 학술발표대회 발표논문초록집
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    • pp.52-52
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    • 2003
  • Granulocyte-macrophage colony stimulating factor (GM-CSF) is synthesized in the female reproductive tract and has been shown to play an important role in human and murine embryo development and implantation. However, the mechanism of GM-CSF on the embryo development is unknown. Recent studies suggested that GM-CSF may be increase the expression of implantation relented genes, such as interleukin-1 (IL-1) system. Our aim of this study was to compare the interleukin-1$\alpha$ (IL-1$\alpha$), interleukin-1$\beta$ (IL-1$\beta$) and interleukin-1 receptor antagonist (IL-lra) mRNA between the GM-CSF supplemented group and control group in mouse embryos. Mouse 2-cell embryos were cultured in P-1 medium supplemented with or without mouse GM-CSF (10 ng/ml). The number of total and apoptotic cell in blastocyst were assessed by TUNEL. And then, the expression of IL-1$\alpha$, IL-1$\beta$ and IL-1ra mRNA in blastocyst were examined by RT-PCR.

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