• Title, Summary, Keyword: Interleukin(IL)-$1{\beta}$

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Effect of $17{\beta}$-Estradiol and 1,25-Dihydroxyvitamin $D_3$ on Interleukin-6 Production of Periodontal Ligament Cells (($17{\beta}$-Estradiol 및 1,25-Dihydroxyvitamin $D_3$가 치주인대 세포의 Interleukin-6의 생성에 미치는 영향)

  • Kwak, Wall-Ah;Choi, Bong-Kyu;Lee, Hyun-Jung;Yoo, Yun-Jung
    • 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.

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ACTIONS OF RECOMBINANT $INTERLEUKIN-1{\beta}$, TUMOR NECROSIS $FACTOR-{\alpha}$ AND INTERLEUKIN-6 ON BONE RESORPTION IN VITRO (RECOMBINANT $INTERLEUKIN-1{\beta}$, TUMOR NECROSIS $FACTOR-{\alpha}$ 및 INTERLEUKIN-6의 골흡수 유도 효과에 관한 연구)

  • Lee, Yong-Moo;Choi, Sang-Mook
    • Journal of Periodontal and Implant Science
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    • v.24 no.1
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    • pp.155-164
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    • 1994
  • 치조골흡수는 만성치주질환의 전형적인 증상이다. 골흡수에 작용하는 여러 요인들 중에서도, 특히 최근에 들어서 몇몇 cytokine들에 대한 관심이 높아지고 있는데, interleukin-1(IL-1), tumor necrosis factor(TNF) 및 interleukin-6(IL-6) 등이 치주질환의 진행과정에서 중요한 치조골흡수요인으로 제안되고 있다. 본 연구의 목적은 신생쥐의 골조직 배양실험을 통해서 recombinant human $interleukin-1{\beta}$ ($rHuIL-1{\beta}$), recombinant human tumor necrosis $factor-{\alpha}$($rHuTNF-{\alpha}$) 및 recombinant human interleukin-6(rHuIL-6) 의 골흡수 유도효과를 알아보고, cyclooxygenase 억제제인 indomethacin과 recombinant murine $interferon-{\gamma}$($rMurIFN-{\gamma}$)가 이들 cytokine의 골흡수 유도능력에 미치는 영향을 알아봄으로써 이들 cytokine의 작용기구에 대해서 알아보고자 하는데 있다. 생후 1-2일된 쥐에게 $1{\mu}Ci^{45}CaCl_2$를 피하주사하고 4일 후에 쥐를 희생시켜 $^{45}Ca$ 로 표지된 두개골을 얻어 24시간 전배양 후, 각 cytokine ($rHuIL-1{\beta}$, $rHuTNF-{\alpha}$ 및 rHuIL-6)과 cytokine 및 첨가약제 (indomethacin 및 $rMurIFN-{\gamma}$)가 함유된 배지로 교환하여 48시간 배양한다. 골흡수 유도효과는 두개골에서 48시간의 배양 중 유리되는 $^{45}Ca$의 방사능 정도로 평가하였다. 본 연구를 통해 다음과 같은 결과를 얻었다. 1. $rHuIL-1{\beta}$ ($10^{-12}-10^{-9}M$) 및 $rHuTNF-{\alpha}$ ($10^{-10}-10^{-8}M$)는 농도변화에 따르는 골흡수 유도효과를 보였으나 , rHuIL-6 ($10^{-10}-10^{-8}M$)는 유의할 만한 효과를 보이지 않았다. 2. Indomethacin ($10^{-6}M$)은 $rHuIL-1{\beta}$$rHuTNF-{\alpha}$의 골흡수 유도작용에 유의할 만한 억제효과를 나타내지 않았다. 3. $rMurIFN-{\gamma}$ (1000 U/ml) 은 $rHuIL-1{\beta}$$rHuTNF-{\alpha}$의 골흡수 유도작용에 유의한 억제효과를 나타내었다. 본연구를 통해 치주질환 환자의 치주조직에서 검출되는 $IL-1{\beta}$$TNF-{\alpha}$가 치조골 흡수에 중요한 역할을 할 것으로 생각된다.

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Study on Relationship between Abdominal Connective Tissue Weakness and Interleukin-1 Gene Polymorphism in Iris Constitution Analysis Study on Relationship between Abdominal Connective Tissue Weakness and Interleukin-1 Gene Polymorphism in Iris Constitution Analysis (홍채 체질 분석에서 복부 결합조직 허약 체질과 인터루킨-1 유전자 다형성과의 상관성 연구)

  • 도금록;황우준;금경수;최성용;김종욱;조재운
    • The Journal of Korean Medicine
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    • v.25 no.1
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    • pp.31-39
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    • 2004
  • Objectives : The purpose of this study is to report the relationship between iridological constitution and interleukin 1 beta (IL-1 $\beta$) gene polymorphism. Methods : Iris constitution were diagnosed by automatic Iris analysis system, Bexel Irina(Korea). The blood was stored at - $20^{\circ}$... until it was ready to be extracted. The genomic DNA was extracted by inorganic procedure. The concentration of DNA was estimated by absorbance at 260 nm. The interleukin-1 beta (IL-1 $\beta$) gene polymorphism was detected by PCR amplification. Results & Conclusions : The author classified 166 individuals according to Iris constitution, and determined IL-1 $\beta$ genotype. The frequencies of Iris constitutions as follows : neurogenic type, 41 (24.7%); abdominal connective tissue weakness type, 53(31.9%); cardio-renal connective tissue weakness type, 50 (30.1%); the others type, 22 (13.3%). Especially, the frequency of abdominal connective tissue weakness type was significantly higher in err genotype than in the remaining constitutions. As a result, The author demonstrated the association among IL-1 $\beta$ genotype, IBD and Iris constitution.

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EFFECT OF INTERLEUKIM-10 ON THE BONE RESORPTION INDUCED BY INTERLEUKIN-1B (Interleukin-10 이 $interleukin-1{\beta}$로 유도되는 골흡수에 미치는 효과)

  • Yu, Yun-Jung;Kang, Yun-Sun;Lee, Syng-Ill
    • Journal of Periodontal and Implant Science
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    • v.24 no.2
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    • pp.321-339
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    • 1994
  • The cytokines released by osteoblasts induce bone resorption via the differentiation of osteoclast precursors. In this process, $interleukin-1{\beta}$($IL-1{\beta}$)-induced bone resorption is mediated by granulocyte macrophage-colony stimulation factor(GM-CSF), interleukin-6 (IL-6), and tumor necrosis factor ${\alpha}$($TNF-{\alpha}$) released from osteoblasts. Since these cytokines (GM-CSF, IL-6, $TNF-{\alpha}$) are produced by not only osteoblasts but also monocytes, and interleukin-10(I1-10) inhibits the secretion of these cytokines from monocytes, it may be speculated that IL 10 could modulate the production of GM-CSF, IL-6, and $TNF-{\alpha}$ by osteoblasts, then control $IL-1{\beta}-induced$ bone resorption. Therefore, the aims of the present study were to examine the effects of IL-10 on bone resorption. The sixten or seventeen-day pregnant ICR mice were injected with $^{45}Ca$ and sacrificed one day after injection. Then fetal mouse calvaria prelabeled with $^{45}Ca$ were dissected out. In order to confirm the degree of bone resorption, mouse calvaria were treated with Lipopolysaccharide(LPS), $TNF-{\alpha}$, $IL-1{\alpha}$, IL-8, $IL-1{\beta}$, and $IL-1{\alpha}$, Then, IL-10 and $interferon-{\gamma}$ ($IFN-{\gamma}$) were added to calvarial medium, in an attempt to evaluate the effect of $IL-1{\beta}-induced$ bone resorption. In addition, osteoclasts formation in bone marrow cell cultures, and the concentration of IL-6, $TNF-{\alpha}$, and GM-CSF produced from mouse calvarial cells were investigated in response to $IL-1{\beta}$ alone and simultaneously adding f $IL-1{\beta}$ and IL-10. The degree of bone resorption was expressed as the ratio of $^{45}Ca$ release(the treated/the control). The osteoclasts in bone marrow cultures were indentified by tartrate resistant acid phosphatase(TRAP) stain and the concentration of the cytokines was quantified using enzyme linked immunosorbent method. As results of these studies, bone resorption was induced by LPS(1 ng/ml ; the ratio of $^{45}Ca$ release, $1.14{\pm}0.07$). Also $IL-1{\beta}$(1 ng/ml), $IL-1{\alpha}$(1 ng/ml), and $TNF-{\alpha}$(1 ng/ml) resulted in bone resorption(the rations of $^{45}Ca$ release, $1.61{\pm}0.26$, $1.77{\pm}0.03$, $1.20{\pm}0.15$ respectively), but IL-8 did not(the ratio of $^{45}Ca$ release, $0.93{\pm}0.21$). The ratios of $^{45}Ca$ release in response to IL-10(400 ng/ml) and $IFN-{\gamma}$(100 ng/ml) were $1.24{\pm}0.12$ and $1.08{\pm}0.04$ respectively, hence these cytokines inhibited $IL-1{\beta}$(1 ng/ml)-induced bone resorption(the ratio of $^{45}Ca$ release $1.65{\pm}0.24$). While $IL-1{\beta}$(1 ng/ml) increased the number of TRAP positive multinulcleated cells in bone marrow cultures($20{\pm}11$), simultaneously adding $IL-1{\beta}$(1 ng/ml) and IL-10(400 ng/ml) decreased the number of these cells($2{\pm}2$). Nevertheless, IL-10(400 ng/ml) did not affect the IL-6, GM-CSF, and $TNF-{\alpha}$ secretion from $IL-1{\beta}$(1 ng/ml)-activated mouse calvarial cells. From the above results, it may be suggested that IL-10 inhibites $IL-1{\beta}-induced$ osteoclast differntiation and bone resorption. However, the inhibitory effect of IL-10 on the osteoclast formation seems to be mediated not by the reduction of IL-6, GM-CSF, and $TNF-{\alpha}$ production, but by other mechanisms.

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Study on Alteration of Interleukin-$1{\beta}$, -2, -6 Production and Serum Level in Schizophrenic Patients (정신분열증 환자에서 Interleukin-$1{\beta}$, -2, -6 생산능과 혈청농도 변화에 관한 연구)

  • Kim, Yong-Ku;Lee, Min-Soo;Suh, Kwang-Yoon
    • Korean Journal of Biological Psychiatry
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    • v.1 no.1
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    • pp.98-108
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    • 1994
  • The etiology and pathophysiology of schizophrenia remain unknown. It has been postulated that infectious-autoimmune process may play a role in the pathogenesis of symptoms in some schizophrenic patients. Findings of altered interleukin(IL) regulation have been regarded as additional proof that schzophrenia has an infectious-autoimmune background. In the present study, we measured mitogen-stimulated production of and serum level of IL-$1{\beta}$, IL-2, IL-6 using ELISA in 16 neuroleptic-free schizophrenic patients and in 16 age, sex matched healthy controls. The results were as follows : 1) There was a significant decrease of IL-2 production in schizophrenic patients than in normal controls(respectively $1.90{\pm}0.13ng/m{\ell}$, $2.79{\pm}0.14ng/m{\ell}$, p<0.001). But there was no significant difference of IL-$1{\beta}$ production and IL-6 production between schizophrenic patients and normal controls. 2) There was a significant increase of serum level of IL-2 in schizophrenic pateitns than in normal controls(respectively $184.8{\pm}12.8pg/m{\ell}$, $104.2{\pm}34.2pg/m{\ell}$, p<0.01). Serum level of IL-$1{\beta}$ was partially detected in both groups and serum level of IL-6 was not detected in both groups. 3) There was no significant differences of IL-$1{\beta}$, -2, -6 production & serum level of IL-2 according to male vs female, paranoid type vs undifferentiated type, drug-naive group vs drug-free group in schizophrenic patients. 4) There was significant correlation between IL-$1{\beta}$ and IL-6 production(r=0.86, p<0.001). No correlation between IL-$1{\beta}$, -2, -6 production, serum level of IL-2 and age, duration of illness, and BPRS score was found. It has been suggested that the low lymphocyte production of IL-2 in the patients with autoimmune disease occurs because the T cells are activated and lymphocyte-derived IL-2 has been released into the serum. The authors suggest that decreased IL-2 production in our schizophrenic patients is due to increased IL-2 serum level in those patients. Thus our finding of low IL-2 production and high serum level of IL-2 in our schizophrenic patients is compatible with the possibility that our patients have an autoimmune process. Further study on relationship between IL alteration and other immunological abnormalities(the presence of serum autoantibody and of anti-brain antibody, $CD4^+$, $CD8^+$ cell index, etc) in schizophrenic patients will be warranted.

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Assessment of interleukin-1beta and interleukin-6 in the crevicular fluid around healthy implants, implants with peri-implantitis, and healthy teeth: a cross-sectional study

  • Yaghobee, Siamak;Khorsand, Afshin;Ghohroudi, Amir Alireza Rasouli;Sanjari, Khashayar;Kadkhodazadeh, Mahdi
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.40 no.5
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    • pp.220-224
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    • 2014
  • Objectives: This study aimed to assess and compare the levels of interleukin-1beta (IL-$1{\beta}$) and interleukin-6 (IL-6) in the crevicular fluid around healthy implants, implants with peri-implantitis, and healthy teeth. Materials and Methods: This study evaluated 16 dental implants in 8 patients (4 males and 4 females). These patients had at least one healthy implant and one implant with peri-implantitis next to healthy teeth. The crevicular fluid was collected using absorbent cones and transferred to the laboratory. Specimens were evaluated by ELISA for interleukin levels. Data were analyzed using repeated measures ANOVA and Bonferroni tests (P<0.05). Results: Levels of IL-$1{\beta}$ in the crevicular fluid around implants with peri-implantitis were significantly higher than around healthy implants (P=0.002); the latter was significantly higher than around healthy teeth (P=0.015). A significant difference was found in the level of IL-6 in the crevicular fluid around implants with peri-implantitis and healthy implants (P=0.049) and also between implants with peri-implantitis and healthy teeth (P<0.001). Conclusion: Within the limitations of this study, significant differences exist in the levels of IL-$1{\beta}$ and IL-6 in the crevicular fluid of implants with peri-implantitis, healthy implants, and healthy teeth. More studies with larger sample sizes in different populations are necessary.

Inhibitory Effect of Phorbol 12-Myristate 13-Acetate on NO Production Induced by Interleukin-1 beta in Aortic Vascular Smooth Muscle Cells of Rats (혈관평활근세포에서 Phorbol 12-Myristate 13-Acetate의 전처리가 Interleukin-1β에 의한 Nitrite생성에 미치는 영향)

  • 윤병헌;김인겸;박태규;김중영
    • Journal of Life Science
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    • v.13 no.4
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    • pp.441-447
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    • 2003
  • To examine the role of protein kinase C (PKC) in regulation of interleukin-1 beta (IL-1$\beta$)-induced iNOS expression, IL-1$\beta$-induced nitrite production was observed in cultured vascular smooth muscle (VSM) cells pretreated with phorbol 12-myristate 13-acetate (PMA) and phorbol 12,13-butyrate (PDB) as PKC activator; 4$\alpha$-phorbol-didecanoate (PDD) as PKC non-activator. Nitrite production induced by IL-1$\beta$ was increased by the presence of increasing concentration of PMA ranging from 2 to 200 nM. However, in VSM cells pretreated with PMA and PDB, IL-1$\beta$-induced $NO_2$ production was decreased in proportion to the duration of pretreatment, and most significantly decreased in pretreatment time of 24 hours. Using RT-PCR method, the expression of iNOS mRNA induced by IL-1$\beta$ was decreased in VSM cells pretreated with PMA 200 nM for 24 hours. These results suggest that decrease in IL-I$\beta$-induced nitrite production by the pretreatment of PMA result from inhibition of iNOS expression and the inhibition related to PMA-induced PKC down-regulation.

Changes of Interleukin-12 and Transforming Growth Factor Beta 1 before and after Antipsychotic Treatments in Schizophrenic Patients (정신분열병 환자에서 Interleukin-12와 Transforming Growth Factor Beta 1의 치료 전후의 변화)

  • Kim, Sung-Jae;Lee, Bun-Hee;Kim, Yong-Ku
    • Korean Journal of Biological Psychiatry
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    • v.12 no.2
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    • pp.143-150
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    • 2005
  • Background:Several reports have suggested that cytokine alterations could be related to the pathophysiology of schizophrenia. In this study, we measured plasma level of interleukin-12(IL-12), a proinflammatory T helper 1(Th1) cytokine and transforming growth factor-${\beta}1$(TGF-${\beta}1$), an anti-inflammatory Th3 cytokine before and after antipsychotic treatment in schizophrenic patients. Methods:The plasma concentrations of IL-12 and TGF-${\beta}1$ were measured by using quantitative ELISA in 23 schizophrenic patients and 31 normal controls at admission and 8 weeks later. The psychopathology was measured by Brief Psychiatric Rating Scale(BPRS). Results:IL-12 and TGF-${\beta}1$ levels were significantly higher in schizophrenic patients than in controls before treatment. At the 8 week of treatment, the TGF-${\beta}1$ levels returned to control values, while IL-12 levels were not significantly changed. There were no significant correlations between the changes of BPRS scores and the changes of IL-12 or TGF-${\beta}1$ levels in schizophrenic patients. Conclusion:Cytokine abnormalities in schizophrenia might be involved in the pathophysiology of the illness. It is possible that TGF-${\beta}1$ plays an important role in the schizophrenia.

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The Effects of Oviduct and Uterine Epithelial Cells on the Expression of Interleukin-$1\beta$ Gene in Preimplantation Mouse Embryos (생쥐 초기배아에서 Interleukin-$1\beta$ 유전자의 발현에 미치는 수란관과 자궁내막세포의 영향)

  • 홍석호;계명찬;김종월;이정복;오은정;조동제;최규완;김문규
    • Development and Reproduction
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    • v.3 no.1
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    • pp.59-67
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    • 1999
  • To investigate the role of interleukin-l$\beta$ (IL-1$\beta$) in the embryonic development, in vivo and in vitro expression patterns of IL-1$\beta$ gene in the preimplantation mouse embryos were examined by RT-PCR, and the effects of explanted mouse ovi-duct and uterine epithelial cells on the expression of IL-1$\beta$ gene in the pleimplantation mouse embryos were examined by co-culture. IL-1$\beta$ mRNA was detected in the embryos from 4-cell stage to blastocyst stage in vivo and from morula stage to hatching blastocyst stage in vitro. This transcript was not detected from the GV stage to late 2-cell stage in vivo, and not at the 4-cell and 8-cell stages in vitro. For the co-culture of late 2-cell embryos with the explanted mouse oviduct and uterine epithelial cells, oviducts and uterine epithelial cells were isolated at 48 hour alter the hCG injection. The explanted oviduct and uterine epithelial cells in co-culture groups facilitated the IL-1$\beta$ gene expression of the mouse embryos in comparison with the control. Taken together these results suggest that the presence of IL-1$\beta$ plays an important role in preimplantation embryonic development. In addition, the up-regulation of IL-1$\beta$ gene expression by the explanted oviduct and uterine epithelial cells demonstrates that embryonic expression of IL-l$\beta$ gene may be regulated by the interaction with oviductal and uterine factor (s).

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Mycobacterium tuberculosis-induced Expression of Interleukin-1 Beta is Mediated Via Protein Kinase C Signaling Pathway

  • Cho, Jang-Eun;Lee, Kyung-Hong;Son, Sin-Jee;Park, Sang-Jung;Lee, Hye-Young;Kim, Yoon-Suk
    • Biomedical Science Letters
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    • v.16 no.2
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    • pp.119-122
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    • 2010
  • Interleukin-1${\beta}$ $(IL-1{\beta})$ is one of the key proinflammatory cytokines and it plays an important role for the antimycobacterial host defense mechanisms. In this study, we examined Mycobacterium tuberculosis (MTB)-stimulated induction of IL-1${\beta}$ and evaluated the associated signal transduction pathways. In PMA-differentiated THP-1 cells, MTB infection increased mRNA expression of IL-$1{\beta}$ in a dose-dependent manner. The expression of IL-1${\beta}$ mRNA began to be induced at 1.5 h after infection, and induced expression of IL-1${\beta}$ was retained for 48 h after MTB infection. The increase in expression of IL-1${\beta}$ caused by MTB was reduced in cells treated with Ro-31-8425 (an inhibitor of PK$C{\alpha}$, ${\beta}I$, ${\beta}II$, ${\gamma}$, ${\varepsilon}$) or PD98059 (an inhibitor of MEK1), meanwhile, pre-treatment with $G\ddot{o}6976$ (an inhibitor of $Ca^{2+}$ dependent PK$C{\alpha}$ and PK$C{\beta}I$) or Rottlerin (an inhibitor of PK$C{\delta}$) has no effect on MTB-induced expression of $IL-1{\beta}$ mRNA. These results show that the expression of $IL-1{\beta}$ mRNA caused by MTB may be mediated via MEK1 and PKC isoforms including PK$C{\beta}II$, $PKC{\gamma}$, or $PKC{\varepsilon}$. Further studies are required to determine whether other PKC isoforms $(PKC {\eta},\;{\theta},\;{\varepsilon},\;and\;{\lambda}/{\iota})$, except $PKC{\delta}$, $PKC{\alpha}$, and $PKC{\beta}I$, are also involved in $IL-1{\beta}$ mRNA expression after mycobacterial infection.