• The korean journal of orthodontics
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• v.28 no.1 s.66
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• pp.165-174
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• 1998

The turnover of collagen is controlled by the balance between collagen synthesis and degradation. The production of collagenase (matrix metalloproteinase-1) and its inhibitor, tissue inhibitor of matrix metallopmteinase-1 (TIMP-1) are one of the substances which regulate this balance. The periodontal ligament fibroblast plays an important role in collagen metabolism during orthodontic treatment and is believed to be an origin of the osteoblast in the alveolar bone. The collagenase secreted by the periodontal ligament fibroblast and the osteoblast initiates the bone resorption by removing the osteoid layer in the alveloar bone. The interleukin-$1{\beta}$ is secreted by the macrophage during orthodontic treatment. The present study was undertaken to assess the effect of mechanical stress and interleukin-$1{\beta}$ on the expression of collagenase and TIMP-1 in the periodontal ligament fibroblasts using reverse transcription polymerase chain reaction and immunohistochemical staining. The periodontal ligament fibroblasts were stitched by placing the $Petriperm dish^{\circledR}$ dish on the top of spheroidal convex watch glass ($5\%$ surface increase) and tented with interleukin-$1{\beta}$ (1.0 ng/ml), or treated with both of them. Treatment with mechanical stress and/or interleukin-$1{\beta}$ resulted in increased collagenase mRNA expression. The mechanical stress treated group (1.61, 1.62, 1.37 fold increase), the interleukin-$1{\beta}$, tented group (1.68, 1.60, 3.78 fold increase), the mechanical stress and interleukin-$1{\beta}$ treated group (1.89, 1.72, 5.48 fold increase) induced increases in collagenase mRNA compared with the control group after 2, 4, 8 hours respectively. But TIMP-1 mRNA expressions at experimental groups were decreased after 2, 4 hours and increased after 8 hours. The mechanical stress treated group (0.16, 0.49 fold decrease and 3.77 fold increase), the interleukin-$1{\beta}$ treated group (0.15,0.44 fold decrease and 4.46 fold increase), the mechanical stress and interleukin-$1{\beta}$ tented group (0.15, 0.69 fold decrease and 4.81 fold increase) induced changes in TIMP-1 mRNA compared with the control group after 2, 4, 8 hours, respectively. Immunohistochemical stain showed that increased collagenase and TIMP-1 staining of the mechanical stress tented group, the interleukin-$1{\beta}$ treated group, and the mechanical stress and interleukin-$1{\beta}$ treated group compared with that of the control group after 8 hours. These findings suggest that mechanical stress and interleukin-$1{\beta}$ regulate expression of collagenase and TIMP-1.

• 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.

• 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.

• YAKHAK HOEJI
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• v.42 no.4
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• pp.408-413
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• 1998

To establish prediabetes in vitro/ model concerning the etiology of Insulin Dependent Diabetes Mellitus (IDDM) in cellular level we have designed experimental prediabefic model in pancreatic beta cells. RINm5F, HIT-T15 and isolated rat islets were chosen as pancreatic beta cells. Since interleukin-$1{\beta}$-induced beta cell cytotoxicity has been implicated in the autoimmune cytotoxicity of IDDM, we used inteleukin-$1{\beta}$ as diabetogenic agent. For establishment of prediabetic in vitro model, the degree of beta cell deterioration was determined by cell proliferation, insulin release and morphological appearance. Cell proliferation, insulin release and morphology were changed dose-dependently in condition that inteleuldn-$1{\beta}$ was exposured to pancreatic beta cells. The concentration and exposure time of interleukin-$1{\beta}$ to set up prediabetic model in beta cell lines and isolated rat islets were 100${\sim}$1000U/ml, 48hr. And 25${\sim}$100U/ml, 48hr, respectively.

• 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 $rHuIL-1{\beta}$ 및 $rHuTNF-{\alpha}$의 골흡수 유도작용에 유의할 만한 억제효과를 나타내지 않았다. 3. $rMurIFN-{\gamma}$ (1000 U/ml) 은 $rHuIL-1{\beta}$ 및 $rHuTNF-{\alpha}$의 골흡수 유도작용에 유의한 억제효과를 나타내었다. 본연구를 통해 치주질환 환자의 치주조직에서 검출되는 $IL-1{\beta}$ 및 $TNF-{\alpha}$가 치조골 흡수에 중요한 역할을 할 것으로 생각된다.

• 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.

• YAKHAK HOEJI
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• v.40 no.6
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• pp.684-689
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• 1996

PALMIWON is composed of 8 oriental herbs which has been known to show some pharmacological effects in kidney, blood vessels and immune systems, and used for the treatment of kid ney disease, hypertension, nervous disease and diabetic mellitus in the Orient for a long time. Based on our previous report that PALMIWON showed different effects on immune cells and ${\beta}$-cells, the immunoreactivity of ICSA (Islet Cell Surface Antibody) with ${\beta}$-cell (RINm5F) and the cell proliferation and function of interleukin-1${\beta}$ damaged ${\beta}$-cells in the presence of PALMIWON were examined. It was observed that PALMIWON significantly inhibited the immunoreactivity of ICSA with ${\beta}$-cell, and markedly increased cell proliferation and insulin release of interleukin-1${\beta}$ damaged ${\beta}$-cells.

• Journal of Gastric Cancer
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• v.4 no.3
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• pp.149-155
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• 2004

Purpose: According to the recent studies, it is shown that the polymorphism of Interleukin $1\beta$ gene is associated with the incidence of gastric cancer caused by the Helicobacter pylori infection. Interleukin $1\beta$ is a cytokine markedly inhibiting gastric acid secretion. Interleukin $1\beta$ production associated with Helicobacter pylori gastric infection may exacerbate mucosal damage including chronic gastritis and atrophic gastritis, may induce eventual neoplasia. Among these Interleukin $1\beta$ gene polymorphisms, polymorphisms at -31 portion and -511 portion may associated with these processes, eventually increase the risk of gastric cancer. We investigated the risk of gastric cancer according to the Helicobacter pylori infection and genetic polymorphism of Interleukin $1\beta$ in gastric cancer patients. Materials and Methods: 176 individuals with gastric cancer and 40 healthy controls were analyzed. Each group was divided into two groups whether they infected with Helicobacter pylori or not. DNA was extracted from the peripheral blood in all groups. The PCR-RFLP method was used for investigating the distribution of genotype of C/C, C/T, T/T at -31 portion and -511 portion. Results: T/T genotype at -511 portion was $19.3\%$ in gastric cancer cases and $10\%$ in controls, which was statistically significant. (P=0.0432) The risk of gastric cancer was increased 4.86 ($1.26\∼18.77$) in group which had T/T genotype. In gastric cancer cases, C/C genotype at 31 portion was $27.6\%$ in group with Helicobacter pylori infection and $12.8\%$ in group without infection, which was statistically significant. (P=0.0047) The risk of gastric cancer was increased 4.82 ($1.81\~12.81$) in group which had C/C genotype. Conclusion: T genotype at -511 portion among the Interleukin $1\beta$ genetic polymorphisms may be the risk factor of gastric cancer. And, with Helicobacter pylori infection, C genotype at -31 portion may be the risk factor of gastric cancer.

• 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.

• 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.