• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.1
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• pp.254-259
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• 2004

Jeongshin-tang (JST) is a Korean herbal prescription, which has been successfully applied for the various neuronal diseases. However, it's effect remains unknown in experimental models. To investigate the biological effect of JST in Alzheimer's disease (AD) in vitro model, we analized the production of interleukin (IL)-6 and IL-8, and expression of cyclooxygenase (COX)-2 in IL-1β plus β-amyloid [25-35] fragment (A)-stimulated human astrocytoma cell line U373MG. JST alone had no effect on the cell viability. The production of IL-6 and IL-8 was significantly inhibited by pretreatment with JST (1mg/㎖) on IL-1β plus A-stimulated U373MG cells. Maximal inhibition rate of IL-6 and IL-8 production by JST was about 41.22% (P<0.01) and 34.45% (P<0.05), respectively. The expression level of COX-2 protein was up-regulated by IL-1β plus A but the increased level of COX-2 was inhibited by pretreatment with JST (1 mg/㎖). These data indicate that JST has a regulatory effect on cytokine production and COX-2 expression, which might explain it's beneficial effect in the treatment of AD.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.1
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• pp.51-57
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• 2015

The etiology of periodontal disease is multifactorial. Exogenous stimuli such as bacterial pathogens can interact with toll-like receptors to activate intracellular calcium signaling in gingival epithelium and other tissues. The triggering of calcium signaling induces the secretion of pro-inflammatory cytokines such as interleukin-8 as part of the inflammatory response; however, the exact mechanism of calcium signaling induced by bacterial toxins when gingival epithelial cells are exposed to pathogens is unclear. Here, we investigate calcium signaling induced by bacteria and expression of inflammatory cytokines in human gingival epithelial cells. We found that peptidoglycan, a constituent of grampositive bacteria and an agonist of toll-like receptor 2, increases intracellular calcium in a concentration-dependent manner. Peptidoglycan-induced calcium signaling was abolished by treatment with blockers of phospholipase C (U73122), inositol 1,4,5-trisphosphate receptors, indicating the release of calcium from intracellular calcium stores. Peptidoglycan-mediated interleukin-8 expression was blocked by U73122 and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis (acetoxymethyl ester). Moreover, interleukin-8 expression was induced by thapsigargin, a selective inhibitor of the sarco/endoplasmic reticulum calcium ATPase, when thapsigargin was treated alone or co-treated with peptidoglycan. These results suggest that the gram-positive bacterial toxin peptidoglycan induces calcium signaling via the phospholipase C/inositol 1,4,5-trisphosphate pathway, and that increased interleukin-8 expression is mediated by intracellular calcium levels in human gingival epithelial cells.

• Restorative Dentistry and Endodontics
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• v.28 no.5
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• pp.409-418
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• 2003

본 연구는 치수 염증 시 IL-8과 MCP-1 분비에서 neuropeptide의 역할에 대해 관찰하고자 발거된 건전한 치아를 수직 파절시켜 치수조직을 채취하여 배양된 치수세포 및 혈관내피세포(ECV 304세포)를 각기 다른 농도의 Substance P(SP)로 12시간 자극하였고, 24시간 동안 4시간 간격으로 시간대별로 자극하였으며, 또 치수세포를 Calcitonin gene-related peptide (CGRP)로 12시간 자극하였다. 이들 세포를 SP길항제 (Spantide)로 15분간 차단한 후 SP로 12시간 재 자극하였으며, SP와 CGRP혼합액을 12시간 자극하였다. 상기의 실험 후 부유물로 ELISA를 시행하여 IL-8과 MCP-1의 분비 량을 측정하였다. 치수세포는 SP로 자극 시 IL-8이 현저히 증가한 반면, CGRP는 효과가 없었으며, SP와 CGRP를 혼합자극 시 시너지 효과 또한 없었고, Spantide는 치수세포의 IL-8과 MCP-1의 분비를 차단시켰다. 치수세포를 SP로 24시간 동안 4시간 간격으로 자극 시 8시간 후 최대의 IL-8은 분비량 나타내었으며, 8시간과 12시간 사이에서 최대의 MCP-1 분비량을 나타내었다. ECV 304세포를 SP로 자극 시 IL-8과 MCP-1 분비량이 미약하게 증가하였으며, Spantide는 ECV 304세포의 IL-8과 MCP-1 분비를 억제시켰다.

• Development and Reproduction
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• v.23 no.3
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• pp.231-238
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• 2019

Interleukin-8 (IL-8) is an inflammatory cytokine that plays an important role in the inflammatory response through the activation of neutrophil cells. The expression of IL-8 was investigated in early developmental stages of the olive flounder and in tissues of 8-month-old individuals. The expression of IL-8 increased after the initiation of the immune system rather than at the early stage of development, and high expression was observed in the gills and spleen, the organs associated with immunity and metabolism. In addition, IL-8 expression after infection by viral hemorrhagic septicemia virus significantly increased in the fin, gill, muscles, and spleen. These results suggest that IL-8 is closely related to inflammation and immune regulation in the immune response of the olive flounder and may be used as a basis for studies on the immune systems of other fish.

• Biomolecules & Therapeutics
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• v.8 no.3
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• pp.276-280
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• 2000

In order to identify the domains of the G$_{\alpha}$16 subunit G protein that are responsible for its activation by the Interleukin-8 receptor, a serious of chimeras between G$_{\alpha}$16 and G$_{\alpha}$11 were assessed for their abilities to be activated by these receptors. Co-expression of IL-8 receptor and chimeras in which the carboxyl-terminal regions of G$_{\alpha}$11 were replaced from 30 up to 156 amino acid residues with the corresponding regions of G$_{\alpha}$16 demonstrated that C-terminal 156 amino acid residues of the G$_{\alpha}$16 were not sufficient to confer IL-8 receptor interaction specificity. Testing of a reciprocal serious of chimeras composed of G$_{\alpha}$16 sequences at the amino terminus and G$_{\alpha}$11 sequences at the carboxyl terminals revealed that sequences extending from the amino tar- minus to amino acid 209 of G$_{\alpha}$16 were sufficient to 7ndow the chimera with 75-80% of interaction specificity for 7-8-induced activation. These results suggest th,.7t combined interactions of the C-terminal 30 amino acid residues and certain domains extending from the arts.ino terminus to amino acid 209 of Gal 6 protein may be involved in its couplings to IL-8 receptor.tain domains extending from the arts.ino terminus to amino acid 209 of Gal 6 protein may be involved in its couplings to IL-8 receptor.

• Parasites, Hosts and Diseases
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• v.33 no.4
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• pp.357-364
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• 1995

The protozoan parasite, Entcmoeba histoIWticc, is one of major causative agents of intestinal disease all over the world. In acute experimental infection, the early host response to 5. histoIHtica is characterized by an infiltration of neutrophils. However, the chemotactic signal for this response is not well known. Based on the (jading that human epithelial cells produce the potent neutrophil chemoattractant and activator, interleukin-8 (IL-8), IL-8 gene expression was examined thoroughly in human colon epithelial cells exposed to 5. histolvtica trophozoites. Cellular RNAs were extracted from HT-29 or Caco-2 human colon epithelial cells exposed to 5. histoLvtica trophozoites for 30 minutes, 1 and 3 hours. IL-8 mRNA transcripts were measured by reverse transcriptional polprnerase chain reaction (RT-PCR) using synthetic standard RNA. The number of IL-8 mRNA molecules increased from 30 minutes to 3 hours of exposure period, reaching 3.1 H 107 molecules/ug of total RNA. Expression pattern of IL-8 mRNA transcripts was parallel to the amounts of IL-8 protein measured by enzyme-linked immunosorbent assay (ELISA) . Lysates of 5. histoIVtica also induced expression of mRNA for IL-8 in colon epithelial cells. These results sugf:esc that acute inflammatory reaction by 5. histoIVticc may be initially triggered by proinflammatory cytokines such as IL-8 secreted from epithelial cells of the colon.

• Journal of Microbiology and Biotechnology
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• v.17 no.7
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• pp.1120-1126
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• 2007

This study was performed to screen probiotic bifidobacteria for their ability to bind and neutralize lipopolysaccharides (LPS) from Escherichia coli and to verify the relationship between LPS-binding ability, cell surface hydrophobicity (CSH), and inhibition of LPS-induced interleukin-8 (IL-8) secretion by HT-29 cells of the various bifidobacterial strains. Ninety bifidobacteria isolates from human feces were assessed for their ability to bind fluorescein isothiocyanate (FITC)-labeled LPS from E. coli. Isolates showing 30-60% binding were designated LPS-high binding (LPS-H) and those with less than 15% binding were designated LPS-low binding (LPS-L). The CSH, autoaggregation (AA), and inhibition of LPS-induced IL-8 release from HT-29 cells of the LPS-H and LPS-L groups were evaluated. Five bifidobacteria strains showed high levels of LPS binding, CSH, AA, and inhibition of IL-8 release. However, statistically significant correlations between LPS binding, CSH, AA, and reduction of IL-8 release were not found. Although we could isolate bifidobacteria with high LPS-binding ability, CSH, AA, and inhibition of IL-8 release, each characteristic should be considered as strain dependent. Bifidobacteria with high LPS binding and inhibition of IL-8 release may be good agents for preventing inflammation by neutralizing Gram-negative endotoxins and improving intestinal health.

• The Journal of the Korean Society for Microbiology
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• v.34 no.6
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• pp.573-582
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• 1999

Cytokines are hormone-like proteins which mediate and regulate inflammatory and immune responses. The purpose of this study was to investigate the effect of lipopolysaccharide (LPS), Staphylococcus enterotoxin B (SEB), and Mycoplasma lysates on regulation of IL-6 and IL-8 production by human nasal fibroblasts. Primary cultured cells were incubated with LPS ($1.0\;{\mu}g/ml$) from E.coli, SEB ($1.0\;{\mu}g/ml$) from S.aureus, or Mycoplasma lysates (M.pneumoniae, Mp; M. fermentans, Mf; M. hominis, Mh, each $1.0\;{\mu}g/ml$). The culture supernatants were collected at 2, 6, and 24 hr and assessed for IL-6 and IL-8 production by enzyme-linked immunosorbent assay. The production of IL-6 in the culture supernatant was downregulated by LPS, SEB, or Mycoplasma lysates. But IL-6 was upregulated by mixed exposure with Mp+LPS (2 hr), Mp+LPS+SEB (24 hr), Mf+LPS (24 hr), Mf+LPS+SEB (2 hr), Mh+LPS (24 hr), Mh+SEB (24 hr), or Mh+LPS+SEB (24 hr). The production of IL-8 in the culture supernatant was similar to that of IL-6 by same stimulants. But IL-8 was upregulated by mixed exposure with Mf+LPS+SEB (2 hr), Mh+LPS (24 hr), Mh+ SEB (24 hr), or Mh+LPS+SEB (24 hr). These studies show that costimulation of LPS or SEB with Mycoplasma whole cell lysates upregulates the production of IL-6 and IL-8.

• IMMUNE NETWORK
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• v.6 no.1
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• pp.20-26
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• 2006

Background: Rheumatoid arthritis (RA) is a chronic and systemic inflammatory disease that is characterized by invasive synovial hyperplasia, leading to progressive joint destruction. Recent studies have described that RA is caused by virus, bacteria or outside material. Approximately 2 to 20% of RA cases arc reported to be associated with infected hepatitis C virus (HCV). However, the mechanisms underlying virus-induced RA are still unknown. Moreover, few molecular studies have addressed the inflammatory aspects of HCV-associated autoimmune RA. In this study, we aimed to determine whe ther or not another HCV core protein transactivates the IL-8 gene expression, prototypic chemokine, in synovial cell. Methods: To establish the HCV core expressing stable synovial cell line, pCI-neo-core, a plasmid encoding HCV core protein, were transfected to HIG-82 cell line that is an established cell line from rabbit periaricular soft tissue. We examined the morphological changes and cell cycle distribution of HIG-82 cells with expression of HCV core protein by inverted microscopy and flow cytometry analysis, respectively. Also, we determined the mRNA levels of Interleukin (IL)-6 and IL-8 related to the inflammation by RT-PCR and then analyzed regulation of IL-8 expression by the NF-${\kappa}B$ pathway. Results: Our study showed no significant differences in morphology and cell cycle between HIG-82 control cell line and HIG-82 expressing HCV core protein. However, expression of HCV core protein induces the IL-8 mRNA expression in HIG-82 core cells via activated NF-${\kappa}B$ pathway. Conclusion: These results suggest that HCV core protein can lead to enhanced IL-8 expression. Such a proinflammatory role may contribute to the etiologic pathogenesis in RA patients with HCV infection.

• 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.