• Parasites, Hosts and Diseases
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• v.51 no.1
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• pp.85-92
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• 2013

IL-23 and IL-12 are structurally similar and critical for the generation of efficient cellular immune responses. Toxoplasma gondii induces a strong cell-mediated immune response. However, little is known about IL-23 secretion profiles in T. gondii-infected immune cells in connection with IL-12. We compared the patterns of IL-23 and IL-12 production by THP-1 human monocytic cells in response to stimulation with live or heat-killed T. gondii tachyzoites, or with equivalent quantities of either T. gondii excretory/secretory proteins (ESP) or soluble tachyzoite antigen (STAg). IL-23 and IL-12 were significantly increased from 6 hr after stimulation with T. gondii antigens, and their secretions were increased with parasite dose-dependent manner. IL-23 concentrations were significantly higher than those of IL-12 at the same multiplicity of infection. IL-23 secretion induced by live parasites was significantly higher than that by heat-killed parasites, ESP, or STAg, whereas IL-12 secretion by live parasite was similar to those of ESP or STAg. However, the lowest levels of both cytokines were at stimulation with heat-killed parasites. These data indicate that IL-23 secretion patterns by stimulation with various kinds of T. gondii antigens at THP-1 monocytic cells are similar to those of IL-12, even though the levels of IL-23 induction were significantly higher than those of IL-12. The detailed kinetics induced by each T. gondii antigen were different from each other.

• The Journal of Internal Korean Medicine
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• v.27 no.1
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• pp.228-236
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• 2006

Objectives : Macrophage has an important innate defense role in the immune system. When we are infected with pathogens, macrophage ingests them through phagocytosis or endocytosis, and then secretes many cytokines, such as IL-1, IL-6 and $TGF{\alpha}$, which are regulators of immune responses. The aim of this study is to determine how Samjunghwan effects the expression of cytokine and other immune-related genes in macrophages. Methods : Cells were treated directly with Samjunghwan and/or LPS at regular intervals. Total RNA of cells was isolated using TRIzol reagent, and the changes in cytokine gene expressions were investigated using RT-PCR, western blot and ELISA. Results : $IL-1{\alpha},\;IL-1{\beta}$ and COX-2 genes were inducibly expressed specifically by Samjunghwan in macrophage. Especially, $IL-1{\beta}$ gene was induced most strongly by treatment with Samjunghwan. Over time, treatment with Samjunghwan showed that the expression levels of $IL-1{\alpha}\;and\;$IL-1{\beta}$ genes increased from 1 to 4h, and then decreased from 4 to ISh. However, the expression level of COX-2 gene increased continuously up to 11h. $IL-1{\alpha},\;IL-1{\beta}$ and COX-2 genes were expressed synergistically by a simultaneous treatment of both Samjunghwan and LPS in macrophages. Secretion levels of translated $IL-1{\beta}$ increased continuously up to 11h. Conclusions : Though this study is only a start in the investigation of the efficasy of Samjunghwan, these results suggest that Samjunghwan has positive effects on immune responses.

• Journal of Life Science
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• v.19 no.3
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• pp.411-416
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• 2009

Chitosan is derived from chitin by a process of controlled deacetylation. In the present study, we investigated the effects of chitosan on the production of cytokines such as interleukin-2 (IL-2), interferon-$\gamma$ (IFN-$\gamma$), interleukin-4 (IL-4), and interleukin-10 (IL-10) in mice. The culture supernatants of splenocytes exposed with chitosan alone or chitosan plus cell stimulants, lipopolysaccharide (LPS), concanavalin A (Con A), and phytohemagglutinin-P (PHA-P) were harvested to assay IL-2, IFN-$\gamma$, IL-4, and IL-10 production. IL-2, IFN-$\gamma$, and IL-4 from splenocytes exposed to chitosan showed a greater increase compared to the PBS control group. IL-2 and IFN-$\gamma$ levels in the culture supernatants from splenocytes exposed to LPS+chitosan were higher than those of the groups exposed to LPS alone. IL-4 and IL-10 levels in the culture supernatants from splenocytes exposed to LPS+chitosan were lower than those of the groups exposed to LPS only. These findings demonstrate that chitosan upregulates the immune responses by Th1 cytokines (IL-2 and IFN-$\gamma$) and downregulates those by Th2 cytokines (IL-4 and IL-10) in LPS-associated immunity. These results show the potential of its usefulness for balancing the Th1/Th2 immune response, if more research results were accumulated.

• IMMUNE NETWORK
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• v.5 no.1
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• pp.16-22
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• 2005

Background: IL-18 was originally cloned as a IFN-${\gamma}$ inducing factor in primed T cells. In synergy with IL-12, IL-18 has been shown to induce strikingly high levels of IFN-${\gamma}$ production by T cells and to enhance Th1 development. Also this cytokine exerts induction of Th2 development through IL-4 induction. Methods: Resting $CD4^+$ T cells were sorted by negative selection and activated by anti-CD3 plus anti-CD28 Ab. Expression of IL-12 binding sites, IL-18 binding sites, IL-18R ${\alpha}$, and GATA-3 mRNA were analysed by FACS and RT-PCR, respectively. Results: Resting $CD4^+$ T cells expressed IL-18R ${\alpha}$ chain but not IL-18 binding sites, suggesting a lack of IL-18R ${\beta}$ expression. IL-18R ${\alpha}$ was maintained on the Th1 and Th2 committed cells. IL-18 binding sites were induced on the Th1 but not Th2 cells. Exposure of these cells to IL-18 led to up-regulation of GATA-3 mRNA expression only in Th2 committed cells. To elucidate the relationship between IL-18R ${\alpha}$ expression and GATA-3 induction by IL-18, Th1 and Th2 committed cells were further cultured in medium with or without IL-12 for 2 days. IL-12 binding sites were maintained on the Th1 and Th2 cells regardless of IL-12 treatment, but IL-18R a expression was rapidly down-regulated on the IL12-untreated Th2 cells which did not induce GATA-3 mRNA expression followed by IL-18 stimulation. Conclusion: IL-12 supports expression of IL-18R ${\alpha}$ and GATA-3 mRNA expression was induced by IL-18 through IL-18R ${\alpha}$ without expression of IL-18 binding site in Th2 cells.

• Animal cells and systems
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• v.13 no.4
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• pp.391-397
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• 2009

The house dust mite (Dermatophagoides pteronissinus) is an important factor in triggering allergic diseases. The function of eosinophils, particularly in the production of cytokine or chemokine, is critical in understanding the pathogenesis of inflammatory diseases. In this study, we examined whether D. pteronissinus extract (DpE) induces the expression of monocyte chemotactic protein 1 (MCP-1)/CCL2, IL-8/CXCL8, and IL-6 that mediate in the infiltration and activation of immune cells and in its signaling mechanism in the human eosinophilic cell line, EoL-1. DpE increased the mRNA and protein expression of MCP-1, IL-8, and IL-6 in a time- and dose-dependent course in EoL-1 cells. In our experiments using signal-specific inhibitors, we found that the increased expression of MCP-1, IL-8, and IL-6 due to DpE is associated with Src family tyrosine kinase and protein kinase C $\delta$ (PKC $\delta$). In addition, the activation of extracellular signal-regulated kinase (ERK) is required for MCP-1 and IL-8 expression while p38 mitogen-activated protein kinase (MAPK) is involved in IL-6 expression. DpE induced the phosphorylation of ERK and p38 MAPK. PP2, an inhibitor of Src family tyrosine kinase, and rottlerin, an inhibitor of PKC $\delta$, blocked the activation of ERK and p38 MAPK. DpE induces the activation of ERK and p38 MAPK via Src family tyrosine kinase and PKC $\delta$ for MCP-1, IL-8, or IL-6 production. Increased cytokine release due to the house dust mite and the characterization of its signal transduction may be valuable in understanding the eosinophil-related pathogenic mechanism of inflammatory diseases.

• Journal of Microbiology and Biotechnology
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• v.31 no.6
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• pp.794-802
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• 2021

In this study we investigated the role and mechanism of cardamonin on IL-1β induced injury in OA. CHON-001 cells were treated with cardamonin and IL-1β and transfected with silencing nuclear factor erythroid 2-related factor 2 (siNrf2). Cell viability was detected by Cell Counting Kit-8 assay and flow cytometer assay was utilized for cell apoptosis assessment. IL-6, IL-8, TNF-α and Nrf2 mRNA expression was tested by qRT-PCR. Western blot was employed to evaluate MMP-3, MMP-13, Collagen II, Nrf2, NQO-1, NLRP3, Caspase 1 and apoptosis-associated speck-like protein containing a caspase-1 recruitment domain (ASC) protein levels. In CHON-001 cells, IL-1β suppressed cell viability and Collagen II level while promoting cell apoptosis and expression of pro-inflammatory cytokines (IL-6, IL-8, TNF-α), MMPs (MMP-3, MMP-13), NQO-1, and NLRP3 inflammasome (NLRP3, Caspase 1 and ASC), with no significant influence on Nrf2. Cardamonin reversed the effect of IL-1β on cell viability, cell apoptosis, pro-inflammatory cytokines, MMPs, Collagen II, and NLRP3 inflammasome levels. In addition, cardamonin advanced Nrf2 and NQO-1 expression of CHON-001 cells. SiNrf2 reversed the function of cardamonin on IL-1β-induced cell apoptosis and expression of pro-inflammatory cytokines, Nrf2, NQO-1, and NLRP3 inflammasome in chondrocytes. Taken together Cardamonin inhibited IL-1β induced injury by inhibition of NLRP3 inflammasome via activating Nrf2/NQO1 signaling pathway in chondrocyte.

• Restorative Dentistry and Endodontics
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• v.24 no.1
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• pp.49-54
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• 1999

Ko, Lim found some differences in the concentrations of bone resorptive cytokines, especially IL-$1{\alpha}$ and IL-$1{\beta}$ in periapical lesions and inflamed pulps. And they suppose that these differences may be due to the type of cells which produce each cytokine. The purpose of this study was to analyze the human odontogenic cysts & cystic fluid for their contents of IL-$1{\alpha}$, IL-$1{\beta}$ and TNF-$1{\alpha}$ and to compare the concentrations of each cytokine according to the cytokine producing cells. The cystic tissues used in this experiment, were obtained from periapical surgery or cyst enucleation surgery. Cystic fluid was obtained from root canal during routine endodontic therapy(n=5). Cystic tissues were subdivided into two groups, inflammatory radicular cyst group(n=15) and developmental odontogenic keratocyst group(n=3). Normal periapical tissues of extracted third molar(n=5) were also obtained to be used as control group. Each specimen was incubated in 0.5ml homogenizing buffer (0.1mol/L potassium chloride, 0.02mol/L TRIS;pH=7.6) for two hours and then homogenized with glass homogenizer. Each specimen was centrifuged in a microcentrifuge for 3 minutes, and supernatants were extracted. The concentrations of cytokines were measured with R&D ELISA kit. The data were analyzed by Mann-Whitney U test for the differences among the diseases and t test for the correlations among each cytokine. Following results were obtained ; 1. For IL-$1{\alpha}$ and IL-$1{\beta}$, all experimental groups showed significantly higher concentrations of each cytokine than the control group (p<0.05). 2. In radicular cysts, the concentrations of IL-$1{\alpha}$ were higher than IL-$1{\beta}$, but not stastically significant (p>0.05). In odontogenic keratocysts, the concentrations of IL-$1{\alpha}$ were significantly higher than IL-$1{\beta}$ (p<0.05). In cystic fluid, the concentration of IL-$1{\beta}$ was significantly higher than IL-$1{\alpha}$ (p<0.05). 3. Between odontogenic keratocysts and radicular cysts, the concentrations of IL-$1{\alpha}$ were significantly higher in odontogenic keratocysts than in radicular cysts (p<0.05). 4. For TNF-${\alpha}$, only cystic fluid group showed significantly higher concentrations than the control group (p<0.05).

• Journal of Life Science
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• v.26 no.9
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• pp.1082-1087
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• 2016

The intestinal tight junction (TJ) plays an important role as a paracellular barrier. Impaired TJ permeability and enhanced proinflammatory cytokine production are crucial pathophysiological mechanisms in inflammatory bowel diseases (IBDs). Although proinflammatory cytokines, tumor necrosis factor-alpha and interluekin-1 beta, which are markedly increased in IBD patients, have been reported to increase intestinal TJ permeability, the role of interleukin-1 alpha (IL-1α) in the TJ has not been studied. Phytochemicals could prevent proinflammatory cytokine-caused TJ alteration. Curcumin (CCM), a biologically active component of turmeric, has a strong anti-inflammatory activity. The purpose of this study was to elucidate the effect of IL-1α on intestinal epithelial TJ permeability and the role of CCM in IL-1α′s action on TJ in an in vitro intestinal epithelial system, Caco-2 monolayers. The TJ integrity of Caco-2 monolayers was estimated by measuring the flux of FITC-labeled dextran and transepithelial electrical resistance (TEER). Apical IL-1α (100 ng/ml) treatment elevated TJ permeability and suppressed TEER of Caco-2 monolayers. Pretreatment with CCM (20 μM) for 30 min significantly inhibited IL-1α-induced TJ alterations, such as increased TJ permeability and decreased in TEER values. These results demonstrated that IL-1α-induced increases in Caco-2 TJ permeability and CCM blocked the action of IL-1α in the TJ.

• Korean Journal of Medicinal Crop Science
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• v.15 no.1
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• pp.38-45
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• 2007

Korean mistletoe (Viscum album L) extract has been found to posses immunoregulating activity. In this study, Korean mistletoe extract, M11C (non-lectin components), was used to know whether this extract activates splenocytes to secret interleukin $1\beta(IL-1\beta)$. The splenocytes were treated with M11C, and then collected the supernatant and cell lysate that were prepared to analyze the level of $IL-1\beta$, using ELISA, immunoblotting, and RT-PCR. Maximum effective dose and time of M11C on $IL-1\beta$ secretion from splenocytes were $200{\mu}g/m\ell$ and 8 hours, respectively. Treatment dose and time for the maximum expression of $IL-1\beta$ mRNA were $200{\mu}g/m\ell$ and 4 hours, respectively. Saccharide degradation enzyme Viscozyme L completely blocked the effect of M11C on $IL-1\beta$ secretion from splenocytes. As the result, among non-lectin components saccharide could be regarded as a main component for $IL-1\beta$ expression from splenocytes.

• Korean Journal of Psychosomatic Medicine
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• v.10 no.2
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• pp.130-141
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• 2002

Objectives : Stress induces alteration of gastrointestinal function in which interleukin (IL) and hypothalamo-pituitary-axis are involved. Depression again is associated with functional gastrointestinal disorders (FGID) and interleukins. The author attempted to look into the role of interleukins in the FGID also the association of depression and stress in this context. Methods : Entered were 20 patients with FGID, diagnosed by Rome IT criteria and 20 healthy controls. Depression was measured by Hamilton Rating Scale for Depression (HAM-D), and stress of the last one year by Schedule of Recent Experience (SRE). Serum levels of IL-$1\beta$, IL-2, IL-6 were measured by Enzyme-linked Immunosorbent Assay and serum cortisol by Fluorescence Polarization Immunoassay. The results were as follows : Results: 1) Serum levels of IL-$1\beta$, IL-2 were significantly lower in the patients with FGID than those in the controls, but level of IL-6 did not differ between two groups. 2) The patient group showed significantly higher level of serum cortisol as well as higher degrees of depression and stress. 3) Positive correlation was noted between depression and serum cortisol, and between depression and IL-2. A trend of negative correlation was seen between depression IL-$1\beta$. Positive correlation was noted between SRE and IL-6 and IL-6 and serum cortisol. Conclusions : It was concluded that FGID might be related to depression and stress. Changes of the interleukins might be involved with elevated cortisol level.