• Clinical and Experimental Pediatrics
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• v.48 no.6
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• pp.634-639
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• 2005

Purpose : An understanding of the immunological process is required if primary prevention of atopic diseases is to be developed in early childhood. But, it is too hard to distinguish atopy from nonatopy under the age of two clinically, because the expression of phenotype and cytokines is vague in early childhood. We evaluated DNA methylation changes at Th2 interleukin-4 gene in peripheral blood from atopic children. Methods : We selected 15 allergic children(mild : eight, moderate to severe : seven) and seven normal controls by using family allergy scores and clinical histories. We measured Total IgE and Der f II specific IgE levels and cultured peripheral blood mononuclear cells with Der f II stimulation and extracted DNA from Der f II specific T cells. We examined the change of CpG methylation in DNA from atopic and nonatopic children. Results : In T cells from normal children, IL-4 DNA were predominantly methylated; otherwise, CpG demethylation occurred in Der f II specific T cells from allergic children. Conclusion : IL-4 DNA methylation changes occurred in T genes from allergic children and DNA methylation assay in early childhood.

• Journal of Microbiology and Biotechnology
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• v.24 no.8
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• pp.1133-1142
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• 2014

Interleukin-32 (IL-32) is a cytokine and inducer of various proinflammatory cytokines such as $TNF{\alpha}$, IL-$1{\beta}$, and IL-6 as well as chemokines. There are five splicing variants (${\alpha}$, ${\beta}$, ${\gamma}$, ${\delta}$, and ${\varepsilon}$) and IL-$32{\gamma}$ is the most active isoform. We generated human IL-$32{\gamma}$ transgenic (IL-$32{\gamma}$ TG) mice to express high level of IL-$32{\gamma}$ in various tissues, including immune cells. The pathology of sepsis is based on the systemic inflammatory response that is characterized by upregulating inflammatory cytokines in whole body, particularly in response to gram-negative bacteria. We investigated the role of IL-$32{\gamma}$ in a mouse model of experimental sepsis by using lipopolysaccharides (LPS). We found that IL-$32{\gamma}TG$ mice resisted LPS-induced lethal endotoxemia. IL-$32{\gamma}$ reduced systemic cytokines release after LPS administration but not the local immune response. IL-$32{\gamma}TG$ increased neutrophil influx into the initial foci of the primary injected site, and prolonged local cytokines and chemokines production. These results suggest that neutrophil recruitment in IL-$32{\gamma}TG$ occurred as a result of the local induction of chemokines but not the systemic inflammatory cytokine circulation. Together, our results suggest that IL-$32{\gamma}$ enhances an innate immune response against local infection but inhibits the spread of immune responses, leading to systemic immune disorder.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.2
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• pp.485-489
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• 2016

Objective: to investigate the effect and side effects of recombinant human interleukin - 11 (rhIL - 11, in Chinese Juheli, produced by Qi Lu Biotechnology CO., LTD) in the second prevention of chemotherapy induced thrombocytopenia (CIT). Methods: Cancer patients with CIT were recruited and were treated with rhIL - 11 (treatment phase, TP), and in the following cycle, all these patients administered with rhIL - 11 24 hours immediately after chemotherapy (preventive treatment phase, PTP). Duration and severity of thrombocytopenia between two phases were compared. Results: for patients in TP or PTP, nadir values of platelet were ($29.28{\pm}20.08){\times}10^9/L$ and ($45.24{\pm}19.66){\times}10^9/L$, duration of thrombocytopenia in TP and PTP was ($11.52{\pm}4.33$) and ($8.20{\pm}+2.77$)days, recovery time was ($19.40{\pm}3.89$)and ($13.44{\pm}3.02$)days, duration of rhIL - 11 administration was ($10.68{\pm}2.46$)and ($6.28{\pm}1.77$)days, number of patients needing platelet infusion was 16and4 respectively, all differences were statistically significant (p value were 0.007, 0.002, 0.000, 0.000, 0.034 respectively). For TP and PTP, number of patients with hemorrhage was 8 and 4, duration of bleeding was ($5.00{\pm}0.82$) and ($4.50{\pm}0.71$) days respectively, with no statistically significant difference. Adverse reactions mainly included fever, edema, arrhythmia, joint pain, fatigue, skin rash, headache, dizziness, etc., all were not statistically significant between TP and PTP. Conclusion: rhIL - 11 could be well tolerated and is effective that could reduce the duration, severity of CIT, platelet transfusion, and incidence of bleeding, as well as shorten the recovery time, duration of rhIL - 11 administration. Thus, rhIL - 11 could be commended in the second prevention of CIT for patients with cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.1
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• pp.265-271
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• 2014

Interleukin-7 (IL-7) is a potent anti-apoptotic cytokine that enhances immune effector cell functions and is essential for lymphocyte survival. While it known to induce differentiation and proliferation in some haematological malignancies, including certain types of leukaemias and lymphomas, little is known about its role in solid tumours, including breast cancer. In the current study, we investigated whether IL-7 could enhance the in vivo antitumor activity of tumor-reactive $CD8^+$ T cells with induction of IFN-${\gamma}$ in a murine breast cancer model. Human IL-7 cDNA was constructed into the eukaryotic expression plasmid pcDNA3.1, and then the recombinational pcDNA3.1-IL-7 was intratumorally injected in the TM40D BALB/C mouse graft model. Serum and intracellular IFN-${\gamma}$ levels were measured by ELISA and flow cytometry, respectively. $CD8^+$ T cell-mediated cytotoxicity was analyzed using the MTT method. Our results showed that IL-7 administration significantly inhibited tumor growth from day 15 after direct intratumoral injection of pcDNA3.1-IL-7. The anti-tumor effect correlated with a marked increase in the level of IFN-${\gamma}$ and breast cancer cells-specific CTL cytotoxicity. In vitro cytotoxicity assays showed that IL-7-treatment could augment cytolytic activity of $CD8^+$ T cells from tumor bearing mice, while anti-IFN-${\gamma}$ blocked the function of $CD8^+$ T cells, suggesting that IFN-${\gamma}$ mediated the cytolytic activity of $CD8^+$ T cells. Furthermore, in vivo neutralization of $CD8^+$ T lymphocytes by CD8 antibodies reversed the antitumor benefit of IL-7. Thus, we demonstrated that IL-7 exerts anti-tumor activity mainly through activating $CD8^+$ T cells and stimulating them to secrete IFN-${\gamma}$ in a murine breast tumor model. Based on these results, our study points to a potential novel way to treat breast cancer and may have important implications for clinical immunotherapy.

• Korean Journal of Psychosomatic Medicine
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• v.7 no.2
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• pp.196-202
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• 1999

The purpose of the study was to determine the effect of vitamin B complex on stress-induced immune alteration. 21 medical students participated in the study 4 weeks before an academic examination period(baseline), 2 weeks before the exam period and during the exam period. Among them, 10 subjects were given vitamin B complex for 4 weeks, and 11 were not given vitamin B during the whole period. Cell-mediated immune function was measured by lymphocyte proliferative response to phytohemagglutinin(PHA) and interleukin-2(IL-2) production. Global assessment of recent stress(GARS) scale and symptom checklist-90-revised(SCL-90-R) were used to measure the level of subjective stress and psychopathology. Vitamin group had significantly lower scores of anxiety scale on SCL-90-R than non-vitamin group. No significant differences were found in lymphocyte proliferative response to PHA and IL-2 production between vitamin and non-vitamin groups during each period. There were no significant differences in change of of each of the two immune parameters over time as well as between vitamin and non-vitamin groups. However, lymphocyte proliferative response to PHA was significantly increased over time. In conclusion, it was suggested that vitamin B complex is likely to decrease anxiety level, and that exam stress might enhance lymphocyte proliferation regardless of vitamin B.

• Journal of Applied Biological Chemistry
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• v.57 no.1
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• pp.1-5
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• 2014

The roots of Opuntia humifusa (OHR) were extracted with 80% aqueous MeOH and the concentrated extract was partitioned with EtOAc, n-butanol and $H_2O$, successively. The fractions were tested using DPPH and ABST radical scavenging method. The all fractions showed potent scavenging effects. The scavenging effect of the EtOAc fraction was higher than the other fractions, with $IC_{50}$ values as DPPH; $77.0{\pm}1.38{\mu}g/mL$, ABTS: $26.3{\pm}2.02{\mu}g/mL$. And, we investigated anti-inflammatory activities by examining the effects of the OHR fractions on pro-inflammatory cytokine release in the human mast cells (HMC-1). Treatment with OHR fractions clearly reduced the release of the proinflammatory cytokines tumor necrosis factor-alpha (TNF-${\alpha}$), interleukin (IL)-$1{\beta}$, interleukin (IL)-6 and interleukin (IL)-8) in PMACI-stimulated HMC-1 cells. The results showed the potential of OHR as an excellent antioxidant substance and inhibiting inflammatory mediators. Therefore, OHR may be used as a therapeutic approach to various inflammatory diseases.

• THE JOURNAL OF KOREAN ORIENTAL ONCOLOGY
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• v.4 no.1
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• pp.159-175
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• 1998

In order to investigate the antitumor effect by Chungsangbohahwan after B-16 cells were transplanted in C57BL/6 mice, and the immune responses in mice induced by methotrexate, the extract of Chungsangbohahwan was orally administered to the mice for 21 days. Experimental studies were performed for measurance of metastasis, cell cytotoxicity in vitro, natural killer cell activity, productivity of interleukin-2. The results were summarized as follows: 1. Inhibition of metastasis in Chungsangbohahwan-treated group was higher than control group with significance on 7th day and 14th day. 2. On the MTT assay, cell viability was significantly inhibited by $5{\mu}g/well$, $2.5{\mu}g/well$, $1.25{\mu}g/well$, and $0.625{\mu}g/well$ of Chungsangbohahwan concentration inhibited cell viability significantly(P<0.05). $IC_{50}$ for cell viability was $2.17{\mu}g/well$. 3. Natural killer cell activity in Chungsangbohahwan-treated group was significantly increased on 100:1, 50:1 E/T(effect cell/target cell) ratio(P<0.05). 4. Production of interleukin-2 in Chungsangbohahwan-treated group was significantly increased(P<0.05).

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.4
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• pp.205-209
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• 2008

Recently, Sun et al (2008) reported that the IL6R polymorphism is associated with schizophrenia. Therefore, to detect the association between polymorphisms of interleukin 31 receptor A (IL31RA) and schizophrenia, we genotyped 9 SNPs [rs9292101 (intron 1), rs1009639 (exon 2, Pr043Pro), rs2161582 (intron 2), rs68761890 (intron 5), rs16884629 (intron 6), rs11956465 (intron 12), rs12153724 (intron 12), and rs16884641 (intron 14)] using the Golden Gate assay on Illumina BeadStation 500 GX. Two hundred eighteen patients with schizophrenia and 379 normal subjects were recruited. Patients with schizophrenia were diagnosed according to DSM-IV, and control subjects without history of psychiatric disorders were selected. We used SNPStats, Haploview, HapAnalyzer, SNPAnalyzer, and Helixtree programs for the evaluation of genetic data. Of nine polymorphisms, three SNPs (rs9292101, rs1009639, and rs11956465) were associated with schizophrenia. The rs9292101 and rs11956465 showed significant associations with the risk of schizophrenia in the codominant [rs9292101, odds ratio (OR)=0.74, 95% confidence interval (CI)=0.58${\sim}$0.95, p=0.017] and recessive (rs11956465, OR=0.64, 95% CI=0.42${\sim}$0.96, p=0.034) models, respectively. The rs1009639 also was statistically related to schizophrenia in both codominant (OR=0.76, 95% CI=0.60${\sim}$0.97, p=0.025) and dominant (OR=0.66, 95% CI=0.44${\sim}$0.98, p=0.035) models. Two linkage disequilibrium (LD) blocks were made. In the analysis of haplotypes, a haplotype (GCT) in block 1 and a haplotype (CCACAG) in block 2 showed significant associations between schizophrenia and control groups (haplotype GCT, frequency=0.509, chi square=4.199, p=0.040; haplotype CCACAG, frequency=0.289, chi square=5.691, p=0.017). The results suggest that IL31RA may be associated with risk of schizophrenia in Korean population.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.38 no.4
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• pp.311-319
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• 2012

Seborrheic dermatitis (SD) is the skin disease occurred because of Malassezia yeast which grows on the skin and scalp, and this yeast lives on sebum lipid, and their metabolite, free lipid acids are thought to be the main irritant on skin. To find out effective cosmeceutical ingredients to treat SD symptoms, we established novel cell-based in vitro model mimicking SD symptoms. This in vitro model adopted the co-culture system with primary sebocyte & HaCaT keratinocyte. We used M. globosa yeast extract, arachidonic acid, linoleic acid and dihydrotestosterone as SD inducers. In the co-culture system with optimized concentrations for SD-inducing cocktail, the production of IL-8 and sebum lipids increased up to 2-fold, and then we screened with commercial essential oils by monitoring IL-8 as a key inflammatory biomarker. Then we found that Cinnamomum zeylanicum oil, Mentha arvensis oil effectively down-regulated IL-$1{\alpha}$, IL-6, IL-8 cytokines which over-produced by SD-inducing cocktail. Additionally, two essential oils also showed inhibitory effect on sebum lipid synthesis from primary sebocyte and growth inhibitory effect to M. globosa yeast (MICs were lower than 0.0625 %). Our recent results suggest that Cinnamomum zeylanicum oil and Mentha arvensis oil could be effective natural herbal remedies to relieve or protect scalp seborrheic dermatitis.

• Journal of Sasang Constitutional Medicine
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• v.12 no.1
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• pp.186-200
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• 2000

The purpose of this research was to investigate the effects of Indongdeungjikolpitang water extract(IJTE) on the complication of diabetes. IJTE did not affect the level of blood glucose in alloxan- or streptozotocin-induced hyperglycemic mice, but inhibited the motility of gastrointestine. IJTE inhibited the writhing syndrome induced by acetic acid, the permeability of evans blue into peritoneal cavity induced by acetic acid, the paw edema induced by histamine, and the formation of cotton pellet granuloma. IJTE increased the cell viability of thymocytes and splenocytes. IJTE decreased the release of ${\gamma}-interferone$(${\gamma}-IFN$) and interleukin-2(IL-2), but did not affect the release of interleukin-4(IL-4) from murine thymocytes. IJTE increased the release of IL-4 and decreased the release of tumor necrosis $factor-{\alpha}$($TNF-{\alpha}$) and $interleukin-1{\beta}$($IL-1{\beta}$), but did not affect of ${\gamma}-IFN$ and IL-2 from murine splenocytes. IJTE decreased the release of $TNF-{\alpha}$ and $IL-1{\beta}$ from murine peritoneal macrophages. IJTE decreased the production of niric oxide(NO) from murine peritioneal macrophages and increased the phagocytic activity of murine peritoneal macrophages. These results suggest that IJTE has an anti-inflammatory action via the inhibition of $TNF-{\alpha}$, $IL-1{\beta}$ and NO production from immune cells.