• 제목/요약/키워드: Interleukin 6

검색결과 1,851건 처리시간 0.036초

Intracellular Signaling Pathways for Type II IgE Receptor (CD23) Induction by Interleukin - 4 and Anti - CD40 Antibody

  • Kim, Hyun-Il;Park, Hee-Jeoung;Lee, Choong-Eun
    • BMB Reports
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    • 제30권6호
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    • pp.431-437
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    • 1997
  • Since the role of CD40 on the interleukin-4(IL-4) -induced B cell activation has been strongly implicated in the agumentation of IgE production and response, we have investigated the intracelluar signaling pathways utilized by IL-4 and CD40 for type II IgE receptor (CD23) expression. IL-4 and anti-CD40 antibody treatment of human B cells, independently caused a rapid induction of CD23 gene activation within 2 h. There was a noticeable synergism between the action of the two agents inducing CD23 expression: the addition of anti-CD40 to the IL-4-treated culture significantly agumented the IL-4-induced CD23 on both mRNA and surface protein levels, and the inclusion of IL-4 in the anti-CD40-treated cells caused a further increase of CD23 expression far above the maximal level induced by anti-CD40. Protein tyrosine kinase (PTK) inhibitors effectively suppressed the both IL-4- and anti -CD40-induced CD23 expression. whereas protein kinase C (PKC) inhibitors had no effects. Electrophoretic mobility shift assays (EMSA) have shown that IL-4 and anti-CD40 induce the activation of NF-IL-4 and $NF-_{K}B$, respectively, binding to the CD23 promoter, both in a PKC-independent and PTK-dependent manner. These data suggest that the synergistic activation of CD23 gene expression by IL-4 and anti-CD40 is mediated by co-operative action of distinct nuclear factors. each of which is rapidly activated via PKC-independent and PTK-dependent process.

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Henoch-$Sch\ddot{o}nlein$ Purpura에서 Interleukin $1{\beta}$ 유전자 다형성과 신장 침범과의 연관성 (The Relationship Between Interleukin $1{\beta}$ Gene Polymorphism and Renal Involvement in Henoch-$Sch\ddot{o}nlein$ Purpura)

  • 나형준;고일용;윤준호;예병일;김황민
    • Childhood Kidney Diseases
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    • 제10권2호
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    • pp.125-131
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    • 2006
  • Purpose : High interleukin-1 beta(IL-$1{\beta}$) expression in the skin biopsy specimens of patients with Henoch-$Sch\ddot{o}nlein$ Purpura(HSP) has been observed. We examined IL-$1{\beta}$ gene polymorphism in patients with HSP. The purpose of this study is to examine the relationship between IL-$1{\beta}$ gene polymorphism and renal involvement in HSP. Methods : Patients from mideast Korea with HSP were studied. All patients had at least 6 months of follow up. Patients and ethnically matched controls were genotyped for IL-$1{\beta}$ gene polymorphism by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP). Results : Thirty-four patients(all younger than 15 years old) who had been diagnosed with HSP and 27 controls were examined. No allele or genotype differences between the HSP and control groups were observed. No significant association between the carriage of IL-$1{\beta}$(-511) T allele and renal involvement(P=0.525, OR:1.417, CI:0.545-3.686) was found. Conclusion : In unselected patients with HSP, carriage of IL-$1{\beta}$(-511) T allele does not appear to influence renal involvement.

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Expression of Human Interleukin-ll and Granulocyte-Macrophage Colony-Stimulating Factor in Transgenic Plants

  • LEE BO-YE;LEE JEONG-HYUN;YOON HOON-SEOK;KANG KYUNG HO;KIM KYUNG-NAM;KIM JAE-HONG;KIM JU-KON;KIM JEONG-KOOK
    • Journal of Microbiology and Biotechnology
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    • 제15권6호
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    • pp.1304-1309
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    • 2005
  • The production of therapeutic proteins for human diseases in plants results in many economic benefits, including reduced risk of animal virus contamination, high yields, and reduced production and storage costs. Human cytokines, interleukin-11 (hlL-11) and granulocyte-macrophage colony-stimulating factor (hGM-CSF), cDNAs were introduced into rice or tobacco, using either the maize ubiquitin promoter or the 35S promoter. The primary hIL-11 transgenic rice plants exhibited stunted growth and a sterile phenotype, whereas the hIL-11 transgenic tobacco plants did not. This suggests that hIL-11 expression in rice disrupts the normal growth and development of the plant. The regeneration efficiency of rice calli transformed with hGM-CSF was found to be approximately a quarter of that seen with the hIL-11, suggesting that hGM-CSF expression is more deleterious to the regeneration of rice calli than is hIL-11. However, the surviving hGM-CSF transgenic rice plants exhibited a normal phenotype of growth. Therefore, it appears that only those transgenic rice lines that expressed the human cytokines in small quantities were able to survive the selection process.

Effect of Defibrotide on Rat Reflux Esophagitis

  • Kim, Hyoung-Ki;Choi, Soo-Ran;Choi, Sang-Jin;Chio, Myung-Sup;Shin, Yong-Kyoo
    • The Korean Journal of Physiology and Pharmacology
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    • 제8권6호
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    • pp.319-327
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    • 2004
  • This study was aimed at evaluating the effect of defibrotide on the development of the surgically induced reflux esophagitis, on gastric secretion, lipid peroxidation, polymorphonuclear leukocytes (PMNs) accumulation, polymorphonuclear leukocytes adherence, superoxide anion and hydrogen peroxide production in PMNs, scavenge of hydroxyl radical and hydrogen peroxide, cytokine (interleukin-1 ${\beta}$, tumor necrosis $factor-{\alpha}$) production in blood, and intracelluar calcium mobilization in PMNs. Defibrotide did not inhibit the gastric secretion and not change the gastric pH. Treatment of esophagitis rats with defibrotide inhibited lipid peroxidation, and myeloperoxidase (MPO) in the esophagus in comparison with untreated rats. Defibrotide significantly decreased the PMN adherence to superior mesenteric artery endothelium in a dose-dependent manner, Superoxide anion and hydrogen peroxide production in $1{\mu}M$ formylmethionylleucylphenylalanine (fMLP)- or $0.1{\mu}g/ml$ N-phorbol 12-myristate 13-acetate (PMA)-activated PMNs was inhibited by defibrotide in a dose-dependent fashion. Defibrotide effectively scavenged the hydrogen peroxide but did not scavenge the hydroxyl radical. Treatment of esophagitis rats with defibrotide inhibited interleukin-1 ${\beta}$ production in the blood in comparison with untreated rats, but tumor necrosis $factor-{\alpha}$ production was not affected by defibrotide. The fMLP-induced elevation of intracellular calcium in PMNs was inhibited by defibrotide. The results of this study suggest that defibrotide may have partly beneficial protective effects against reflux esophagitis by the inhibition lipid peroxidation, PMNs accumulation, PMNs adherence to endothelium, reactive oxygen species production in PMNs, inflammatory cytokine production(i.e. interleukin-1 ${\beta}$), and intracellular calcium mobilization in PMNs in rats.

Adenosine derived from Staphylococcus aureus-engulfed macrophages functions as a potent stimulant for the induction of inflammatory cytokines in mast cells

  • Ma, Ying Jie;Kim, Chan-Hee;Ryu, Kyoung-Hwa;Kim, Min-Su;So, Young-In;Lee, Kong-Joo;Garred, Peter;Lee, Bok-Luel
    • BMB Reports
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    • 제44권5호
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    • pp.335-340
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    • 2011
  • In this study, we attempted to isolate novel mast cell-stimulating molecules from Staphylococcus aureus. Water-soluble extract of S. aureus cell lysate strongly induced human interleukin-8 in human mast cell line-1 and mouse interleukin-6 in mouse bone marrow-derived mast cells. The active molecule was purified to homogeneity through a $C_{18}$ reverse phase HPLC column. By determination of its structure by MALDITOF and $^1H$- and $^{13}C$-NMR, adenosine was revealed to be responsible for the observed cytokine induction activities. Further studies using 8-sulfophenyl theophylline, a selective adenosine receptor blocker, verified that purified adenosine can induce interleukin-8 production via adenosine receptors on mast cells. Moreover, adenosine was purified from S. aureus-engulfed RAW264.7 cells, a murine macrophage cell line, used to induce phagocytosis of S. aureus. These results show a novel view of the source of exogenous adenosine in vivo and provide a mechanistic link between inflammatory disease and bacterial infection.

Interleukin-8 and Matrix Metalloprotease 9 as Salivary Biomarkers of Pain in Patients with Temporomandibular Disorder Myalgia: A Pilot Study

  • Park, Yang Mi;Ahn, Yong-Woo;Jeong, Sung-Hee;Ju, Hye-Min;Jeon, Hye-Mi;Kim, Kyung-Hee;Ok, Soo-Min
    • Journal of Oral Medicine and Pain
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    • 제44권4호
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    • pp.160-168
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    • 2019
  • Purpose: To search the salivary factors that objectively indicate an pain in myalgia patients with temporomandibular joint disorder (TMD) and determine the possibility of the factors as pain-biomarkers. Methods: Participants consisted of pain-free 15 persons (male 7, female 8, mean age±standard deviation (SD); 26.8±16.04 years) and 45 myalgia patients with TMD (male 21, female 24, mean age±SD; 27.98±13.01 years). They were divided into a pain-free group (numerical rating scale [NRS] score 0), a mild pain group (NRS 1-4), a moderate pain group (NRS 5-6), and a severe pain group (NRS 7-10) and members of all groups were age, sex matched. Interleukin-8 (IL-8) and matrix metalloprotease 9 (MMP-9) were selected as pain biomarkers, by searching the Gene Expression Omnibus database and analyzing pain-related genes. Enzyme-linked immunosorbent assays were used to measure the concentration of IL-8 and MMP-9 in the patients' saliva. Results: IL-8 and MMP-9 levels were statistically significantly higher in pain groups than in the pain-free group. Greater differences were observed in patients with acute pain (with painful duration under 3 months) than in the control group and in female patients than in male. Conclusions: Salivary IL-8 and MMP-9 may play a role as biomarkers of myalgia in patients with TMD.

Synergistic Effect of Interleukin-18 on the Expression of Lipopolysaccharide-Induced IP-10 (CXCL-10) mRNA in Mouse Peritoneal Macrophages

  • Kim, Hyo-Young;Kim, Jae-Ryong;Kim, Hee-Sun
    • Journal of Microbiology and Biotechnology
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    • 제16권10호
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    • pp.1605-1612
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    • 2006
  • Interleukin (IL)-18, a member of the family of IL-l cytokine, is one of the principal inducers of $interferon-{\gamma}(IFN-{\gamma})$ in T lymphocytes and natural killer cells. The objective of the present study was to evaluate the effect of IL-18 on the expression of chemokine IP-10 (CXCL-10) mRNA in mouse peritoneal macrophages. IL-18 had very weak direct effect or synergistic effect with IL-12 on the expression of IP-10 mRNA in C57BL/6 mouse peritoneal macrophages. However, IL-18 pretreatment was found to playa cooperative role in the expression of lipopolysaccharide (LPS)-induced IP-10 mRNA. For the expression of LPS-induced IP-10 mRNA, the synergistic effect was detected after 16 h of IL-18 pretreatment prior to LPS stimulation. The expression level of CD14 in cells stimulated with LPS was not changed by IL-18 pretreatment, and the level of $IFN-{\gamma}$ production during IL-18 pretreatment plus LPS stimulation was barely discernible ($0.36{\pm}0.31pg/ml$). Namely, the synergistic effect of IL-18 pretreatment was not related to a change of LPS receptor, CD14 expression, and the production of $IFN-{\gamma}$ by the interaction between IL-18 and LPS. The synergistic effect of IL-18 pretreatment on the expression of LPS-induced IP-10 was related to not NF-kB but AP-1 activation, and associated with the extracellular signal-regulated kinase (ERK) pathway, one of the mitogen-activated protein kinase signaling pathways. These results provide useful information that may elucidate the mechanisms underlying the effect of IL-18 on the expression of IP-10 mRNA.

Comparison of Interleukin-8 Levels in Long-Distance Runners and Healthy Sedentary Non-Athletic Control Subjects

  • Shin, Young-Oh;Bae, Jun-Sang;Min, Ji-Won;Lee, Jeong-Beom;Kim, Jung-Kyu;Song, Young-Ju;Yang, Hun-Mo;Min, Young-Ki
    • The Korean Journal of Physiology and Pharmacology
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    • 제11권6호
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    • pp.263-267
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    • 2007
  • We have previously demonstrated that the level of leukocytes and neutrophils significantly increased immediately and 30 min after exercise. Interleukin-8 (IL-8) is an inflammatory cytokine that acts as a chemokine on neutrophils. In the present study, we evaluated the correlation between the number of neutrophils and leukocytes, and between the number of neutrophils and plasma IL-8 level. Long-distance trained runners (TRs, n = 10) and untrained sedentary control subjects (SEDs, n = 10) ran for one hour at 70% of heart rate reserve. In the TR, the number of neutrophils correlated significantly with the number of leukocytes in the blood. However, there was no correlation between the number of neutrophils and the plasma IL-8 concentration in both groups. Expressions of IL-8 protein and mRNA were markedly higher in the TRs as compared to the SEDs at three time intervals (pre-exercise, immediately after exercise, and post exercise). In conclusion, our results show that 1) the neutrophil level was dependent on the level of leukocytes 2) there was no correlation between the neutrophils count and plasma IL-8 concentration and 3) a higher plasma IL-8 level in athletes may be a unique characteristic of intensive training.

Association of a genetic polymorphism of IL1RN with risk of acute pancreatitis in a Korean ethnic group

  • Park, Jin Woo;Choi, Ja Sung;Han, Ki Joon;Lee, Sang Heun;Kim, Eui Joo;Cho, Jae Hee
    • The Korean journal of internal medicine
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    • 제33권6호
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    • pp.1103-1110
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    • 2018
  • Background/Aims: Several epidemiological studies have validated the association of interleukin gene polymorphisms with acute pancreatitis (AP) in different populations. However, there have been few studies in Asian ethnic groups. We aimed to investigate the relationships between inflammatory cytokine polymorphisms and AP as pilot research in a Korean ethnic group. Methods: Patients who had been diagnosed with AP were prospectively enrolled. DNA was extracted from whole blood, and DNA sequencing was subsequently performed. Single-nucleotide polymorphisms (SNPs) of the interleukin $1{\beta}$ (IL1B), interleukin 1 receptor antagonist (IL1RN), and tumor necrosis factor ${\alpha}$ (TNFA) genes of patients with AP were compared to those of normal controls. Results: Between January 2011 and January 2013, a total of 65 subjects were enrolled (40 patients with AP vs. 25 healthy controls). One intronic SNP (IL1RN -1129T>C, rs4251961) was significantly associated with the risk of AP (odds ratio, 0.304; 95% confidence interval, 0.095 to 0.967; p = 0.043). However, in our study, AP was not found to be associated with polymorphisms in the promoter regions of inflammatory cytokine genes, including IL1B (-118C>T, c47+242C>T, +3954C/T, and -598T>C) and TNFA (-1211T>C, -1043C>A, -1037C>T, -488G>A, and -418G>A). Conclusions: IL1RN -1129T>C (rs4251961) genotypes might be associated with a significant increase of AP risk in a Korean ethnic group.

Synthesis of Thienopyrimidine Derivatives as Inhibitors of STAT3 Activation Induced by IL-6

  • Jang, Hyun-Jae;Kim, Sung Min;Rho, Mun-Chual;Lee, Seung Woong;Song, Yang-Heon
    • Journal of Microbiology and Biotechnology
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    • 제29권6호
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    • pp.856-862
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    • 2019
  • A series of thienopyrimidine compounds (6Aa-g and 6Ba-d) were synthesized and characterized by NMR spectroscopy and mass spectrometry. These compounds (6Aa-g and 6Ba-d) potently inhibited STAT3 expression induced by IL-6 in a dose-dependent manner with $IC_{50}$ values of $5.73-0.32{\mu}M$. Among the prepared thienopyrimidine derivatives, 6Aa, 6Ab, 6Ba and 6Bc significantly suppressed the phosphorylation of STAT3 and ERK1/2 stimulated by IL-6 in Hep3B cells. Furthermore, the synthesized compounds might be useful remedies for the treatment of inflammatory diseases by inhibiting the action of IL-6.