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Bae, Suyoung,Choi, Jida,Hong, Jaewoo,Lee, Siyoung,Her, Erk,Choi, Wonhyuk,Kim, Sangmin,Choi, Youngbum,Kim, Soohyun Mary Ann Liebert 2010 Hybridoma Vol.29 No.1
<P>Proteinase 3 (PR3), a neutrophil granule serine protease, is the major autoantigen for autoantibodies in the systemic vasculitic disease, Wegener's granulomatosis. It is also found to be involved in various inflammatory diseases including Crohn's disease, rheumatoid arthritis, cystic fibrosis, and gingivitis. However, there is no high quality antibody available to detect endogenous PR3 in biological samples such as plasma and tissue. Several commercial anti-PR3 monoclonal antibodies (MAbs) were obtained by using HMC-1/PR3 cell granule extracts as the antigen, but the resulting antibodies could not be applied for immunoblotting or other immunological methods. Therefore, we produced human recombinant PR3 in Escherichia coli and developed several MAbs that are highly sensitive and can be used for immunoblotting, FACS analysis, and immunofluorescent staining. The PR3 MAbs recognized both rhPR3 and human plasma-derived neutrophil PR3 in reducing and non-reducing conditions at low nanogram levels. In addition, new MAbs detect endogenous PR3 from normal human plasma and urine with high specificity. The new anti-PR3 MAbs will be an essential tool for investigating the role of PR3 in inflammatory and autoimmune diseases.</P>
BIRB 796 has Distinctive Anti-inflammatory Effects on Different Cell Types
Ryoo, Soyoon,Choi, Jida,Kim, Jaemyung,Bae, Suyoung,Hong, Jaewoo,Jo, Seunghyun,Kim, Soohyun,Lee, Youngmin The Korean Association of Immunobiologists 2013 Immune Network Vol.13 No.6
The pro-inflammatory cytokines tumor necrosis factor-${\alpha}$ (TNF${\alpha}$) and interleukin (IL)-$1{\beta}$ are crucial mediators involved in chronic inflammatory diseases. Inflammatory signal pathways regulate inflammatory cytokine expression-mediated by p38 mitogen activated protein kinase (p38MAPK). Therefore, considerable attention has been given to p38MAPK as a target molecule for the development of a novel anti-inflammatory therapeutics. BIRB 796, one of p38MAPK inhibitor, is a candidate of therapeutic drug for chronic inflammatory diseases. In this study, we investigated the effect of BIRB 796 on inflammatory cytokine productions by lipopolysaccharide (LPS) in different immune cell types. BIRB 796 reduced LPS-mediated IL-8 production in THP-1 cells but not in Raw 264.7 cells. Further analysis of signal molecules by western blot revealed that BIRB 796 sufficiently suppressed LPS-mediated phosphorylation of p38MAPK in both cell types whereas it failed to block inhibitor of kappa B (I-${\kappa}B$) degradation in Raw 264.7 cells. Taken together, these results suggest that the anti-inflammatory function of BIRB 796 depends on cell types.
Neutrophil Proteinase 3 Induces Diabetes in a Mouse Model of Glucose Tolerance
Bae, Suyoung,Choi, Jida,Hong, Jaewoo,Jhun, Hyunjhung,Hong, Kwangwon,Kang, Taebong,Song, Keeho,Jeong, Sangmin,Yum, Hokee,Kim, Soohyun Informa Healthcare 2012 Endocrine research Vol.37 No.1
<P>Type 1 diabetes is considered to be an autoimmune disease in which T cells attack pancreatic islet cells. Impaired glucose tolerance with type 2 diabetes has been classified as an obesity-associated metabolic syndrome. However, recent studies have revealed that type 2 diabetes is an autoinflammatory disease due to an imbalance of inflammatory cytokine production and related molecular components that cause inflammation. Insulin-like growth factor (IGF) and the insulin-like growth factor-binding protein-3 (IGFBP3) system are known to be involved in the development of experimental diabetic nephropathy, and urinary IGFBP3 protease activity has been observed in patients with type 2 diabetes. A serine protease was found to be responsible for the proteolytic activity in diabetic urine; however, the identity of the precise enzyme remains unknown. We investigated neutrophil proteinase 3 (PR3) to see whether it has specific enzymatic activity associated with insulin-like growth factor-1 and IGFBP3. In our study, both molecules were sufficiently degraded, which leads us to believe that PR3 may induce insulin resistance in the mouse model utilized. In addition, we found that PR3 in the urine of diabetic patients similarly affects insulin resistance. Moreover, PR3-immunized mice had an increase in glucose clearance due to inhibition of PR3 activity. As such, PR3 can be considered as an inflammatory enzyme directly linking inflammation to type 2 diabetes through downregulation of insulin-like growth factor-1/IGFBP3.</P>
BIRB 796 has Distinctive Anti-inflammatory Effects on Different Cell Types
Soyoon Ryoo,Jida Choi,Jaemyung Kim,Suyoung Bae,홍재우,Seunghyun Jo,김수현,이영민 대한면역학회 2013 Immune Network Vol.13 No.6
The pro-inflammatory cytokines tumor necrosis factor-α (TNFα) and interleukin (IL)-1β are crucial mediators involved in chronic inflammatory diseases. Inflammatory signal pathways regulate inflammatory cytokine expression-mediated by p38 mitogen activated protein kinase (p38MAPK). Therefore, considerable attention has been given to p38MAPK as a target molecule for the development of a novel anti-inflammatory therapeutics. BIRB 796, one of p38MAPK inhibitor, is a candidate of therapeutic drug for chronic inflammatory diseases. In this study, we investigated the effect of BIRB 796 on inflammatory cytokine productions by lipopolysaccharide (LPS) in different immune cell types. BIRB 796 reduced LPS-mediated IL-8 production in THP-1 cells but not in Raw 264.7 cells. Further analysis of signal molecules by western blot revealed that BIRB 796 sufficiently suppressed LPS-mediated phosphorylation of p38MAPK in both cell types whereas it failed to block inhibitor of kappa B (I-κB) degradation in Raw 264.7 cells. Taken together, these results suggest that the anti-inflammatory function of BIRB 796 depends on cell types.
Generation of Monoclonal Antibodies Against Recombinant AtSIZ1
Kim, Kangchang,Bae, Suyoung,Hong, Jaewoo,Choi, Jida,Ryoo, Soyoon,Jhun, Hyunjhung,Lee, Siyoung,Her, Erk,Hong, Kwangwon,Kim, Soohyun Mary Ann Liebert 2010 Hybridoma Vol.29 No.4
<P>Post-translational modifications of target proteins by small ubiquitin-like modifier (SUMO) proteins modulate many cellular processes in yeast and animals. Here we present the development of monoclonal antibodies (MAb) and polyclonal antibodies (PAb) against Arabidopsis SIZ1 (AtSIZ1) protein with high specificity. Mice were immunized with recombinant AtSIZ1 protein for generating monoclonal antibodies via the classic hybridoma production technique. Anti-AtSIZ1 MAb and PAb were able to detect endogenous AtSIZ1 in Arabidopsis wild type and its complementary line formed by transforming C-siz1-2 mutant with construct containing the AtSIZ1 gene under the control of the native promoter, but not the siz1-2 deletion mutant. These results show that these anti-AtSIZ MAbs are highly sensitive to detect endogenous AtSIZ1 and can be used for immunoblotting and other experimental methods. The new anti-AtSIZ1 MAbs will be essential tools used to investigate the role of AtSIZ1 in plant developmental biology.</P>
Lim, Jeong H.,Lee, Jongmin,Choi, Jida,Hong, Jaewoo,Jhun, Hyunjhung,Han, Jinsoo,Kim, Soohyun Mary Ann Liebert 2009 Photomedicine and laser surgery Vol.27 No.5
<P>OBJECTIVE: The aim of this study was to investigate the effects of light-emitting diode (LED) irradiation (radiant power, 0.047 mW; irradiation area, 1.13 cm(2)) at 610 nm and 710 nm on T-lymphocyte subset populations and cytokine expression using an in vivo rat model. BACKGROUND DATA: The proliferation of CD4+ T lymphocytes was induced by polychromatic visible polarized light at the range of 540-780 nm in a previous study, but the specific target wavelength for this effect has not yet been identified. METHODS: Before and after 4 weeks of LED phototherapy, whole blood samples were collected from 610 nm, 710 nm, and control groups. The percentages of CD4+ and CD8+ T lymphocyte populations were determined by flow cytometry. The transcript levels of representative cytokines of CD4+ T-cell (interleukin [IL]-4, interferon [IFN]gamma) and proinflammatory cytokines (IL-1beta, IL-6) were assessed with the reverse transcriptase-polymerase chain reaction. RESULTS: The population of CD4+ T cells increased significantly in 710 nm group on day 28 (p < 0.05), but it did not increase in the 610 nm or control group. The population of CD8+ T cells did not show any significant change after irradiation in all groups. The mRNA expression of IL-4 increased in both the 610 nm and 710 nm groups compared to the control group, but IFNgamma was not detected in any group. The transcripts of IL-1beta and IL-6 were slightly induced in the 710 nm group. CONCLUSION: The in vivo irradiation of 710 nm wavelength LED significantly increases the population of murine CD4+ T cells, which suggests that this new phototherapeutic regimen might be promising for CD4+ T lymphocyte-mediated immune modulation therapy.</P>