Korean Journal of Immunology.1993;15(1):25-35.
Korean Journal of Immunology
2002 (v1, n1) to Present ISSN: 1671-8925
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Korean Journal of Immunology.1993;15(1):11-23.
The immunological characteristics of adhesin in escherichia coli.
Korean Journal of Immunology.1993;15(1):1-9.
Physiological Role of PGE2 and DBcAMP in Bone Cell Metabolism.
Korean Journal of Immunology.1999;21(1):77-84.
One of the primary functions for which bones have evolved is to act as a structural support. To achieve this, bones remodel throughout life so that their structure remains optimal for the prevailing mechanical environment. Bone remodeling consists of an initial phase of osteoclastic bone resorption followed by a bone formation period. Prostaglandins are potent regulators of bone formation and bone resorption that can have both stimulatory and inhibitory effects. Elevation of intracellular cAMP is an important intracellular signaling mechanism involved in the regulation of the expression of many proteins. In this study we examine whether PGE or DBcAMP affects osteoblastic activation or osteoclastic differentiation in mouse bone marrow cells and osteosarcoma ROS 17/2.8 cells. The effect of PGE and DBcAMP on the cell proliferation was measured by the incorporation of [3H]- thymidine into DNA. As a result, PGE2 (0.5-1 ug/ml) and DBcAMP (0.1-0.5 mM) inhibited the [3H]-thymidine incorporation into DNA in a dose dependent manner. The effect of PGE2 and DBcAMP on the induction of alkaline phosphatase (ALP) was investigated in ROS 17/2.8 cells cultured in medium containing 0.4% fetal bovine serum. PGE and DBcAMP stimulated ALP activity in the cells in a dose- dependent manner. PGE2 also increased the intracellular cAMP content in a dose- dependent fashion with a maximal effect at 0.5 ug/ml. ROS 17/2.8 cells release nitric oxide upon stimulation of PGE2 or DBcAMP with interferon-r. PGE2 and DBcAMP increase the phosphorylation level of CREB (cAMP response element binding protein) without any change on the amount of CREB protein. Also, PGE (10-6 M) and DBcAMP (10-4 M) significantly increase the generation of osteoclasts in mouse bone marrow cell culture system. In conclusion, the results of this study suggested that cAMP appears to be an important regulatory molecule in the processes of bone formation and resorption.
Alkaline Phosphatase ; Animals ; Bone Marrow Cells ; Bone Remodeling ; Bone Resorption ; Bucladesine* ; Cell Proliferation ; Cyclic AMP Response Element-Binding Protein ; Dinoprostone* ; DNA ; Metabolism* ; Mice ; Nitric Oxide ; Osteoblasts ; Osteoclasts ; Osteogenesis ; Osteosarcoma ; Phosphorylation ; Prostaglandins ; Prostaglandins E ; Response Elements ; Thymidine
Alkaline Phosphatase ; Animals ; Bone Marrow Cells ; Bone Remodeling ; Bone Resorption ; Bucladesine* ; Cell Proliferation ; Cyclic AMP Response Element-Binding Protein ; Dinoprostone* ; DNA ; Metabolism* ; Mice ; Nitric Oxide ; Osteoblasts ; Osteoclasts ; Osteogenesis ; Osteosarcoma ; Phosphorylation ; Prostaglandins ; Prostaglandins E ; Response Elements ; Thymidine
Korean Journal of Immunology.1999;21(1):71-76.
Carp which receive intraperitoneal injections of sodium alginate show a high survival rate after being challenged with Edwardsiella tarda. To elucidate the immunoenhancement by sodium alginate, its effects on the non-specific defense system of carp were investigated. Sodium alginate had little influence either on the activity of the alternative complement pathway or on the phagocytic and respiratory burst activities of head kidney phagocytes (HKP), yet it greatly enhanced the migration of HKP to the peritoneal cavity (the site of injection) and concurrently elevated their phagocytic activity. The number of phagocytes mobilized by sodium alginate was 2 to 50 times greater than that by the well-known peritoneal exudate cell-eliciting agents when injected at the same dose. Accordingly, it is highly probable that the early elimination of challenge bacteria by such mobilized and activated phagocytes was responsible for the high survival rate of the alginateinjected fish. In chemotaxis assays, it was revealed that sodium alginate stimulated sorne leukocyte subpopulation (s) within the peritoneal cavity to produce and/or secrete chemotactic factor (s), while concurrently enhancing the sensitivity of HKP to the factor (s).
Bacteria ; Carps* ; Chemotaxis ; Complement Pathway, Alternative ; Edwardsiella tarda ; Exudates and Transudates ; Head Kidney ; Injections, Intraperitoneal ; Leukocytes ; Peritoneal Cavity ; Phagocytes ; Respiratory Burst ; Sodium* ; Survival Rate
Bacteria ; Carps* ; Chemotaxis ; Complement Pathway, Alternative ; Edwardsiella tarda ; Exudates and Transudates ; Head Kidney ; Injections, Intraperitoneal ; Leukocytes ; Peritoneal Cavity ; Phagocytes ; Respiratory Burst ; Sodium* ; Survival Rate
Korean Journal of Immunology.1999;21(1):63-70.
Immunoadjuvant activities of the extract (KM-110) from Korean mistletoe ( Viscum album coloratum) on the induction of humoral and cellular responses against Keyhole limpet hemocyanim (KLH) as an antigen and allogenic tumor cells were examined. When mice were immunized subcataneously (s.c.) with KLH admixed with KM-110, more than 1000-times higher antibody titers to KLH than those immunized with KLH alone was observed. KM-110 induced high level of KLH- specific IgG1, IgG2a and IgG2b antibodies. In an in vitro analysis of lymphocytes proliferation to KLH on week 4, the splenocytes of mice treated with KLH and KM- 110 exhibited significantly higher proliferating activity than those treated with KLH alone. In addition, the culture supernatnats obtained from the splenocytes of mice treated with both KLH and KM-110 showed high level of IL-2 and IL-4. In the test of cellular immune responses, KM-110 enhanced the DTH reaction to KLH in mice. Furthemore, cytotoxic T-lymphocyte (CTL) activity using an allogenic CTL induction model where C57BL/6 (H-2b) mice were injected with allogenic P815 (H-2d) mastocytoma cells admixed with or without KM-110, mice treated with P815 cells and KM-110 showed higher cytatoxic activity against allogenic tumor cells than those treated without KM-110. This results suggest that KM-110 may possess adjuvant activities to potentially enhance humoral as well as cellular immune responses against antigens.
Animals ; Antibodies ; B-Lymphocytes ; Immunity, Cellular* ; Immunoglobulin G ; Interleukin-2 ; Interleukin-4 ; Lymphocytes ; Mastocytoma ; Mice ; Mistletoe* ; T-Lymphocytes ; T-Lymphocytes, Cytotoxic ; Viscum album* ; Viscum*
Animals ; Antibodies ; B-Lymphocytes ; Immunity, Cellular* ; Immunoglobulin G ; Interleukin-2 ; Interleukin-4 ; Lymphocytes ; Mastocytoma ; Mice ; Mistletoe* ; T-Lymphocytes ; T-Lymphocytes, Cytotoxic ; Viscum album* ; Viscum*
The Roles of SEK1 in Nitric Oxide (NO) Induced Apoptsis of RAW264.7 cells.
Korean Journal of Immunology.1999;21(1):55-61.
Nitric oxide (NO) induces apoptotic cell death in murine RAW 264.7 macrophages. To elucidate the roles of SEK1/MKK4, a upstream kinase for both c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) and p38 kinase, on NO-induced apoptosis, we generated clones of RAW 264.7 cells which stably overexpressd kinase inactive SEK1 (RAW/SEK1-Kl) or wild type SEK1 (RAW/SEK1-WT). Treatment of kinase inactive SEK1 transfected RAW 264.7 cells (RAW/SEK1-Kl) with sodium nitroprusside (SNP), a NO generating agent, significantly decreased the cell viability up to 20% of RAW control cells which were treated with the same amount of SNP. However, RAW/SEK1-WT cells were less susceptible to NO induced apoptosis. For a while, caspase-3 like activity in NO treated RAW/SEK1-Kl cells was significantly increased with parallell to apoptotic death rate. However, caspase1 like activity was not affected by NO in any transfectants. The NO induced apoptosis in RAW/SEK1-Kl cells was significantly prevented by the addition of caspase-3 like inhibitor (N-Ac- DEVD-CHO). In addition, the phosphotransferase activity of JNK1 in NO-treated RAW/SEK1-WT is significantly increased, but not in RAW/SEK1-Kl cells. These results suggest that SEK1 may play anti-apoptotic role in RAW cells from NO-induced apoptosis.
Apoptosis ; Caspase 3 ; Cell Death ; Cell Survival ; Clone Cells ; Macrophages ; Mortality ; Nitric Oxide* ; Nitroprusside ; Phosphotransferases ; Protein Kinases
Apoptosis ; Caspase 3 ; Cell Death ; Cell Survival ; Clone Cells ; Macrophages ; Mortality ; Nitric Oxide* ; Nitroprusside ; Phosphotransferases ; Protein Kinases
The Differentiation of HL-60 Cells Causes to Lose their Ability to Express TNF mRNA.
Korean Journal of Immunology.1999;21(1):47-53.
It is well known that HL-60 cell, a human promyelocytic line, is differentiated into eosinophil-like cells in the presence of butyric acid, and thus the differentiated HL-60 cells have been used as a model system to study irnmunological properties of peripheral eosinophils which are thought to be terminally differentiated. To study whether HL-60 cells alter their capability of expressing cytokines during differentiation to eosinophil-like cells, we examined TNF mRNA levels in HL-60 cells treated with butyric acid by Ribonuclease Protection Assay (RPA). HL-60 cells were incubated for 3 days in the presence of butyric acid (0.5 mM), and stimulated with PMA and lipopolysaccharide (LPS). The levels of TNF mRNA decreased by 50 % and 95 % upon one and two days of post-treatment of butyric acid, respectively. The decreased pattern in TNF mRNA levels was also observed in HL-60 cells that have been treated with retinoic acid known as an inducer for differentiation of them. In accordance with these results, prominent azurophilic granules typical in eosinophils appeared in the cytoplasm of the differentiated HL-60 cells. The decreased expression of TNF mRNA was not attributable to the presence of serum, since increasing concentrations of serum had no effect. Furthermore, interleukin-5 (IL-5), which is known to be involved in activation and trafficking of eosinophils in vivo and in vitro, failed to affect TNF mRNA production when it was used in place of butyric acid. These data suggest that the differentiated HL-60 cells may have immunological resemblance to eosinophils in that they weakly produce the cytokine mRNA.
Butyric Acid ; Cytokines ; Cytoplasm ; Eosinophils ; HL-60 Cells* ; Humans ; Interleukin-5 ; Ribonucleases ; RNA, Messenger* ; Tretinoin
Butyric Acid ; Cytokines ; Cytoplasm ; Eosinophils ; HL-60 Cells* ; Humans ; Interleukin-5 ; Ribonucleases ; RNA, Messenger* ; Tretinoin
Korean Journal of Immunology.1999;21(1):35-45.
Cortex mori (Morus alba L.: Sangbaikpi), the root bark of mulberry tree, has been used as an antiphlogistic, diuretic, and expectorant in herbal medicine. Previous studies have demonstrated that the phenolic extract of Cortex mori have hypotensive, hypoglycemic, antifungal, antiviral, antiinflammatory, and anticancer effects, and the hot water extract from Cortex mori has inhibitory effects on compound 48/80- induced mast cell degranulation and histamine release from rat peritoneal mast cells (RPMCs). This study was perforrned to investigate the effects of polysaccharide fraction from Cortex mori (PFCM) on compound 48/80-induced degranulation, histamine release, calcium influx, changes of intracellular cAMP and cGMP level, and morphological changes of RPMCs. The results were summarized as follows. 1) Compound 48/80-induced cytomorphological changes such as swelling, degranulation, intracellular vacuoles, and interrupted cell boundary were significantly inhibited by pretreatment with either hot water or polysaccaride fractions frorn Cortex mori (PFCM), 2) the compound 48/80-induced histamine release from RPMCs pretreated with PFCM was significantly inhibited, compared to that of control without PFCM pretreatment, 3) the PFCM inhibited remarkably the compound 48/80-induced calcium influx into the RPMCs, 4) the PFCM increased significantly the intracellular cAMP levels and decreased the intracellular cGMP levels of RPMCs, compared to those of normal control, and 5) the compound 48/80-induced cAMP levels of RPMCs pretreated with PFCM were significantly increased, compared to those of positive control without PFCM, and the compound 48/80-induced cGMP levels of RPMCs pretreated with PFCM were remarkably decreased, compared to those of positive control without PFCM. From the above results, it is suggested that PFCM have an activity to inhibit the compound 48/80-induced mast cell activation.
Animals ; Calcium ; Herbal Medicine ; Histamine Release ; Mast Cells* ; Morus ; Phenol ; Rats ; Trees ; Vacuoles ; Water
Animals ; Calcium ; Herbal Medicine ; Histamine Release ; Mast Cells* ; Morus ; Phenol ; Rats ; Trees ; Vacuoles ; Water
Korean Journal of Immunology.1999;21(1):25-34.
Programmed cell death (PCD), or apoptosis, plays an important role in embryonic development, metamorphsis, hormone-dependent atrophy and tumor growth, as a physiological event regulating the cell number or eliminating damaged cells. Currently hybridoma cell production, resulting from the fusion of myeloma cells with antibody producing spleen cells, is widely used in various fields of life science. This technique requires a hypoxanthine guanine phosphoribosyl transferase (HGPRT) deficient mutant myeloma cell line as a fusion partner. When these rnutant cells are treated with aminopterin plus hypoxanthine-thymidine (HAT) after the cell fusion they are selectively and efficiently eliminated so that one could get only fused hybridoma cells. But there hasn't been any report regarding this selective elimination mechanism of HGPRT mutant myeloma cell. By using HGPRT myeloma V653 as a model system this study demonstrated that PCD was induced by aminopterin treatment of this V653 cell. And this PCD was further characterized by cotreatement of cycloheximide, actinomycin-D, and calcium ionophore A23187 together with aminopterin. The apoptotic endonuclease involved in this PCD process was also detected and characterized. When V653 cells were incubated for the various periods of time in the presence of 0.4 uM aminopterin, the viability was continued to decrease until 48 hours of aminopterin treatment and there was no viable cell affer 36 hours of incubation. DNA fragmentation was detectable 3 hours of incubation and peaked between 12 and 18 hours of aminopterin treatment. The induction of cell death and DNA fragmentation of V653 cells by aminopterin were inhibited by protein synthesis inhibitor, cycloheximide, and RNA synthesis inhibitor, actinomycin-D and maximal inhibitory effects on cell death were seen at concentrations of 2 ug/ml and 0.5 uM, respectively. Ca2+ ionophore A23187 promoted aminopterin-induced cell death of V653. When the cells were coincubated with A23187 in the presence of aminopterin, cell viability was remarkably decreased at concentrations of more than 2 uM and DNA fragmentation was increased at concentrations of more than 0.2 uM. A23187 also induced cell death when the cells were treated with A23187 alone. When endogenous endonuclease activities of nuclei isolated from intact healthy cells and aminopterin-treated cells were compared for four different conditions, there were notable increases in the Ca2+/Mg2+ -independent and the Mg2+ -dependent endonuclease activity after incubation with aminopterin for 12 hours. In northern blot analysis, induction of c-myc gene was observed in aminopterin-treated V653 cell reached peak at 2 hours and thern decreased drastically.
Aminopterin* ; Animals ; Apoptosis* ; Atrophy ; Biological Science Disciplines ; Blotting, Northern ; Calcimycin ; Calcium ; Cell Count ; Cell Death ; Cell Fusion ; Cell Line ; Cell Survival ; Cycloheximide ; DNA Fragmentation ; Embryonic Development ; Female ; Genes, myc ; Guanine ; Hybridomas ; Hypoxanthine ; Hypoxanthine Phosphoribosyltransferase ; Mice* ; Pregnancy ; RNA ; Spleen ; Transferases
Aminopterin* ; Animals ; Apoptosis* ; Atrophy ; Biological Science Disciplines ; Blotting, Northern ; Calcimycin ; Calcium ; Cell Count ; Cell Death ; Cell Fusion ; Cell Line ; Cell Survival ; Cycloheximide ; DNA Fragmentation ; Embryonic Development ; Female ; Genes, myc ; Guanine ; Hybridomas ; Hypoxanthine ; Hypoxanthine Phosphoribosyltransferase ; Mice* ; Pregnancy ; RNA ; Spleen ; Transferases
Country
Republic of Korea
Publisher
Korean Association of Immunobiologists
ElectronicLinks
http://www.ksimm.or.kr/journal/main.html?mod=volEditor-in-chief
Abbreviation
Korean J Immunol
Vernacular Journal Title
대한면역학회지
ISSN
1015-6453
EISSN
Year Approved
2007
Current Indexing Status
Currently Indexed
Start Year
1979
Description
Current Title
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