• BMB Reports
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• v.29 no.2
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• pp.175-179
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• 1996

Viral surface proteins are known to play an essential role in attachment of the virus particle to the host cell membrane. In case of the hepatitis B virus (HBV) several reports have described potential receptors on the target cell side, but no definite receptor protein has been isolated yet. As for the viral side, it has been suggested that the preS region of the envelope protein, especially the preS1 region, is involved in binding of HBV to the host cell. In this study, preS1 region was recombinantly expressed in the form of a maltose binding protein (MBP) fusion protein and used to identify and visualize the expression of putative HBV receptor(s) on the host cell. Using laser scanned confocal microscopy and by FACS analysis, MBP-preS1 proteins were shown to bind to the human hepatoma cell line HepG2 in a receptor-ligand specific manner. The binding kinetic of MBP-preS1 to its cellular receptor was shown to be temperature and time dependent. In cells permeabilized with Triton X-100 and treated with the fusion protein, a specific staining of the nuclear membrane could be observed. To determine the precise location of the receptor binding site within the preS1 region, several short overlapping peptides from this region were synthesized and used in a competition assay. In this way the receptor binding epitope in preS1 was revealed to be amino acid residues 27 to 51, which is in agreement with previous reports. These results confirm the significance of the preS1 region in virus attachment in general, and suggest an internalization pathway mediated by direct attachment of the viral particle to the target cell membrane.

• Parasites, Hosts and Diseases
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• v.52 no.4
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• pp.355-365
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• 2014

The enteric protozoan parasite Entamoeba histolytica is the causative agent of human amebiasis. During infection, adherence of E. histolytica through Gal/GalNAc lectin on the surface of the amoeba can induce caspase-3-dependent or -independent host cell death. Phosphorylinositol 3-kinase (PI3K) and protein kinase C (PKC) in E. histolytica play an important function in the adhesion, killing, or phagocytosis of target cells. In this study, we examined the role of amoebic PI3K and PKC in amoeba-induced apoptotic cell death in Jurkat T cells. When Jurkat T cells were incubated with E. histolytica trophozoites, phosphatidylserine (PS) externalization and DNA fragmentation in Jurkat cells were markedly increased compared to those of cells incubated with medium alone. However, when amoebae were pretreated with a PI3K inhibitor, wortmannin before being incubated with E. histolytica, E. histolytica-induced PS externalization and DNA fragmentation in Jurkat cells were significantly reduced compared to results for amoebae pretreated with DMSO. In addition, pretreatment of amoebae with a PKC inhibitor, staurosporine strongly inhibited Jurkat T cell death. However, E. histolytica-induced cleavage of caspase-3, -6, and -7 were not inhibited by pretreatment of amoebae with wortmannin or staurosporin. In addition, we found that amoebic PI3K and PKC have an important role on amoeba adhesion to host compartment. These results suggest that amebic PI3K and PKC activation may play an important role in caspase-independent cell death in Entamoeba-induced apoptosis.

• The Sea:JOURNAL OF THE KOREAN SOCIETY OF OCEANOGRAPHY
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• v.7 no.4
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• pp.2221-2221
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• 2002

The first laboratory culture of host-parasite system of Prorocentrum minimum- Amoebophrya sp. was established by single cell isolation method. Here, we report the life cycle stages of the parasitic dinoflagellate. Amoebophrya sp. of the red tide dinoflagellate P. minimum as observed by light and epifluorescence microscopy. Infections developed inside the nucleus of P. minimum. The trophont developed to occupy almost all the intracellular space of the host at its late stage. The fully developed trophont finally ruptured through the host cell. “Vermiform stage”, the free-swimming extracellular lift cycle stage is followed by another stage for the sudden release of many individual dinospores. Our laboratory strain of the host-parasite system for P. minimum, a causative species fur the huge red tides in spring and summer in Korean coastal waters, could be a useful living material for the in situ biological control of harmful algal blooms.

• The Sea:JOURNAL OF THE KOREAN SOCIETY OF OCEANOGRAPHY
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• v.7 no.4
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• pp.221-225
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• 2002

The first laboratory culture of host-parasite system of Prorocentrum minimum- Amoebophrya sp. was established by single cell isolation method. Here, we report the life cycle stages of the parasitic dinoflagellate. Amoebophrya sp. of the red tide dinoflagellate P. minimum as observed by light and epifluorescence microscopy. Infections developed inside the nucleus of P. minimum. The trophont developed to occupy almost all the intracellular space of the host at its late stage. The fully developed trophont finally ruptured through the host cell. “Vermiform stage”, the free-swimming extracellular lift cycle stage is followed by another stage for the sudden release of many individual dinospores. Our laboratory strain of the host-parasite system for P. minimum, a causative species fur the huge red tides in spring and summer in Korean coastal waters, could be a useful living material for the in situ biological control of harmful algal blooms.

• ALGAE
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• v.19 no.3
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• pp.201-205
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• 2004

An ectoparasitic din flagellate infesting plank tonic chaetognath, Sagitta crassa Tokioka was found, for the first time, from Korean coasts. In order to identify the species, we investigated detailed morphology of the din flagellate using Nomarski interference optics as well as epifluorescent microscopes. The parasitic din flagellate consists of an oval to rod-shaped cell with a peduncle, by which the organism attaches to the host. The cell is covered with polygonal thecal plates. The nucleus displays two different shapes according to cell cycle stages: in young trophont the nucleus is elongated and shows typical din flagellate nucleus (dinokaryon), while in matured trophont, the nucleus is dome-shaped and non-dinokaryotic. The peduncle is variable in length and is ornamented with the longitudinal striations. All these characteristics point to identity that the ectoparasitic din flagellate infecting Sagitta crassa in Korean coasts is Oodinium inlandicum Horiguchi et Ohtsuka, originally described from the Seto Inland Sea of Japan. Relationship between prevalence and host sizes differed from those in Japan.

• IMMUNE NETWORK
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• v.7 no.4
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• pp.167-172
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• 2007

Various cell types that express regulatory function may influence the pathogenesis of most and perhaps all infections. Some regulatory cells are present at the time of infection whereas others are induced or activated in response to infection. The actual mechanisms by which different types of infections signal regulatory cell responses remain poorly understood. However a most likely mechanism is the creation of a microenvironment that permits the conversion of conventional T cells into cells with the same antigen specificity that have regulatory function. Some possible means by which this can occur are discussed. The relationship between regulatory cells and infections is complex especially with chronic situations. The outcome can either be of benefit to the host or damage the disease control process or in rare instances appears to be a component of a finely balanced relationship between the host and the infecting agent. Manipulating the regulatory cell responses to achieve a favorable outcome of infection remains an unfulfilled objective of therapeutic immunology.

• Asian-Australasian Journal of Animal Sciences
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• v.21 no.6
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• pp.801-806
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• 2008

A classical technique to study somitic cell fate is to employ the cross-transplantation of quail somites into a chick host. The densely stained nucleoli of the quail cells makes it possible to assess the fate of the donor quail cells in the chick host. Classical somite transplantation techniques have been hampered by the necessity of a small opening in the chick eggshell, difficulty in hatching the offspring and interspecies post-hatch graft rejection. With the advent of transgenic chicken technology, it is now possible to use embryos from transgenic chickens expressing reporter genes in somite cross-transplantation techniques to remove any possibility of interspecies graft rejection. This report describes using a surrogate eggshell system in conjunction with transgenic chick:chick somitic cell cross-transplantation to generate viable chimeric embryos and offspring. Greater than 40% of manipulated embryos survive past 10 days of incubation, and ~80% of embryos successfully cultured past 10 days of incubation hatched to produce viable offspring.

• Research in Plant Disease
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• v.11 no.2
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• pp.98-105
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• 2005

All viruses have few genes relative to their hosts. Viruses, thus, utilize many host factors for efficient viral replication in host cell. Virus-host interactions are crucial determinations of host range, replication, and pathology. Host factors participate in most steps of positive-strand RNA virus infection, including entry, viral gene expression, virion assembly, and release. Recent data show that host factors play important roles in assembling the viral RNA replication complex, selecting and recruiting viral RNA replication templates, activating the viral complex for RNA synthesis, and the other steps. These virus-host interactions may contribute to the host specificity and/or pathology. Positive-strand RNA viruses encompass over two-thirds of all virus genera and include numerous pathogens. This review focuses on the importance of host factors involved in positive strand plant RNA virus genome replication.

• Journal of Periodontal and Implant Science
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• v.30 no.3
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• pp.675-687
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• 2000

Multiple periodontal pathogens sequentially colonize the subgingival niche during the conversion from gingivitis to destructive periodontal disease. An animal model of sequential immunization with key periodontal pathogens has been developed to determine whether T and B lymppocyte effector functions are skewed and fail to protect the host from pathogenic challenge. The present study was performed to evaluate immunomodulatory effect of exposure to Fusobacterium nucleatum(F. nucleatum) prior to Porphyromonas gingivalis(P. gingi - valis). Group 1(control) mice were immunized with phosphate-buffered saline, Group 2 were immunized with F. nucleatum prior to P. gingivalis, while Group 3 were immunized P. gingivalis alone. All the T cell clones derived from Group 2 demonstrated type 2 helper T cell clone(Th2 subsets), while those from Group 3 mice demonstrated Th1 subsets. Exposure of mice to F . nucleatum prior to P. gingivalis interfered with opsonophagocytosis function of sera against P. gingivalis. In adoptive T cell transfer experiments, in vivo protective capacity type 2 helper T cell clones(Th2) from Group 2 was significantly lower than type 1 helper T cell clones(Th1) from Group 3 against the lethal dose infection of P. gingivalis. Western blot analysis indicated the different pattern of recognition of P .gingivalis fimbrial proteins between sera from Group 2 and Group 3. In conclusion, these study suggest that colonization of the subgingival niche by F .nucleatum prior to the periodontal pathogen, P. gingivalis, modulates the host immune responses to P. gingivalis at humoral, cellular and molecular levels.

• IMMUNE NETWORK
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• v.15 no.3
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• pp.125-134
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• 2015

Acute graft-versus-host-disease (GVHD) is characterized by selective damage to the liver, the skin, and the gastrointestinal tract. Following allogeneic hematopoietic stem cell transplantation, donor bone marrow (BM) cells repopulate the immune system of the recipient. We previously demonstrated that the acute intestinal GVHD (iGVHD) mortality rate was higher in MyD88-deficient BM recipients than that in the control BM recipients. In the present study, the role of MyD88 (expressed by donor BM) in the pathophysiology of hepatic GVHD (hGVHD) was examined. Unlike iGVHD, transplantation with MyD88-deficient T-cell depleted (TCD) BM attenuated hGVHD severity and was associated with low infiltration of T cells into the liver of the recipients. Moreover, GVHD hosts, transplanted with MyD88-deficient TCD BM, exhibited markedly reduced expansion of $CD11b^+Gr-1^+$ myeloidderived suppressor cells (MDSC) in the liver. Adoptive injection of the MDSC from wild type mice, but not MyD88-deficient mice, enhanced hepatic T cell infiltration in the MyD88-deficient TCD BM recipients. Pre-treatment of BM donors with LPS increased MDSC levels in the liver of allogeneic wild type BM recipients. In conclusion, hGVHD and iGVHD may occur through various mechanisms based on the presence of MyD88 in the non-T cell compartment of the allograft.