• Title/Summary/Keyword: host cell

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Change of Infection Properties of Subcultured Marine Birnavirus in Several Fish Cell Lines (어류 주화세포에서의 계대배양에 의한 해양버나바이러스의 감염특성의 변화)

  • Jung, Sung-Ju
    • Journal of fish pathology
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    • v.11 no.2
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    • pp.89-96
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    • 1998
  • Marine birnavirus (MABV) has wide host range in marine organisms. To clarify various infection properties of MABV in different host species, in vitro study was performed by subculture for 10 passages in several fish cell lines. In CHSE-214, RTG-2 and RSBK-2 cells, the virus produced high yield of virus. Typical CPE with high protein expression was observed in these cells. On the contrary, the virus grown in EPC, FHM and BF-2 cells exhibited no CPE appearance although virus protein was detected. In EPC and FHM cells, the virus titer increased in later passages. The plaque size was distinctly bigger in CHSE-214, RTG-2 and RSBK-2 cells than in other cell lines. The nucleotide sequence of VP2/NS junction region on genome segment A exhibited one specific nucleotide change at 195. The different infection properties in several cell types performed in the present work might reflect in vivo MABV infection in various host species occurring in natural conditions.

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Host-Microbe Interactions Regulate Intestinal Stem Cells and Tissue Turnover in Drosophila

  • Ji-Hoon Lee
    • International Journal of Stem Cells
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    • v.17 no.1
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    • pp.51-58
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    • 2024
  • With the activity of intestinal stem cells and continuous turnover, the gut epithelium is one of the most dynamic tissues in animals. Due to its simple yet conserved tissue structure and enteric cell composition as well as advanced genetic and histologic techniques, Drosophila serves as a valuable model system for investigating the regulation of intestinal stem cells. The Drosophila gut epithelium is in constant contact with indigenous microbiota and encounters externally introduced "non-self" substances, including foodborne pathogens. Therefore, in addition to its role in digestion and nutrient absorption, another essential function of the gut epithelium is to control the expansion of microbes while maintaining its structural integrity, necessitating a tissue turnover process involving intestinal stem cell activity. As a result, the microbiome and pathogens serve as important factors in regulating intestinal tissue turnover. In this manuscript, I discuss crucial discoveries revealing the interaction between gut microbes and the host's innate immune system, closely associated with the regulation of intestinal stem cell proliferation and differentiation, ultimately contributing to epithelial homeostasis.

Modulatory Activity of Bifidobacterium sp. BGN4 Cell Fractions on Immune Cells

  • Kim Nam-Ju;Ji Geun-Eog
    • Journal of Microbiology and Biotechnology
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    • v.16 no.4
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    • pp.584-589
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    • 2006
  • Bifidobacteria has been suggested to exert health promoting effects on the host by maintaining microbial flora and modulating immune functions in the human intestine. We assessed modulatory effects of the different cell fractions of Bifidobacterium sp. BGN4 on macrophage cells and other immune cells from the spleen and Peyer's patches (PP) of mouse. Cell free extracts (CFE) of the BGN4 fractions induced well-developed morphological changes in the macrophages and increased the phagocytic activity more effectively than other fractions in the mouse peritoneal cells. Nitric oxide (NO) production was significantly reduced by both the cell walls (CW) and CFE in the cultured cells from the spleen and PP. The production of interleukin-6 (IL-6) and interleukin-10 (IL-10) was eminent in the spleen cells treated with experimental BGN4 cell fractions. However, in the PP cells, IL-6 was slightly decreased by the treatment with the whole cell (WC) and CW, whereas IL-10 was significantly increased by the treatment with the CW and CFE. These results suggest that different types of bifidobacterial cell fractions may have differential immunomodulatory activities depending on their location within the host immune system.

A Handoff Improvement Method of High Speed Mobile Host to use LiFA (LIFA를 이용한 고속 이동체의 핸드오프 개선 방안)

  • 김동근;정상운;김상복;김용수
    • Journal of Korea Multimedia Society
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    • v.6 no.1
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    • pp.105-113
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    • 2003
  • In CDMA cellular system, inefficient Channel assignment for high-speed mobile host increase call blocking probability For it has been method proposed to guarantee QoS upon tn the speed of hierarchical cell that is allocated Queues and dedicated channels of high speed mobile host's speed. In this paper, We allocated the dedicated channel of high-speed handoff In FA (Foreign Agent), only if the receive signal strength of mobile host in current cell that there is low traffic in HA (Home Agent). also, we created new Circular queue LiFA (Limited Foreign Agent) for high-speed handoff call that signal strength is weak in certain FA, and had this High-speed handoff call to be ready for Life time to the new Circular queue LiFA. Thus improve the rate of the forced call termination.

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Shigella flexneri Inhibits Intestinal Inflammation by Modulation of Host Sphingosine-1-Phosphate in Mice

  • Kim, Young-In;Yang, Jin-Young;Ko, Hyun-Jeong;Kweon, Mi-Na;Chang, Sun-Young
    • IMMUNE NETWORK
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    • v.14 no.2
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    • pp.100-106
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    • 2014
  • Infection with invasive Shigella species results in intestinal inflammation in humans but no symptoms in adult mice. To investigate why adult mice are resistant to invasive shigellae, 6~8-week-old mice were infected orally with S. flexneri 5a. Shigellae successfully colonized the small and large intestines. Mild cell death was seen but no inflammation. The infected bacteria were cleared 24 hours later. Microarray analysis of infected intestinal tissue showed that several genes that are involved with the sphingosine-1-phosphate (S1P) signaling pathway, a lipid mediator which mediates immune responses, were altered significantly. Shigella infection of a human intestinal cell line modulated host S1P-related genes to reduce S1P levels. In addition, co-administration of S1P with shigellae could induce inflammatory responses in the gut. Here we propose that Shigella species have evasion mechanisms that dampen host inflammatory responses by lowering host S1P levels in the gut of adult mice.

Ultrastructures of Colletotrichum orbiculare in Cucumber Leaves Expressing Systemic Acquired Resistance Mediated by Chlorella fusca

  • Kim, Su Jeung;Ko, Eun Ju;Hong, Jeum Kyu;Jeun, Yong Chull
    • The Plant Pathology Journal
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    • v.34 no.2
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    • pp.113-120
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    • 2018
  • Chlorella, one single-cell green algae organism that lives autotrophically by photosynthesis, can directly suppress some plant diseases. The objective of this study was to determine whether pre-spraying with Chlorella fusca suspension could induce systemic acquired resistance (SAR) in cucumber plants against anthracnose caused by Colletotrichum orbiculare. In order to illustrate SAR induced by algae, infection structures in host cells were observed under a transmission electron microscope (TEM). Cytological changes as defense responses of host mesophyll cells such as accumulation of vesicles, formation of sheath around penetration hyphae, and thickness of cell wells adjoining with intracellular hyphae were demonstrated in cucumber leaves. Similar defense responses were also found in the plant pre-treated with DL-3-aminobutyric acid, another SAR priming agent. Images showed that defense response of host cells was scarcely observed in untreated leaf tissues. These cytological observations suggest that C. fusca could induce SAR against anthracnose in cucumber plants by activating defense responses of host cells.

Microbial Components and Effector Molecules in T Helper Cell Differentiation and Function

  • Changhon Lee;Haena Lee;John Chulhoon Park;Sin-Hyeog Im
    • IMMUNE NETWORK
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    • v.23 no.1
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    • pp.7.1-7.27
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    • 2023
  • The mammalian intestines harbor trillions of commensal microorganisms composed of thousands of species that are collectively called gut microbiota. Among the microbiota, bacteria are the predominant microorganism, with viruses, protozoa, and fungi (mycobiota) making up a relatively smaller population. The microbial communities play fundamental roles in the maturation and orchestration of the immune landscape in health and disease. Primarily, the gut microbiota modulates the immune system to maintain homeostasis and plays a crucial role in regulating the pathogenesis and pathophysiology of inflammatory, neuronal, and metabolic disorders. The microbiota modulates the host immune system through direct interactions with immune cells or indirect mechanisms such as producing short-chain acids and diverse metabolites. Numerous researchers have put extensive efforts into investigating the role of microbes in immune regulation, discovering novel immunomodulatory microbial species, identifying key effector molecules, and demonstrating how microbes and their key effector molecules mechanistically impact the host immune system. Consequently, recent studies suggest that several microbial species and their immunomodulatory molecules have therapeutic applicability in preclinical settings of multiple disorders. Nonetheless, it is still unclear why and how a handful of microorganisms and their key molecules affect the host immunity in diverse diseases. This review mainly discusses the role of microbes and their metabolites in T helper cell differentiation, immunomodulatory function, and their modes of action.

Analysis of the morphological change and the expression of secretory leukocyte protease inhibitor (SLPI) in various cell lines after lipopolysaccharide stimulation

  • Choi, Baik-Dong;Choi, Jeong-Yoon;Jeong, Soon-Jeong;Park, Joo-Cheol;Kim, Heung-Joong;Bae, Chun-Sik;Lim, Do-Seon;Jeong, Moon-Jin
    • 한국전자현미경학회:학술대회논문집
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    • 2005.11a
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    • pp.127-129
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    • 2005
  • Bacterial lipopolysaccharide(LPS) is can stimulate the most LPS-responsive cells in the mammalian host. The macrophage response to LPS can protect the host from infection but high levels, contribute to systemic inflammatory response syndrome and destruction of host itself, The previously study, secretory leukocyte pretense inhibitor (SLPI) was known LPS-induced product of macrophage and had the function that antagonizes their LPS-induced activation of pro-inflammation signaling factors. Purpose of this study was to identify the expression of SLPI involving the infection in various cell lines including odontoblast cell line. Therefore, we conducted in vitro researches, which treated the LPS to the MDPC-23, and compared to NIH3T3, RAW264.7. To investigate the expressionof SLPI in mRNA level, the methods was used RT-PCR and western blotting for protein expression of SLPI. Moreover, we performed the scanning electron microscopic (SEM) observation for the morphological change. This work was supported by Korea Science and Engineering Foundation.

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Ultrastructure of Compatible and Incompatible Interactions of Pumpkin Stems Infected with Phytophthora capsici

  • Lee, Byung-Kook;Hong, Jeum-Kyu;Hwang, Byung-Kook
    • The Plant Pathology Journal
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    • v.17 no.1
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    • pp.29-35
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    • 2001
  • Early infection process of Phytophthora capsici in pumpkin stems was similar in the compatible and incompatible interactions 24 h after inoculation. Intercellularly growing hyphae penetrated host parenchyma cells by growing hyphae penetrated host parenchyma cells by forming haustoria. An extrahaustorial matrix was found around the haustoria in both compatible and incompatible interactions. No wall appositions were observed at the infection sites in the parenchyma cells. In the compatible interaction, infecting hyphae grew well in the intercellular spaces between xylem vessels in stem tissues. Degraded host cell wall, plasmolysis of plasma membrane, and degenerated chloroplasts were pathological features of pumpkin stem tissues in both compatible and incompatible interactions. A characteristic host response in the resistant pumkin cultivar Danmatmaetdol was rapid cytoplasmic movement of host cells toward the oomycete haustoria.

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Ubiquitin-regulating effector proteins from Legionella

  • Jeong, Minwoo;Jeon, Hayoung;Shin, Donghyuk
    • BMB Reports
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    • v.55 no.7
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    • pp.316-322
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    • 2022
  • Ubiquitin is relatively modest in size but involves almost entire cellular signaling pathways. The primary role of ubiquitin is maintaining cellular protein homeostasis. Ubiquitination regulates the fate of target proteins using the proteasome- or autophagy-mediated degradation of ubiquitinated substrates, which can be either intracellular or foreign proteins from invading pathogens. Legionella, a gram-negative intracellular pathogen, hinders the host-ubiquitin system by translocating hundreds of effector proteins into the host cell's cytoplasm. In this review, we describe the current understanding of ubiquitin machinery from Legionella. We summarize structural and biochemical differences between the host-ubiquitin system and ubiquitin-related effectors of Legionella. Some of these effectors act much like canonical host-ubiquitin machinery, whereas others have distinctive structures and accomplish non-canonical ubiquitination via novel biochemical mechanisms.