• Title/Summary/Keyword: host cell

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Involvement of NOX2-derived ROS in human hepatoma HepG2 cell death induced by Entamoeba histolytica

  • Young Ah Lee ;Myeong Heon Shin
    • Parasites, Hosts and Diseases
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    • v.61 no.4
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    • pp.388-396
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    • 2023
  • Entamoeba histolytica is an enteric tissue-invasive protozoan parasite causing amoebic colitis and liver abscesses in humans. Amoebic contact with host cells activates intracellular signaling pathways that lead to host cell death via generation of caspase-3, calpain, Ca2+ elevation, and reactive oxygen species (ROS). We previously reported that various NADPH oxidases (NOXs) are responsible for ROS-dependent death of various host cells induced by amoeba. In the present study, we investigated the specific NOX isoform involved in ROS-dependent death of hepatocytes induced by amoebas. Co-incubation of hepatoma HepG2 cells with live amoebic trophozoites resulted in remarkably increased DNA fragmentation compared to cells incubated with medium alone. HepG2 cells that adhered to amoebic trophozoites showed strong dichlorodihydrofluorescein diacetate (DCF-DA) fluorescence, suggesting intracellular ROS accumulation within host cells stimulated by amoebic trophozoites. Pretreatment of HepG2 cells with the general NOX inhibitor DPI or NOX2-specific inhibitor GSK 2795039 reduced Entamoeba-induced ROS generation. Similarly, Entamoeba-induced LDH release from HepG2 cells was effectively inhibited by pretreatment with DPI or GSK 2795039. In NOX2-silenced HepG2 cells, Entamoeba-induced LDH release was also significantly inhibited compared with controls. Taken together, the results support an important role of NOX2-derived ROS in hepatocyte death induced by E. histolytica.

Host and Non-Host Disease Resistances of Kimchi Cabbage Against Different Xanthomonas campestris Pathovars

  • Lee, Young-Hee;Hong, Jeum-Kyu
    • The Plant Pathology Journal
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    • v.28 no.3
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    • pp.322-329
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    • 2012
  • This study was conducted to investigate host and non-host disease resistances of kimchi cabbage plants to bacterial infection. Kimchi cabbage leaves responded differently to infections with a virulent strain of Xanthomonas campestris pv. campestris (Xcc) 8004 and two strains (85-10 and Bv5-4a.1) of non-host bacteria X. campestris pv. vesicatoria (Xcv). Non-host bacteria triggered a rapid tissue collapse of the leaves showing as brown coloration at the infected sites, highly increased ion leakage, lipid peroxidation and accumulation of UV-stimulated autofluorescence materials at the inoculated sites. During the observed interactions, bacterial proliferations within the leaf tissues were significantly different. Bacterial number of Xcc 8004 progressively increased within the inoculated leaf tissues over time, while growths of two non-host bacteria Xcv strains were distinctly limited. Expressions of pathogenesis-related genes, such as GST1, PR1, BGL2, VSP2, PR4 and LOX2, were differentially induced by host and non-host bacterial infections of X. campestris pathovars. These results indicated that rapid host cellular responses to the non-host bacterial infections may contribute to an array of defense reactions to the non-host bacterial invasion.

Ultrastructural Study on the Haustorial Cells of Cuscuta australis R. Brown in the Region of the Host Parenchyma (기주식물의 유조직 속에서 생장하는 실새삼(Cuscuta australis R. Brown) 흡기세포의 미세구조)

  • 이규배
    • Journal of Plant Biology
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    • v.34 no.2
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    • pp.129-136
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    • 1991
  • Two cell types, tip cells and hyphal cells, were found at the front of Cuscuta australis endophyte growing into the stem parenchyma of the host plant, Trifolium repens. Each tip cell developed into an elongate, filamentous hypha. The cells of both types possessed a dense cytoplasm including abundant organelles and enlarged nuclei with the deeply lobed envelope. The unevenly thick walls were observed in certain tip cells. The wall penetrated through the middle lamellae of the host cells and engulfed the debris of broken host cells. Some front cells had the plasmalemma-wall invaginations, which increased the surface area and would facilitate material uptake from the host No plasmodesmata between the host and parasite cells were found; instead, an apoplastic continuity was established by fused cell walls at the interface of the two partners. The apoplast was thought to be the main route for water and nutrients transport.nsport.

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Infectivity of Orientia tsutsugamushi to Various Eukaryotic Cells and Their Cellular Invasion Mechanism (Orientia tsutsugamushi의 유핵세포내 감염능 분석 및 기전)

  • Ihn, Kyung-Soo;Han, Seung-Hoon;Kim, Hang-Rae;Seong, Seung-Yong;Kim, Ik-Sang;Choi, Myung-Sik
    • The Journal of the Korean Society for Microbiology
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    • v.34 no.5
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    • pp.435-443
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    • 1999
  • Orientia tsutsugamushi is obligate intracellular bacterium that grows within the cytoplasm of the eukaryotic host cells. Therefore capability of the attachment, entry into the host cell and intracellular survival should be critical process for oriential infection. In this study we investigated the cellular invasion mechanism of Orientia tsutsugamushi and the role of transmembrane heparan sulfate proteoglycan, which binds diverse components at the cellular microenvironment and is implicated as host cell receptors for a variety of microbial pathogens. First of all Orientia tsutsugamushi can invade a wide range of nonprofessional phagocytic cells including fibroblast, epithelial cells and endothelial cells of various host species, including Band T lymphocytes. Thus, it was postulated that the attachment of O. tsutsugamushi requires the recognition of ubiquitous surface structures of many kinds of host cells. Treatments with heparan sulfate and heparin inhibited the infection of Orientia tsutsugamushi in dose-dependent manner for L cell, mouse fibroblast, whereas other glycosaminoglycans such as chondroitin sulfate had no effect. Collectively, these findings provide strong evidence that initial interaction with heparan sulfate proteoglycan is required for the oriential invasion into host cells.

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An Ultrastructural Investigation of Infection Threads in Sesbania rostrata Stem Nodules Induced by Sinorhizobium sp. Strain MUS10

  • Krishnan Hari B.
    • KOREAN JOURNAL OF CROP SCIENCE
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    • v.49 no.4
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    • pp.316-324
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    • 2004
  • Sinorhizobium sp. strain MUS10 forms nitrogen-fixing stem nodules on Sesbania rostrata, a tropical green manure crop. In this study, the ultrastructural events associated with the formation of stem nodules were investigated. Sinorhizobium sp. strain MUS10 entered the host tissue through cracks created by the emerging adventitious root primordia and multiplied within the intercellular spaces. During early phases of infection, host cells adjacent to invading bacteria revealed cellular damage that is typical of hypersensitive reactions, while the cells at the inner cortex exhibited meristematic activity. Infection threads were numerous in S-day-old nodules and often were associated with the host cell wall. In several cases, more than one infection thread was found in individual cells. The junction at which the host cell walls converged was often enlarged due to fusion of intracellular branches of infection threads resulting in large infection pockets. The infection threads were made up of a homogeneous, amorphous matrix that enclosed the bacteria. Several finger-like projections were seen radiating from these enlarged infection threads and were delineated from the host cytoplasm by the plasma membrane. As in Azorhizobium caulinodans induced root nodules, the release of Sinorhizobia from the infection threads into the plant cells appears to be mediated by 'infection droplets'. A 15-day­old Sesbania stem nodule revealed typical ultrastructure features of a determinate nodule, containing several bacterioids within symbiosomes.

Influence of calcium ion on host cell invasion and intracellular replication by Toxoplasma gondii

  • Song, Hyun-Ouk;Ahn, Myoung-Hee;Ryu, Jae-Sook;Min, Duk-Young;Joo, Kyoung-Hwan;Lee, Young-Ha
    • Parasites, Hosts and Diseases
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    • v.42 no.4
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    • pp.185-193
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    • 2004
  • Toxoplasma gondii is an obligate intracellular protozoan parasite, which invades a wide range of hosts including humans. The exact mechanisms involved in its invasion are not fully understood. This study focused on the roles of $Ca^{2+}$ in host cell invasion and in T. gondii replication. We examined the invasion and replication of T. gondii pretreated with several calcium modulators, the conoid extrusion of tachyzoites. Calmodulin localization in T. gondii were observed using the immunogold method, and $Ca^{2+}$ levels in tachyzoites by confocal microscopy. In light microscopic observation, tachyzoites co-treated with A23187 and EGTA showed that host cell invasion and intracellular replication were decreased. The invasion of tachyzoites was slightly inhibited by the $Ca^{2+}$ channel blockers, bepridil and verapamil, and by the calmodulin antagonist, calmidazolium. We observed that calcium saline containing A23187 induced the extrusion of tachyzoite conoid. By immunoelectron microscopy, gold particles bound to anti-calmodulin or anti-actin mAb, were found to be localized on the anterior portion of tachyzoites. Remarkably reduced intracellular $Ca^{2+}$ was observed in tachyzoites treated with BAPTA/AM by confocal microscopy. These results suggest that host cell invasion and the intracellular replication of T. gondii tachyzoites are inhibited by the calcium ionophore, A23187, and by the extracellular calcium chelator, EGTA.

Combined application of Astragali Radix and chlorambucil on anticancerous effect and host safety in Lukemia Cell(P388D1 cell) and its bearing mice (황기와 Chlorambucil 병용(倂用)이 P388D1 백혈병(白血病) 세포(細胞) 및 담암(擔癌)생쥐에 미치는 영향(影響))

  • Jeon, Jeong-Hoi;Kim, Jin-Sung;Yoon, Sang-Hyub;Ryu, Bong-Ha;Ryu, Ki-Won
    • The Journal of Internal Korean Medicine
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    • v.26 no.2
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    • pp.291-301
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    • 2005
  • Objective : Anticancerous and host safety effects of the combination of Astragali Radix and chlorambucil are studied when it is applied to leukemia cell(P388D1 cell) related disease. Methods : After 5 groups of mice are treated by respective procedures (HG, CHL, HG+CHL, etc), the quantitative analyses (cell proliferation assay, mutagenesis test, survival rate, weight shift observation, tissue and blood analyses, etc) are conducted. Results : While sole injection of Astragali Radix extends the survival period and deter the liver and marrow function deterioration, combined injection (HG+CHL) shows more strong anticancerous effect than sole injection of Astragali Radix or Cholrambucil, and also does not cause any mutation on the normal cells and virulence on marrow and liver caused by leukemia. Conclusions : The combined application of Astragali Radix and chlorambucil has more effective anticancerous and host safety effects than independent use of them.

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Design and VLSI Implementation of Reassembly Controller for ATM/AAL Layer (ATM/AAL 처리를 위한 재조립 처리기의 설계 및 VLSI 구현)

  • 박경철;심영석
    • Journal of the Institute of Electronics Engineers of Korea SD
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    • v.40 no.5
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    • pp.369-378
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    • 2003
  • This paper presents design and VLSI implementations of a reassembly processor for ATM/AAL. The assembly processor is responsible for processing ATM cells from the receive physical interface. It controls the transfer of the AAL payload to host memory and performs all necessary SAR and CPCS checks. We propose the improved structure of cell identification algorithm and smart scatter method for host memory management. The proposed cell identification algorithm quickly locates the appropriate reassembly VC table based on the received VPI./VCI channel value in the ATM header. The cell identification algorithm also allow complete freedom in assignment of VCI/VPI values. The reassembly processor uses a smart scatter method to write cell payload data to host memory. It maintains the scatter operation and controls the incoming DMA block during scatter DMA to host memory. The proposed reassembly processor can perform reassembly checks on AAL. OAM cell. For an AAL5 connection, only CPCS checks, including the CRC32, are performed. In this paper, we proposed a practical reassembly architecture. The design of reassembly processor has become feasible using 0.6${\mu}{\textrm}{m}$ CMOS gate array technology.

Toxoplasma gondii Induces Apoptosis via Endoplasmic Reticulum Stress-Derived Mitochondrial Pathway in Human Small Intestinal Epithelial Cell-Line

  • Wang, Hao;Li, Chunchao;Ye, Wei;Pan, Zhaobin;Sun, Jinhui;Deng, Mingzhu;Zhan, Weiqiang;Chu, Jiaqi
    • Parasites, Hosts and Diseases
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    • v.59 no.6
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    • pp.573-583
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    • 2021
  • Toxoplasma gondii, an intracellular protozoan parasite that infects one-third of the world's population, has been reported to hijack host cell apoptotic machinery and promote either an anti- or proapoptotic program depending on the parasite virulence and load and the host cell type. However, little is known about the regulation of human FHs 74 small intestinal epithelial cell viability in response to T. gondii infection. Here we show that T. gondii RH strain tachyzoite infection or ESP treatment of FHs 74 Int cells induced apoptosis, mitochondrial dysfunction and ER stress in host cells. Pretreatment with 4-PBA inhibited the expression or activation of key molecules involved in ER stress. In addition, both T. gondii and ESP challenge-induced mitochondrial dysfunction and cell death were dramatically suppressed in 4-PBA pretreated cells. Our study indicates that T. gondii infection induced ER stress in FHs 74 Int cells, which induced mitochondrial dysfunction followed by apoptosis. This may constitute a potential molecular mechanism responsible for the foodborne parasitic disease caused by T. gondii.

Skin Graft-versus-host Disease Following Autologous Stem Cell Transplantation for Multiple Myeloma

  • Lee, Sung-Eun;Yoon, Jae-Ho;Shin, Seung-Hwan;Park, Gyeongsin;Min, Chang-Ki
    • IMMUNE NETWORK
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    • v.13 no.3
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    • pp.107-110
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    • 2013
  • Graft-versus-host disease (GVHD) is a common complication of allogeneic stem cell transplantation (allo-SCT). However, a similar syndrome has been reported in autologous stem cell transplantation (ASCT) as well. The target organs of GVHD in ASCT are the skin, liver and gastrointestinal (GI) tract, which are consistent with those in allo-SCT. Histologic findings from the skin and the mucosa of the GI tract also show similar features. Here we describe a case of autologous GVHD involving the skin of a patient who underwent ASCT for multiple myeloma. In this patient, the response to a total prednisone dose of 0.5 mg/kg/day was unsatisfactory, and the patient required more intensive and prolonged immunosuppressive therapy with slow tapering.