• Title/Summary/Keyword: host cells

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Expression of Heat Shock Protein Protein 70 in Umbilical Vein Endothelial Cells Infected by Staphylococcus aureus

  • Chang, Hyun-Ah;Chang, Jun-Keun;Kim, Jong-Won;Kim, Mal-Nam
    • Journal of Microbiology and Biotechnology
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    • v.10 no.2
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    • pp.137-142
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    • 2000
  • Environmental stres is known to induce heat shock proteins (HSPs) in eukaryotic cells. However, the induction of HSPs in host cells by microbial infection has not yet been well explained. Staphylococcus aureus (S. aureus) is one of the major pathogens in the pathogenesis of endovascular diseases such as infective endocarditis. In this study, the synthesis of stress-inducible 70 kDa HSP was investigated in the endothelial cells (ECs) after 3 h to 20 h of incubation with S. aureus. The dffect of S. aureus infection on the expression of HSP70 in cultured ECs was analyzed using laser scanning confocal microscopy (LSCM). The increase of HSP70 expression in ECs infected by S. aureus ($10^4{\;}cfu/ml$) for 20 h was 1.1-fold higher than that in heat shock treated ECs and 2.2-fold higher than that in untreated cells. Heat shock is known to induce intranucleus HSP70 expression in mammalian cells, whereas the S. aureus infection induced perinuclear expression in ECs as observed by LSCM. Consequently, the expression of HSP70 in ECs plays an important role in the pathogenesis of endovascular infection.

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Marine birnavirus (MABV)'s 5' terminal region of segment A acts as internal ribosome entry site (IRES)

  • Kim, So Yeon;Kim, Ki Hong
    • Journal of fish pathology
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    • v.34 no.1
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    • pp.17-22
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    • 2021
  • Eukaryotic translation is initiated by either cap-dependent or cap-independent way, and the cap-independent translation can be initiated by the internal ribosomal entry site (IRES). In this study, to know whether the 5'UTR leader sequence of marine birnavirus (MABV) segment A and segment B can act as IRES, bicistronic vectors harboring a CMV promoter-driven red fluorescent gene (mCherry) and poliovirus IRES- or MABV's leader sequence-driven green fluorescent gene (eGFP) were constructed, then, transfected into a mammalian cell line (BHK-21 cells) and a fish cell line (CHSE-214 cells). The results showed that the poliovirus IRES worked well in BHK-21 cells, but did not work in CHSE-214 cells. In the evaluation of MABV's leader sequences, the reporter eGFP gene under the 5'UTR leader sequence of MABV's segment A was well-translated in CHSE-214 cells, indicating 5'UTR of MABV's segment A initiates translation in the cap-independent way and can be used as a fish-specific IRES system. However, the 5'UTR leader sequence of MABV's segment B did not initiate translation in CHSE-214 cells. As the precise mechanism of birnavirid IRES-mediated translation is not known, more elaborate investigations are needed to uncover why the leader sequence of segment B could not initiate translation in the present study. In addition, further studies on the host species range of MABV's segment A IRES and on the screening of other fish-specific IRESs are needed.

Anticancer Drugs at Low Concentrations Upregulate the Activity of Natural Killer Cell

  • Hyeokjin Kwon;Myeongguk Jeong;Yeeun Kim;Go-Eun Choi
    • Biomedical Science Letters
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    • v.29 no.3
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    • pp.178-183
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    • 2023
  • Natural killer (NK) cells are innate cytotoxic lymphoid cells that actively prevent neoplastic development, growth, and metastatic dissemination in a process called cancer immunosurveillance. Regulation of the cytotoxic activity of NK cells relies on integrated interactions between inhibitory receptors and numerous activating receptors that act in tandem to eliminate tumor cells efficiently. Conventional chemotherapy is designed to produce an anti-proliferative or cytotoxic effect on early tumor cell division. Therapies designed to kill cancer cells and simultaneously maintain host anti-tumor immunity are attractive strategies for controlling tumor growth. Depending on the drug and dose used, several chemotherapeutic agents cause DNA damage and cancer cell death through apoptosis, immunogenic cell death, or other forms of non-killing (i.e., mitotic catastrophe, senescence, autophagy). Among stress-induced immunostimulatory proteins, changes in the expression levels of NK cell activating and inhibitory ligands and tumor cell death receptors play an important role in the detection and elimination by innate immune effectors including NK cells. Therefore, we will address how these cytotoxic lymphocytes sense and respond to high and low concentrations of drug-induced stress to the drug cisplatin, among the various types of drugs that contribute to their anticancer activity.

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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Mitophagy: a balance regulator of NLRP3 inflammasome activation

  • Kim, Min-Ji;Yoon, Joo-Heon;Ryu, Ji-Hwan
    • BMB Reports
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    • v.49 no.10
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    • pp.529-535
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    • 2016
  • The NLRP3 inflammasome is activated by a variety of external or host-derived stimuli and its activation initiates an inflammatory response through caspase-1 activation, resulting in inflammatory cytokine IL-1β maturation and secretion. The NLRP3 inflammasome activation is a kind of innate immune response, most likely mediated by myeloid cells acting as a host defense mechanism. However, if this activation is not properly regulated, excessive inflammation induced by overactivated NLRP3 inflammasome can be detrimental to the host, causing tissue damage and organ dysfunction, eventually causing several diseases. Previous studies have suggested that mitochondrial damage may be a cause of NLRP3 inflammasome activation and autophagy, which is a conserved self-degradation process that negatively regulates NLRP3 inflammasome activation. Recently, mitochondria-selective autophagy, termed mitophagy, has emerged as a central player for maintaining mitochondrial homeostasis through the elimination of damaged mitochondria, leading to the prevention of hyperinflammation triggered by NLRP3 inflammasome activation. In this review, we will first focus on the molecular mechanisms of NLRP3 inflammasome activation and NLRP3 inflammasome-related diseases. We will then discuss autophagy, especially mitophagy, as a negative regulator of NLPP3 inflammasome activation by examining recent advances in research.

Targeted Nanomedicine that Interacts with Host Biology

  • Ju, Jin-Myeong
    • Proceedings of the Korean Institute of Surface Engineering Conference
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    • 2017.05a
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    • pp.81-81
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    • 2017
  • Nanotechnology is of great importance to molecular biology and medicine because life processes are maintained by the action of a series of molecular nanomachines in the cell machinery. Recent advances in nanoscale materials that possess emergent physical properties and molecular organization hold great promise to impact human health in the diagnostic and therapeutic arenas. In order to be effective, nanomaterials need to navigate the host biology and traffic to relevant biological structures, such as diseased or pathogenic cells. Moreover, nanoparticles intended for human administration must be designed to interact with, and ideally leverage, a living host environment. Inspired by nature, we use peptides to transfer biological trafficking properties to synthetic nanoparticles to achieve targeted delivery of payloads. In this talk, development of nanoscale materials will be presented with a particular focus on applications to three outstanding health problems: bacterial infection, cancer detection, and traumatic brain injury. A biodegradable nanoparticle carrying a peptide toxin trafficked to the bacterial surface has antimicrobial activity in a pneumonia model. Trafficking of a tumor-homing nanoprobes sensitively detects cancer via a high-contrast time-gated imaging system. A neuron-targeted nanoparticle carrying siRNA traffics to neuronal populations and silences genes in a model of traumatic brain injury. Unique combinations of material properties that can be achieved with nanomaterials provide new opportunities in translational nanomedicine. This framework for constructing nanomaterials that leverage bio-inspired molecules to traffic diagnostic and therapeutic payloads can contribute on better understanding of living systems to solve problems in human health.

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Inprovement of Handoff Protocol for Real-Time Packet Transmission in Cellular Wireless Networks (셀룰라 무선 망에서 실시간 패킷 전송을 위한 핸드오프 프로토콜 개선)

  • Han, Seung-Jin;Lee, Jung-Hyun
    • The Transactions of the Korea Information Processing Society
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    • v.7 no.11S
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    • pp.3675-3683
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    • 2000
  • The Handoff is the core technical factor that is required when mobile host moves from one area to another, while transmitting and receiving data. The existing works try to minimize the loss of pockets by forwarding packets to the Cell which a mobile host will move to. However, though the loss quantity is little, the accumulated loss can del(rade the performance of the TCP, and can be a serious problem if data is sensitive to the loss of packets. In this paper, we can reduce a memory requesting in FA by restricting the mobile host to move within at most 2 movable cells and design the improved handoff protocol for Mil to receive packets seamlessly in spite of handoff. We can evaluate that the suggested method is superior to the previous method, as a result of comparing with it.

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Ultrastructural Changes of Chinese Cabbage Root Tissues Associated with Pathogenesis of Plasmodiophora brassicae

  • Sung, Mi-Joo;Kim, Young-Soon;Kim, Young-Ho
    • The Plant Pathology Journal
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    • v.17 no.2
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    • pp.94-100
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    • 2001
  • Roots of Chinese cabbage (Brassica campestris var. chinensis) seedlings infected with Plasmodiophora brassicae were examined by light and electron microscopy to reveal histopathological changes related to pathogenesis in the susceptible host. The pathogen colonized the cortex and partly the stele as well, invading up to the xylem. Gall tissues could be differentiated from the initially infected tissues, involving less compact organization and new vascular development. The infected cells were much hypertrophied, and contained one to several plasmodia. Except cellular hypertrophy, no pathological ultrastructural modification was noted in the infected calls. Infected cytoplasm became dense with ground cytoplasm, inconspicuous central vacuole, and increased cellular organelles such as mitochondria and dictyosomes. There were two types of nuclear states of plasmodium, uninucleate and multinucleate. Both plasmodia were structurally similar, filled with lipid droplets, bounded with envelope, and containing mitochondria, endo-plasmic reticulum, and sometimes small vacuoles. Plasmodial fragmentation, which may be regarded as a way to discharge plasmodial materials into host cytoplasm, commonly occurred, forming plasmodial fragments by outgrowth of plasmodial cytoplasm and regional compartmentalization. Plasmodial fragments were degenerated sometimes followed by forming chains of spherical vesicles especially in the uninucleate plasmodial state. These ultrastructural features indicate the biotrophic nature of the pathogen associated with its pathogenesis in the susceptible host.

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Microbe-derived extracellular vesicles as a smart drug delivery system

  • Yang, Jinho;Kim, Eun Kyoung;McDowell, Andrea;Kim, Yoon-Keun
    • Translational and Clinical Pharmacology
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    • v.26 no.3
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    • pp.103-110
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    • 2018
  • The human microbiome is known to play an essential role in influencing host health. Extracellular vesicles (EVs) have also been reported to act on a variety of signaling pathways, distally transport cellular components such as proteins, lipids, and nucleic acid, and have immunomodulatory effects. Here we shall review the current understanding of the intersectionality of the human microbiome and EVs in the emerging field of microbiota-derived EVs and their pharmacological potential. Microbes secrete several classes of EVs: outer membrane vesicles (OMVs), membrane vesicles (MVs), and apoptotic bodies. EV biogenesis is unique to each cell and regulated by sophisticated signaling pathways. EVs are primarily composed of lipids, proteins, nucleic acids, and recent evidence suggests they may also carry metabolites. These components interact with host cells and control various cellular processes by transferring their constituents. The pharmacological potential of microbiome-derived EVs as vaccine candidates, biomarkers, and a smart drug delivery system is a promising area of future research. Therefore, it is necessary to elucidate in detail the mechanisms of microbiome-derived EV action in host health in a multi-disciplinary manner.

Infection of marine diatom Coscinodiscus wailesii(Bacillariophyceae) by the parasitic nanoflagellate Pirsonia diadema(Stramenopiles) from Yongho Bay in Korea

  • Yoo, Jiae;Kim, Sunju
    • Korean Journal of Environmental Biology
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    • v.38 no.4
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    • pp.567-577
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    • 2020
  • The infection of marine diatom Coscinodiscus wailesii by a parasitic protist from the Yongho Bay of Busan, Korea was observed during the diatom bloom events in 2017 through 2018. The morphological and molecular features suggested that the parasitic nanoflagellate Pirsonia diadema was responsible for the infection. During the study period, the parasite prevalence ranged from 0.3% to 3.3%, and infected C. wailesii cells were observed only at surface seawater temperatures ranging between 10.9 and 19.9℃, although the host population appeared at temperatures above 25℃. The parasite and host system was successfully established as cultures. Using the cultures, we determined the morphological features over the infection cycle, parasite generation time, parasite prevalence as a function of inoculum size, and zoospore infectivity and survival time. The diatom C. wailesii was readily infected by the parasite P. diadema, with a parasite prevalence reaching up to 100% and a zoospore to host inoculum ratio above 20:1. The survival and infectivity of the parasite zoospores decreased with age. While the zoospores could survive up to 88 hours, they quickly lost their ability to infect after 48 hours. These results could lead to a better understanding of the biology and ecology of the parasitoid infecting the giant-sized diatoms in coastal waters.