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  1. Article ; Online: Pseudomonas aeruginosa

    Kim, Dae-Kyum / Huh, Jin-Won / Yu, Hyeonseung / Lee, Yeji / Jin, Yongxin / Ha, Un-Hwan

    International journal of molecular sciences

    2023  Volume 24, Issue 21

    Abstract: As members of pathogen-associated molecular patterns, bacterial heat shock proteins (HSPs) are widely recognized for their role in initiating innate immune responses. This study aimed to examine the impact of DnaJ, a homolog of HSP40 derived ... ...

    Abstract As members of pathogen-associated molecular patterns, bacterial heat shock proteins (HSPs) are widely recognized for their role in initiating innate immune responses. This study aimed to examine the impact of DnaJ, a homolog of HSP40 derived from
    MeSH term(s) Inflammasomes/metabolism ; Pseudomonas aeruginosa/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Signal Transduction ; Macrophages/metabolism ; NF-kappa B/metabolism ; Interleukin-1beta/metabolism
    Chemical Substances Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; NF-kappa B ; Interleukin-1beta
    Language English
    Publishing date 2023-11-03
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms242115957
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Integrative single-cell transcriptome analysis provides new insights into post-COVID-19 pulmonary fibrosis and potential therapeutic targets.

    Kim, Yumin / Kim, Yeongmin / Lim, Hyobin Julianne / Kim, Dae-Kyum / Park, Ji-Hwan / Oh, Chang-Myung

    Journal of medical virology

    2023  Volume 95, Issue 11, Page(s) e29201

    Abstract: The global COVID-19 pandemic caused by the severe acute respiratory syndrome coronavirus 2 virus has resulted in a significant number of patients experiencing persistent symptoms, including post-COVID pulmonary fibrosis (PCPF). This study aimed to ... ...

    Abstract The global COVID-19 pandemic caused by the severe acute respiratory syndrome coronavirus 2 virus has resulted in a significant number of patients experiencing persistent symptoms, including post-COVID pulmonary fibrosis (PCPF). This study aimed to identify novel therapeutic targets for PCPF using single-cell RNA-sequencing data from lung tissues of COVID-19 patients, idiopathic pulmonary fibrosis (IPF) patients, and a rat transforming growth factor beta-1-induced fibrosis model treated with antifibrotic drugs. Patients with COVID-19 had lower alveolar macrophage counts than healthy controls, whereas patients with COVID-19 and IPF presented with elevated monocyte-derived macrophage counts. A comparative transcriptome analysis showed that macrophages play a crucial role in IPF and COVID-19 development and progression, and fibrosis- and inflammation-associated genes were upregulated in both conditions. Functional enrichment analysis revealed the upregulation of inflammation and proteolysis and the downregulation of ribosome biogenesis. Cholesterol efflux and glycolysis were augmented in both macrophage types. The study suggests that antifibrotic drugs may reverse critical lung fibrosis mediators in COVID-19. The results help clarify the molecular mechanisms underlying pulmonary fibrosis in patients with severe COVID-19 and IPF and highlight the potential efficacy of antifibrotic drugs in COVID-19 therapy. Collectively, all these findings may have significant implications for the development of new treatment strategies for PCPF.
    MeSH term(s) Humans ; Animals ; Rats ; Pulmonary Fibrosis/drug therapy ; Pulmonary Fibrosis/genetics ; COVID-19/complications ; COVID-19/genetics ; Pandemics ; Single-Cell Gene Expression Analysis ; Inflammation
    Language English
    Publishing date 2023-11-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 752392-0
    ISSN 1096-9071 ; 0146-6615
    ISSN (online) 1096-9071
    ISSN 0146-6615
    DOI 10.1002/jmv.29201
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: SARS-CoV-2 Nonstructural Proteins 1 and 13 Suppress Caspase-1 and the NLRP3 Inflammasome Activation.

    Kim, Na-Eun / Kim, Dae-Kyum / Song, Yoon-Jae

    Microorganisms

    2021  Volume 9, Issue 3

    Abstract: Viral infection-induced activation of inflammasome complexes has both positive and negative effects on the host. Proper activation of inflammasome complexes induces down-stream effector mechanisms that inhibit viral replication and promote viral ... ...

    Abstract Viral infection-induced activation of inflammasome complexes has both positive and negative effects on the host. Proper activation of inflammasome complexes induces down-stream effector mechanisms that inhibit viral replication and promote viral clearance, whereas dysregulated activation has detrimental effects on the host. Coronaviruses, including SARS-CoV and MERS-CoV, encode viroporins that activate the NLRP3 inflammasome, and the severity of coronavirus disease is associated with the inflammasome activation. Although the NLRP3 inflammasome activation is implicated in the pathogenesis of coronaviruses, these viruses must evade inflammasome-mediated antiviral immune responses to establish primary replication. Screening of a complementary DNA (cDNA) library encoding 28 SARS-CoV-2 open reading frames (ORFs) showed that two nonstructural proteins (NSPs), NSP1 and NSP13, inhibited caspase-1-mediated IL-1β activation. NSP1 amino acid residues involved in host translation shutoff and NSP13 domains responsible for helicase activity were associated with caspase-1 inhibition. In THP-1 cells, both NSP1 and NSP13 significantly reduced NLRP3-inflammasome-induced caspase-1 activity and IL-1β secretion. These findings indicate that SARS-CoV-2 NSP1 and NSP13 are potent antagonists of the NLRP3 inflammasome.
    Language English
    Publishing date 2021-02-26
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2720891-6
    ISSN 2076-2607
    ISSN 2076-2607
    DOI 10.3390/microorganisms9030494
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: SARS-CoV-2 Nonstructural Proteins 1 and 13 Suppress Caspase-1 and the NLRP3 Inflammasome Activation

    Na-Eun Kim / Dae-Kyum Kim / Yoon-Jae Song

    Microorganisms, Vol 9, Iss 3, p

    2021  Volume 494

    Abstract: Viral infection-induced activation of inflammasome complexes has both positive and negative effects on the host. Proper activation of inflammasome complexes induces down-stream effector mechanisms that inhibit viral replication and promote viral ... ...

    Abstract Viral infection-induced activation of inflammasome complexes has both positive and negative effects on the host. Proper activation of inflammasome complexes induces down-stream effector mechanisms that inhibit viral replication and promote viral clearance, whereas dysregulated activation has detrimental effects on the host. Coronaviruses, including SARS-CoV and MERS-CoV, encode viroporins that activate the NLRP3 inflammasome, and the severity of coronavirus disease is associated with the inflammasome activation. Although the NLRP3 inflammasome activation is implicated in the pathogenesis of coronaviruses, these viruses must evade inflammasome-mediated antiviral immune responses to establish primary replication. Screening of a complementary DNA (cDNA) library encoding 28 SARS-CoV-2 open reading frames (ORFs) showed that two nonstructural proteins (NSPs), NSP1 and NSP13, inhibited caspase-1-mediated IL-1β activation. NSP1 amino acid residues involved in host translation shutoff and NSP13 domains responsible for helicase activity were associated with caspase-1 inhibition. In THP-1 cells, both NSP1 and NSP13 significantly reduced NLRP3-inflammasome-induced caspase-1 activity and IL-1β secretion. These findings indicate that SARS-CoV-2 NSP1 and NSP13 are potent antagonists of the NLRP3 inflammasome.
    Keywords severe acute respiratory syndrome coronavirus 2 ; nonstructural protein ; inflammasome ; caspase-1 ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2021-02-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Pseudomonas aeruginosa -Derived DnaJ Induces the Expression of IL−1β by Engaging the Interplay of p38 and ERK Signaling Pathways in Macrophages

    Dae-Kyum Kim / Jin-Won Huh / Hyeonseung Yu / Yeji Lee / Yongxin Jin / Un-Hwan Ha

    International Journal of Molecular Sciences, Vol 24, Iss 21, p

    2023  Volume 15957

    Abstract: As members of pathogen-associated molecular patterns, bacterial heat shock proteins (HSPs) are widely recognized for their role in initiating innate immune responses. This study aimed to examine the impact of DnaJ, a homolog of HSP40 derived from ... ...

    Abstract As members of pathogen-associated molecular patterns, bacterial heat shock proteins (HSPs) are widely recognized for their role in initiating innate immune responses. This study aimed to examine the impact of DnaJ, a homolog of HSP40 derived from Pseudomonas aeruginosa ( P. aeruginosa ), on the regulation of IL−1β expression in macrophages. We demonstrated that DnaJ modulates macrophages to secrete IL−1β by activating NF-κB and MAPK signaling pathways. Specifically, ERK was identified as a positive mediator for IL−1β expression, while p38 acted as a negative mediator. These results suggest that the reciprocal actions of these two crucial MAPKs play a vital role in controlling IL−1β expression. Additionally, the reciprocal actions of MAPKs were found to regulate the activation of inflammasome-related molecules, including vimentin, NLRP3, caspase-1, and GSDMD. Furthermore, our investigation explored the involvement of CD91/CD40 in ERK signaling-mediated IL−1β production from DnaJ-treated macrophages. These findings emphasize the importance of understanding the signaling mechanisms underlying IL−1β induction and suggest the potential utility of DnaJ as an adjuvant for stimulating inflammasome activation.
    Keywords HSP40 homolog ; IL−1β ; inflammasome ; MAPK ; NF-κB ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Language English
    Publishing date 2023-11-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Biogenesis and delivery of extracellular vesicles

    Jivin Yu / Saba Sane / Ji-Eun Kim / Sehee Yun / Hyeon-Jai Kim / Kyeong Beom Jo / Jacob P. Wright / Nooshin Khoshdoozmasouleh / Kunwoo Lee / Ho Taek Oh / Keaton Thiel / Afrin Parvin / Xavier Williams / Claire Hannon / Hunsang Lee / Dae-Kyum Kim

    Frontiers in Molecular Biosciences, Vol

    harnessing the power of EVs for diagnostics and therapeutics

    2024  Volume 10

    Abstract: Extracellular vesicles (EVs) are membrane-enclosed particles secreted by a variety of cell types. These vesicles encapsulate a diverse range of molecules, including proteins, nucleic acids, lipids, metabolites, and even organelles derived from their ... ...

    Abstract Extracellular vesicles (EVs) are membrane-enclosed particles secreted by a variety of cell types. These vesicles encapsulate a diverse range of molecules, including proteins, nucleic acids, lipids, metabolites, and even organelles derived from their parental cells. While EVs have emerged as crucial mediators of intercellular communication, they also hold immense potential as both biomarkers and therapeutic agents for numerous diseases. A thorough understanding of EV biogenesis is crucial for the development of EV-based diagnostic developments since the composition of EVs can reflect the health and disease status of the donor cell. Moreover, when EVs are taken up by target cells, they can exert profound effects on gene expression, signaling pathways, and cellular behavior, which makes these biomolecules enticing targets for therapeutic interventions. Yet, despite decades of research, the intricate processes underlying EV biogenesis by donor cells and subsequent uptake by recipient cells remain poorly understood. In this review, we aim to summarize current insights and advancements in the biogenesis and uptake mechanisms of EVs. By shedding light on the fundamental mechanisms governing EV biogenesis and delivery, this review underscores the potential of basic mechanistic research to pave the way for developing novel diagnostic strategies and therapeutic applications.
    Keywords extracellular vesicles ; exosomes ; ectosomes ; biogenesis ; delivery ; uptake ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2024-01-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article: Biogenesis and delivery of extracellular vesicles: harnessing the power of EVs for diagnostics and therapeutics.

    Yu, Jivin / Sane, Saba / Kim, Ji-Eun / Yun, Sehee / Kim, Hyeon-Jai / Jo, Kyeong Beom / Wright, Jacob P / Khoshdoozmasouleh, Nooshin / Lee, Kunwoo / Oh, Ho Taek / Thiel, Keaton / Parvin, Afrin / Williams, Xavier / Hannon, Claire / Lee, Hunsang / Kim, Dae-Kyum

    Frontiers in molecular biosciences

    2024  Volume 10, Page(s) 1330400

    Abstract: Extracellular vesicles (EVs) are membrane-enclosed particles secreted by a variety of cell types. These vesicles encapsulate a diverse range of molecules, including proteins, nucleic acids, lipids, metabolites, and even organelles derived from their ... ...

    Abstract Extracellular vesicles (EVs) are membrane-enclosed particles secreted by a variety of cell types. These vesicles encapsulate a diverse range of molecules, including proteins, nucleic acids, lipids, metabolites, and even organelles derived from their parental cells. While EVs have emerged as crucial mediators of intercellular communication, they also hold immense potential as both biomarkers and therapeutic agents for numerous diseases. A thorough understanding of EV biogenesis is crucial for the development of EV-based diagnostic developments since the composition of EVs can reflect the health and disease status of the donor cell. Moreover, when EVs are taken up by target cells, they can exert profound effects on gene expression, signaling pathways, and cellular behavior, which makes these biomolecules enticing targets for therapeutic interventions. Yet, despite decades of research, the intricate processes underlying EV biogenesis by donor cells and subsequent uptake by recipient cells remain poorly understood. In this review, we aim to summarize current insights and advancements in the biogenesis and uptake mechanisms of EVs. By shedding light on the fundamental mechanisms governing EV biogenesis and delivery, this review underscores the potential of basic mechanistic research to pave the way for developing novel diagnostic strategies and therapeutic applications.
    Language English
    Publishing date 2024-01-03
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2814330-9
    ISSN 2296-889X
    ISSN 2296-889X
    DOI 10.3389/fmolb.2023.1330400
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: SARS-CoV-2 Nonstructural Proteins 1 and 13 Suppress Caspase-1 and the NLRP3 Inflammasome Activation

    Kim, Na-Eun / Kim, Dae-Kyum / Song, Yoon-Jae

    Microorganisms. 2021 Feb. 26, v. 9, no. 3

    2021  

    Abstract: Viral infection-induced activation of inflammasome complexes has both positive and negative effects on the host. Proper activation of inflammasome complexes induces down-stream effector mechanisms that inhibit viral replication and promote viral ... ...

    Abstract Viral infection-induced activation of inflammasome complexes has both positive and negative effects on the host. Proper activation of inflammasome complexes induces down-stream effector mechanisms that inhibit viral replication and promote viral clearance, whereas dysregulated activation has detrimental effects on the host. Coronaviruses, including SARS-CoV and MERS-CoV, encode viroporins that activate the NLRP3 inflammasome, and the severity of coronavirus disease is associated with the inflammasome activation. Although the NLRP3 inflammasome activation is implicated in the pathogenesis of coronaviruses, these viruses must evade inflammasome-mediated antiviral immune responses to establish primary replication. Screening of a complementary DNA (cDNA) library encoding 28 SARS-CoV-2 open reading frames (ORFs) showed that two nonstructural proteins (NSPs), NSP1 and NSP13, inhibited caspase-1-mediated IL-1β activation. NSP1 amino acid residues involved in host translation shutoff and NSP13 domains responsible for helicase activity were associated with caspase-1 inhibition. In THP-1 cells, both NSP1 and NSP13 significantly reduced NLRP3-inflammasome-induced caspase-1 activity and IL-1β secretion. These findings indicate that SARS-CoV-2 NSP1 and NSP13 are potent antagonists of the NLRP3 inflammasome.
    Keywords Coronavirus infections ; Severe acute respiratory syndrome coronavirus 2 ; amino acids ; caspase-1 ; complementary DNA ; inflammasomes ; pathogenesis ; secretion ; virus replication
    Language English
    Dates of publication 2021-0226
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    ZDB-ID 2720891-6
    ISSN 2076-2607
    ISSN 2076-2607
    DOI 10.3390/microorganisms9030494
    Database NAL-Catalogue (AGRICOLA)

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  9. Article ; Online: Gut microbiota promotes stem cell differentiation through macrophage and mesenchymal niches in early postnatal development.

    Kim, Ji-Eun / Li, Bo / Fei, Lijiang / Horne, Rachael / Lee, Dorothy / Loe, Adrian Kwan Ho / Miyake, Hiromu / Ayar, Eda / Gurma, Maria / Kim, Dae-Kyum / Surette, Michael G / Philpott, Dana J / Sherman, Philip / Guo, Guoji / Pierro, Agostino / Kim, Tae-Hee

    Immunity

    2023  Volume 56, Issue 9, Page(s) 2175

    Language English
    Publishing date 2023-09-13
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2023.08.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: A resource of human coronavirus protein-coding sequences in a flexible, multipurpose Gateway Entry clone collection.

    Weller, Benjamin / Lin, Chung-Wen / Pogoutse, Oxana / Sauer, Mayra / Marin-de la Rosa, Nora / Strobel, Alexandra / Young, Veronika / Knapp, Jennifer J / Rayhan, Ashyad / Falter, Claudia / Kim, Dae-Kyum / Roth, Frederick P / Falter-Braun, Pascal

    G3 (Bethesda, Md.)

    2023  Volume 13, Issue 7

    Abstract: The COVID-19 pandemic has catalyzed unprecedented scientific data and reagent sharing and collaboration, which enabled understanding the virology of the SARS-CoV-2 virus and vaccine development at record speed. The pandemic, however, has also raised ... ...

    Abstract The COVID-19 pandemic has catalyzed unprecedented scientific data and reagent sharing and collaboration, which enabled understanding the virology of the SARS-CoV-2 virus and vaccine development at record speed. The pandemic, however, has also raised awareness of the danger posed by the family of coronaviruses, of which 7 are known to infect humans and dozens have been identified in reservoir species, such as bats, rodents, or livestock. To facilitate understanding the commonalities and specifics of coronavirus infections and aspects of viral biology that determine their level of lethality to the human host, we have generated a collection of freely available clones encoding nearly all human coronavirus proteins known to date. We hope that this flexible, Gateway-compatible vector collection will encourage further research into the interactions of coronaviruses with their human host, to increase preparedness for future zoonotic viral outbreaks.
    MeSH term(s) Humans ; COVID-19/epidemiology ; SARS-CoV-2/genetics ; Pandemics
    Language English
    Publishing date 2023-06-02
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2629978-1
    ISSN 2160-1836 ; 2160-1836
    ISSN (online) 2160-1836
    ISSN 2160-1836
    DOI 10.1093/g3journal/jkad105
    Database MEDical Literature Analysis and Retrieval System OnLINE

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