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  1. Article ; Online: Host and microbial regulation of mitochondrial reactive oxygen species during mycobacterial infections.

    Kyung Kim, Jin / Jo, Eun-Kyeong

    Mitochondrion

    2024  Volume 75, Page(s) 101852

    Abstract: Mycobacteria, including Mycobacterium tuberculosis (Mtb) and non-tuberculous mycobacteria (NTM), pose challenges in treatment due to their increased resistance to antibiotics. Following infection, mycobacteria and their components trigger robust innate ... ...

    Abstract Mycobacteria, including Mycobacterium tuberculosis (Mtb) and non-tuberculous mycobacteria (NTM), pose challenges in treatment due to their increased resistance to antibiotics. Following infection, mycobacteria and their components trigger robust innate and inflammatory immune responses intricately associated with the modulation of mitochondrial functions, including oxidative phosphorylation (OXPHOS) and metabolism. Certainly, mitochondrial reactive oxygen species (mtROS) are an inevitable by-product of OXPHOS and function as a bactericidal weapon; however, an excessive accumulation of mtROS are linked to pathological inflammation and necroptotic cell death during mycobacterial infection. Despite previous studies outlining various host pathways involved in regulating mtROS levels during antimicrobial responses in mycobacterial infection, our understanding of the precise mechanisms orchestrating the fine regulation of this response remains limited. Emerging evidence suggests that mycobacterial proteins play a role in targeting the mitochondria of the host, indicating the potential influence of microbial factors on mitochondrial functions within host cells. In this review, we provide an overview of how both host and Mtb factors influence mtROS generation during infection. A comprehensive study of host and microbial factors that target mtROS will shed light on innovative approaches for effectively managing drug-resistant mycobacterial infections.
    MeSH term(s) Humans ; Reactive Oxygen Species/metabolism ; Mycobacterium tuberculosis ; Anti-Bacterial Agents ; Inflammation/metabolism ; Mitochondria/metabolism
    Chemical Substances Reactive Oxygen Species ; Anti-Bacterial Agents
    Language English
    Publishing date 2024-02-13
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2056923-3
    ISSN 1872-8278 ; 1567-7249
    ISSN (online) 1872-8278
    ISSN 1567-7249
    DOI 10.1016/j.mito.2024.101852
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Interplay between host and pathogen: immune defense and beyond.

    Jo, Eun-Kyeong

    Experimental & molecular medicine

    2019  Volume 51, Issue 12, Page(s) 1–3

    MeSH term(s) Animals ; Host-Pathogen Interactions ; Humans ; Immunity, Innate/physiology ; Interferon-gamma/metabolism ; Nitric Oxide Synthase Type II/metabolism ; Th1 Cells/metabolism
    Chemical Substances Interferon-gamma (82115-62-6) ; Nitric Oxide Synthase Type II (EC 1.14.13.39)
    Language English
    Publishing date 2019-12-11
    Publishing country United States
    Document type Editorial
    ZDB-ID 1328915-9
    ISSN 2092-6413 ; 1226-3613 ; 0378-8512
    ISSN (online) 2092-6413
    ISSN 1226-3613 ; 0378-8512
    DOI 10.1038/s12276-019-0281-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: TNF in Human Tuberculosis: A Double-Edged Sword.

    Yuk, Jae-Min / Kim, Jin Kyung / Kim, In Soo / Jo, Eun-Kyeong

    Immune network

    2024  Volume 24, Issue 1, Page(s) e4

    Abstract: TNF, a pleiotropic proinflammatory cytokine, is important for protective immunity and immunopathology ... ...

    Abstract TNF, a pleiotropic proinflammatory cytokine, is important for protective immunity and immunopathology during
    Language English
    Publishing date 2024-01-26
    Publishing country Korea (South)
    Document type Journal Article ; Review
    ZDB-ID 2536191-0
    ISSN 2092-6685 ; 1598-2629
    ISSN (online) 2092-6685
    ISSN 1598-2629
    DOI 10.4110/in.2024.24.e4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Peroxisome Proliferator-Activated Receptor-Targeted Therapies: Challenges upon Infectious Diseases.

    Kim, In Soo / Silwal, Prashanta / Jo, Eun-Kyeong

    Cells

    2023  Volume 12, Issue 4

    Abstract: Peroxisome proliferator-activated receptors (PPARs) α, β, and γ are nuclear receptors that orchestrate the transcriptional regulation of genes involved in a variety of biological responses, such as energy metabolism and homeostasis, regulation of ... ...

    Abstract Peroxisome proliferator-activated receptors (PPARs) α, β, and γ are nuclear receptors that orchestrate the transcriptional regulation of genes involved in a variety of biological responses, such as energy metabolism and homeostasis, regulation of inflammation, cellular development, and differentiation. The many roles played by the PPAR signaling pathways indicate that PPARs may be useful targets for various human diseases, including metabolic and inflammatory conditions and tumors. Accumulating evidence suggests that each PPAR plays prominent but different roles in viral, bacterial, and parasitic infectious disease development. In this review, we discuss recent PPAR research works that are focused on how PPARs control various infections and immune responses. In addition, we describe the current and potential therapeutic uses of PPAR agonists/antagonists in the context of infectious diseases. A more comprehensive understanding of the roles played by PPARs in terms of host-pathogen interactions will yield potential adjunctive personalized therapies employing PPAR-modulating agents.
    MeSH term(s) Humans ; Receptors, Cytoplasmic and Nuclear ; Gene Expression Regulation ; PPAR alpha ; Inflammation ; Communicable Diseases
    Chemical Substances Receptors, Cytoplasmic and Nuclear ; PPAR alpha
    Language English
    Publishing date 2023-02-17
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12040650
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Ginsenosides for therapeutically targeting inflammation through modulation of oxidative stress.

    Paik, Seungwha / Song, Gyu Yong / Jo, Eun-Kyeong

    International immunopharmacology

    2023  Volume 121, Page(s) 110461

    Abstract: Ginsenosides are steroid glycosides derived from ginseng plants such as Panax ginseng, Panax quinquefolium, and Panax notoginseng. Advances in recent studies have identified numerous physiological functions of each type of ginsenoside, i.e., ... ...

    Abstract Ginsenosides are steroid glycosides derived from ginseng plants such as Panax ginseng, Panax quinquefolium, and Panax notoginseng. Advances in recent studies have identified numerous physiological functions of each type of ginsenoside, i.e., immunomodulatory, antioxidative, and anti-inflammatory functions, in the context of inflammatory diseases. Accumulating evidence has revealed the molecular mechanisms by which the single or combined ginsenoside(s) exhibit anti-inflammatory effects, although it remains largely unclear. It is well known that excessive production of reactive oxygen species (ROS) is associated with pathological inflammation and cell death in a variety of cells, and that inhibition of ROS generation ameliorates the local and systemic inflammatory responses. The mechanisms by which ginsenosides attenuate inflammation are largely unknown; however, targeting ROS is suggested as one of the crucial mechanisms for the ginsenosides to control the pathological inflammation in the immune and non-immune cells. This review will summarize the latest progress in ginsenoside studies, particularly in the context of antioxidant mechanisms for its anti-inflammatory effects. A better understanding of the distinct types and the combined action of ginsenosides will pave the way for developing potential preventive and therapeutic modalities in treating various inflammation-related diseases.
    MeSH term(s) Ginsenosides/therapeutic use ; Reactive Oxygen Species/metabolism ; Oxidative Stress ; Panax notoginseng ; Antioxidants/metabolism ; Inflammation/drug therapy
    Chemical Substances Ginsenosides ; Reactive Oxygen Species ; Antioxidants
    Language English
    Publishing date 2023-06-16
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2023.110461
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Itaconate family-based host-directed therapeutics for infections.

    Yuk, Jae-Min / Park, Eun-Jin / Kim, In Soo / Jo, Eun-Kyeong

    Frontiers in immunology

    2023  Volume 14, Page(s) 1203756

    Abstract: Itaconate is a crucial anti-infective and anti-inflammatory immunometabolite that accumulates upon disruption of the Krebs cycle in effector macrophages undergoing inflammatory stress. Esterified derivatives of itaconate (4-octyl itaconate and dimethyl ... ...

    Abstract Itaconate is a crucial anti-infective and anti-inflammatory immunometabolite that accumulates upon disruption of the Krebs cycle in effector macrophages undergoing inflammatory stress. Esterified derivatives of itaconate (4-octyl itaconate and dimethyl itaconate) and its isomers (mesaconate and citraconate) are promising candidate drugs for inflammation and infection. Several itaconate family members participate in host defense, immune and metabolic modulation, and amelioration of infection, although opposite effects have also been reported. However, the precise mechanisms by which itaconate and its family members exert its effects are not fully understood. In addition, contradictory results in different experimental settings and a lack of clinical data make it difficult to draw definitive conclusions about the therapeutic potential of itaconate. Here we review how the immune response gene 1-itaconate pathway is activated during infection and its role in host defense and pathogenesis in a context-dependent manner. Certain pathogens can use itaconate to establish infections. Finally, we briefly discuss the major mechanisms by which itaconate family members exert antimicrobial effects. To thoroughly comprehend how itaconate exerts its anti-inflammatory and antimicrobial effects, additional research on the actual mechanism of action is necessary. This review examines the current state of itaconate research in infection and identifies the key challenges and opportunities for future research in this field.
    MeSH term(s) Humans ; Anti-Inflammatory Agents/therapeutic use ; Inflammation/metabolism
    Chemical Substances itaconic acid (Q4516562YH) ; Anti-Inflammatory Agents
    Language English
    Publishing date 2023-05-16
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1203756
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Editorial: Host-pathogen interactions in nontuberculous mycobacterial infections.

    Lorè, Nicola Ivan / Yamasaki, Sho / Simmonds, Rachel E / Jo, Eun-Kyeong

    Frontiers in immunology

    2023  Volume 14, Page(s) 1201159

    Language English
    Publishing date 2023-05-26
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1201159
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Itaconate, Arginine, and Gamma-Aminobutyric Acid: A Host Metabolite Triad Protective Against Mycobacterial Infection.

    Kim, Jin Kyung / Park, Eun-Jin / Jo, Eun-Kyeong

    Frontiers in immunology

    2022  Volume 13, Page(s) 832015

    Abstract: Immune metabolic regulation shapes the host-pathogen interaction during infection ... ...

    Abstract Immune metabolic regulation shapes the host-pathogen interaction during infection with
    MeSH term(s) Animals ; Arginine/metabolism ; Autophagy ; Host-Pathogen Interactions ; Humans ; Immunity, Innate ; Macrophages/immunology ; Macrophages/microbiology ; Mycobacterium tuberculosis/pathogenicity ; Succinates/metabolism ; Tuberculosis/immunology ; Tuberculosis/metabolism ; gamma-Aminobutyric Acid/metabolism
    Chemical Substances Succinates ; gamma-Aminobutyric Acid (56-12-2) ; Arginine (94ZLA3W45F) ; itaconic acid (Q4516562YH)
    Language English
    Publishing date 2022-02-04
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.832015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Sirtuin 1 in Host Defense during Infection.

    Kim, Jin Kyung / Silwal, Prashanta / Jo, Eun-Kyeong

    Cells

    2022  Volume 11, Issue 18

    Abstract: Sirtuins (SIRTs) are members of the class III histone deacetylase family and epigenetically control multiple target genes to modulate diverse biological responses in cells. Among the SIRTs, SIRT1 is the most well-studied, with a role in the modulation of ...

    Abstract Sirtuins (SIRTs) are members of the class III histone deacetylase family and epigenetically control multiple target genes to modulate diverse biological responses in cells. Among the SIRTs, SIRT1 is the most well-studied, with a role in the modulation of immune and inflammatory responses following infection. The functions of SIRT1 include orchestrating immune, inflammatory, metabolic, and autophagic responses, all of which are required in establishing and controlling host defenses during infection. In this review, we summarize recent information on the roles of SIRT1 and its regulatory mechanisms during bacterial, viral, and parasitic infections. We also discuss several SIRT1 modulators, as potential antimicrobial treatments. Understanding the function of SIRT1 in balancing immune homeostasis will contribute to the development of new therapeutics for the treatment of infection and inflammatory disease.
    MeSH term(s) Autophagy ; Sirtuin 1/metabolism ; Sirtuins/metabolism
    Chemical Substances Sirtuin 1 (EC 3.5.1.-) ; Sirtuins (EC 3.5.1.-)
    Language English
    Publishing date 2022-09-19
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11182921
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  10. Article ; Online: An Interplay Between Autophagy and Immunometabolism for Host Defense Against Mycobacterial Infection.

    Paik, Seungwha / Jo, Eun-Kyeong

    Frontiers in immunology

    2020  Volume 11, Page(s) 603951

    Abstract: Autophagy, an intracellular catabolic pathway featuring lysosomal degradation, is a central component of the host immune defense against various infections ... ...

    Abstract Autophagy, an intracellular catabolic pathway featuring lysosomal degradation, is a central component of the host immune defense against various infections including
    MeSH term(s) AMP-Activated Protein Kinases/metabolism ; Animals ; Autophagy ; Host-Pathogen Interactions ; Humans ; Immunity, Innate ; Mycobacterium tuberculosis/immunology ; Mycobacterium tuberculosis/metabolism ; Mycobacterium tuberculosis/pathogenicity ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism ; Tuberculosis/immunology ; Tuberculosis/metabolism ; Tuberculosis/microbiology
    Chemical Substances TOR Serine-Threonine Kinases (EC 2.7.1.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
    Language English
    Publishing date 2020-11-12
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2020.603951
    Database MEDical Literature Analysis and Retrieval System OnLINE

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