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  1. Book ; Online: Innate Immunity Programming and Memory in Resolving and Non-Resolving Inflammation

    Li, Liwu / McCall, Charles E. / Hu, Xiaoyu

    2020  

    Keywords Medicine ; Immunology ; innate immune memory ; inflammation dynamics ; resolving and non-resolving inflammation ; acute disease ; chronic disease
    Size 1 electronic resource (139 pages)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021231196
    ISBN 9782889635825 ; 2889635821
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article ; Online: The pyruvate dehydrogenase complex: Life's essential, vulnerable and druggable energy homeostat.

    Stacpoole, Peter W / McCall, Charles E

    Mitochondrion

    2023  Volume 70, Page(s) 59–102

    Abstract: Found in all organisms, pyruvate dehydrogenase complexes (PDC) are the keystones of prokaryotic and eukaryotic energy metabolism. In eukaryotic organisms these multi-component megacomplexes provide a crucial mechanistic link between cytoplasmic ... ...

    Abstract Found in all organisms, pyruvate dehydrogenase complexes (PDC) are the keystones of prokaryotic and eukaryotic energy metabolism. In eukaryotic organisms these multi-component megacomplexes provide a crucial mechanistic link between cytoplasmic glycolysis and the mitochondrial tricarboxylic acid (TCA) cycle. As a consequence, PDCs also influence the metabolism of branched chain amino acids, lipids and, ultimately, oxidative phosphorylation (OXPHOS). PDC activity is an essential determinant of the metabolic and bioenergetic flexibility of metazoan organisms in adapting to changes in development, nutrient availability and various stresses that challenge maintenance of homeostasis. This canonical role of the PDC has been extensively probed over the past decades by multidisciplinary investigations into its causal association with diverse physiological and pathological conditions, the latter making the PDC an increasingly viable therapeutic target. Here we review the biology of the remarkable PDC and its emerging importance in the pathobiology and treatment of diverse congenital and acquired disorders of metabolic integration.
    MeSH term(s) Animals ; Pyruvate Dehydrogenase Complex/chemistry ; Pyruvate Dehydrogenase Complex/metabolism ; Energy Metabolism ; Oxidative Phosphorylation ; Citric Acid Cycle/physiology ; Glycolysis
    Chemical Substances Pyruvate Dehydrogenase Complex
    Language English
    Publishing date 2023-03-01
    Publishing country Netherlands
    Document type Journal Article ; Review ; Research Support, U.S. Gov't, P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 2056923-3
    ISSN 1872-8278 ; 1567-7249
    ISSN (online) 1872-8278
    ISSN 1567-7249
    DOI 10.1016/j.mito.2023.02.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Glutathionylation of Pyruvate Dehydrogenase Complex E2 and Inflammatory Cytokine Production During Acute Inflammation Are Magnified By Mitochondrial Oxidative Stress.

    Long, David L / McCall, Charles E / Poole, Leslie B

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Lipopolysaccharide (LPS) is a known inducer of inflammatory signaling which triggers generation of reactive oxygen species (ROS) and cell death in responsive cells like THP-1 promonocytes and freshly isolated human monocytes. A key LPS-responsive ... ...

    Abstract Lipopolysaccharide (LPS) is a known inducer of inflammatory signaling which triggers generation of reactive oxygen species (ROS) and cell death in responsive cells like THP-1 promonocytes and freshly isolated human monocytes. A key LPS-responsive metabolic pivot point is the 9 megadalton mitochondrial pyruvate dehydrogenase complex (PDC), which provides pyruvate dehydrogenase (E1), lipoamide-linked transacetylase (E2) and lipoamide dehydrogenase (E3) activities to produce acetyl-CoA from pyruvate. While phosphorylation-dependent decreases in PDC activity following LPS treatment or sepsis have been deeply investigated, redox-linked processes have received less attention. Data presented here demonstrate that LPS-induced reversible oxidation within PDC occurs in PDCE2 in both THP-1 cells and primary human monocytes. Knockout of PDCE2 by CRISPR and expression of FLAG-tagged PDCE2 in THP-1 cells demonstrated that LPS-induced glutathionylation is associated with wild type PDCE2 but not mutant protein lacking the lipoamide-linking lysine residues. Moreover, the mitochondrially-targeted electrophile MitoCDNB, which impairs both glutathione- and thioredoxin-based reductase systems, elevates ROS similar to LPS but does not cause PDCE2 glutathionylation. However, LPS and MitoCDNB together are highly synergistic for PDCE2 glutathionylation, ROS production, and cell death. Surprisingly, the two treatments together had differential effects on cytokine production; pro-inflammatory IL-1β production was enhanced by the co-treatment, while IL-10, an important anti-inflammatory cytokine, dropped precipitously compared to LPS treatment alone. This new information may expand opportunities to understand and modulate PDC redox status and activity and improve the outcomes of pathological inflammation.
    Language English
    Publishing date 2023-08-04
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.01.26.525791
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Glutathionylation of pyruvate dehydrogenase complex E2 and inflammatory cytokine production during acute inflammation are magnified by mitochondrial oxidative stress.

    Long, David L / McCall, Charles E / Poole, Leslie B

    Redox biology

    2023  Volume 65, Page(s) 102841

    Abstract: Lipopolysaccharide (LPS) is a known inducer of inflammatory signaling which triggers generation of reactive oxygen species (ROS) and cell death in responsive cells like THP-1 promonocytes and freshly isolated human monocytes. A key LPS-responsive ... ...

    Abstract Lipopolysaccharide (LPS) is a known inducer of inflammatory signaling which triggers generation of reactive oxygen species (ROS) and cell death in responsive cells like THP-1 promonocytes and freshly isolated human monocytes. A key LPS-responsive metabolic pivot point is the 9 MDa mitochondrial pyruvate dehydrogenase complex (PDC), which provides pyruvate dehydrogenase (E1), lipoamide-linked transacetylase (E2) and lipoamide dehydrogenase (E3) activities to produce acetyl-CoA from pyruvate. While phosphorylation-dependent decreases in PDC activity following LPS treatment or sepsis have been deeply investigated, redox-linked processes have received less attention. Data presented here demonstrate that LPS-induced reversible oxidation within PDC occurs in PDCE2 in both THP-1 cells and primary human monocytes. Knockout of PDCE2 by CRISPR and expression of FLAG-tagged PDCE2 in THP-1 cells demonstrated that LPS-induced glutathionylation is associated with wild type PDCE2 but not mutant protein lacking the lipoamide-linking lysine residues. Moreover, the mitochondrially-targeted electrophile MitoCDNB, which impairs both glutathione- and thioredoxin-based reductase systems, elevates ROS similar to LPS but does not cause PDCE2 glutathionylation. However, LPS and MitoCDNB together are highly synergistic for PDCE2 glutathionylation, ROS production, and cell death. Surprisingly, the two treatments together had differential effects on cytokine production; pro-inflammatory IL-1β production was enhanced by the co-treatment, while IL-10, an important anti-inflammatory cytokine, dropped precipitously compared to LPS treatment alone. This new information may expand opportunities to understand and modulate PDC redox status and activity and improve the outcomes of pathological inflammation.
    MeSH term(s) Humans ; Dihydrolipoyllysine-Residue Acetyltransferase/genetics ; Dihydrolipoyllysine-Residue Acetyltransferase/metabolism ; Reactive Oxygen Species/metabolism ; Lipopolysaccharides ; Oxidative Stress ; Inflammation ; Pyruvates ; Cytokines/metabolism
    Chemical Substances Dihydrolipoyllysine-Residue Acetyltransferase (EC 2.3.1.12) ; Reactive Oxygen Species ; Lipopolysaccharides ; Pyruvates ; Cytokines
    Language English
    Publishing date 2023-08-06
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2023.102841
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Editorial: The Roles of Mitochondria in Immunity.

    Patil, Naeem K / Bohannon, Julia K / Vachharajani, Vidula / McCall, Charles E

    Frontiers in immunology

    2022  Volume 13, Page(s) 914639

    MeSH term(s) Mitochondria ; Reactive Oxygen Species
    Chemical Substances Reactive Oxygen Species
    Language English
    Publishing date 2022-05-16
    Publishing country Switzerland
    Document type Editorial ; Research Support, N.I.H., Extramural
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.914639
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Temporal associations of plasma levels of the secreted phospholipase A

    Lu, Eric / Hara, Aki / Sun, Shudong / Hallmark, Brian / Snider, Justin M / Seeds, Michael C / Watkins, Joseph C / McCall, Charles E / Zhang, Hao Helen / Yao, Guang / Chilton, Floyd H

    European journal of immunology

    2024  , Page(s) e2350721

    Abstract: Previous research suggests that group IIA-secreted phospholipase ... ...

    Abstract Previous research suggests that group IIA-secreted phospholipase A
    Language English
    Publishing date 2024-04-23
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 120108-6
    ISSN 1521-4141 ; 0014-2980
    ISSN (online) 1521-4141
    ISSN 0014-2980
    DOI 10.1002/eji.202350721
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 489: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
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  7. Article ; Online: Corrigendum to "IL-10 induces an immune repressor pathway in sepsis by promoting S100A9 nuclear localization and MDSC development" [Cell Immunol. 332 (2018) 32-38].

    Bah, Isatou / Kumbhare, Ajinkya / Nguyen, Lam / McCall, Charles E / El Gazzar, Mohamed

    Cellular immunology

    2022  Volume 378, Page(s) 104560

    Language English
    Publishing date 2022-06-09
    Publishing country Netherlands
    Document type Published Erratum
    ZDB-ID 80094-6
    ISSN 1090-2163 ; 0008-8749
    ISSN (online) 1090-2163
    ISSN 0008-8749
    DOI 10.1016/j.cellimm.2022.104560
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 417: Show issues Location:
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  8. Article ; Online: Sirtuins: potential therapeutic targets for regulating acute inflammatory response?

    Vachharajani, Vidula / McCall, Charles E

    Expert opinion on therapeutic targets

    2020  Volume 24, Issue 5, Page(s) 489–497

    Abstract: ... ...

    Abstract Introduction
    MeSH term(s) Acute Disease ; Animals ; Homeostasis ; Humans ; Inflammation/physiopathology ; Inflammation/therapy ; Molecular Targeted Therapy ; NAD/metabolism ; Sirtuins/metabolism
    Chemical Substances NAD (0U46U6E8UK) ; Sirtuins (EC 3.5.1.-)
    Language English
    Publishing date 2020-03-26
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2055208-7
    ISSN 1744-7631 ; 1472-8222
    ISSN (online) 1744-7631
    ISSN 1472-8222
    DOI 10.1080/14728222.2020.1743268
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Corrigendum to "Expression of C/EBPβ in myeloid progenitors during sepsis promotes immunosuppression" [Mol. Immunol. 91 (2017) 165-172].

    Dai, Jun / Kumbhare, Ajinkya / Youssef, Dima / Yao, Zhi Q / McCall, Charles E / El Gazzar, Mohamed

    Molecular immunology

    2022  Volume 150, Page(s) 246

    Language English
    Publishing date 2022-06-15
    Publishing country England
    Document type Published Erratum
    ZDB-ID 424427-8
    ISSN 1872-9142 ; 0161-5890
    ISSN (online) 1872-9142
    ISSN 0161-5890
    DOI 10.1016/j.molimm.2022.06.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 166: Show issues Location:
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  10. Article ; Online: Inhibiting KDM6A Demethylase Represses Long Non-Coding RNA Hotairm1 Transcription in MDSC During Sepsis.

    Bah, Isatou / Youssef, Dima / Yao, Zhi Q / McCall, Charles E / El Gazzar, Mohamed

    Frontiers in immunology

    2022  Volume 13, Page(s) 823660

    Abstract: Myeloid-derived suppressor cells (MDSCs) prolong sepsis by promoting immunosuppression. We reported that sepsis MDSC development requires long non-coding RNA Hotairm1 interactions with S100A9. Using a mouse model that simulates the immunobiology of ... ...

    Abstract Myeloid-derived suppressor cells (MDSCs) prolong sepsis by promoting immunosuppression. We reported that sepsis MDSC development requires long non-coding RNA Hotairm1 interactions with S100A9. Using a mouse model that simulates the immunobiology of sepsis, we find that histone demethylase KDM6A promotes Hotairm1 transcription by demethylating transcription repression H3K27me3 histone mark. We show that chemical targeting of KDM6A by GSK-J4 represses Hotairm1 transcription, which coincides with decreases in transcription activation H3K4me3 histone mark and transcription factor PU.1 binding to the Hotairm1 promoter. We further show that immunosuppressive IL-10 cytokine promotes KDM6A binding at the Hotairm1 promoter. IL-10 knockdown repletes H3K27me3 and reduces Hotairm1 transcription. GSK-J4 treatment also relocalizes nuclear S100A9 protein to the cytosol. To support translation to human sepsis, we demonstrate that inhibiting H3K27me3 demethylation by KDM6A ex vivo in MDSCs from patients with protracted sepsis decreases Hotairm1 transcription. These findings suggest that epigenetic targeting of MDSCs in human sepsis might resolve post-sepsis immunosuppression and improve sepsis survival.
    MeSH term(s) Animals ; Benzazepines/pharmacology ; Calgranulin B/metabolism ; Histone Code ; Histone Demethylases/metabolism ; Histones/genetics ; Histones/metabolism ; Humans ; Immunosuppression Therapy ; Interleukin-10/genetics ; Interleukin-10/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Myeloid-Derived Suppressor Cells/metabolism ; Pyrimidines/pharmacology ; Sepsis/metabolism ; Sepsis/pathology
    Chemical Substances Benzazepines ; Calgranulin B ; GSK-J4 ; Histones ; IL10 protein, human ; MicroRNAs ; Pyrimidines ; histone H3 trimethyl Lys4 ; long non-coding RNA HOTAIRM1, human ; Interleukin-10 (130068-27-8) ; Histone Demethylases (EC 1.14.11.-) ; KDM6A protein, human (EC 1.14.11.-)
    Language English
    Publishing date 2022-01-28
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.823660
    Database MEDical Literature Analysis and Retrieval System OnLINE

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