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  1. Article ; Online: Primary Human M2 Macrophage Subtypes Are Distinguishable by Aqueous Metabolite Profiles.

    Fuchs, Amanda L / Costello, Stephanann M / Schiller, Sage M / Tripet, Brian P / Copié, Valérie

    International journal of molecular sciences

    2024  Volume 25, Issue 4

    Abstract: The complexity of macrophage (MΦ) plasticity and polarization states, which include classically activated pro-inflammatory (M1) and alternatively activated anti-inflammatory (M2) MΦ phenotypes, is becoming increasingly appreciated. Within the M2 MΦ ... ...

    Abstract The complexity of macrophage (MΦ) plasticity and polarization states, which include classically activated pro-inflammatory (M1) and alternatively activated anti-inflammatory (M2) MΦ phenotypes, is becoming increasingly appreciated. Within the M2 MΦ polarization state, M2a, M2b, M2c, and M2d MΦ subcategories have been defined based on their expression of specific cell surface receptors, secreted cytokines, and specialized immune effector functions. The importance of immunometabolic networks in mediating the function and regulation of MΦ immune responses is also being increasingly recognized, although the exact mechanisms and extent of metabolic modulation of MΦ subtype phenotypes and functions remain incompletely understood. In this study, proton (
    MeSH term(s) Humans ; Macrophages/metabolism ; Cytokines/metabolism ; Phenotype ; Receptors, Cell Surface/metabolism ; Macrophage Activation ; Cell Differentiation
    Chemical Substances Cytokines ; Receptors, Cell Surface
    Language English
    Publishing date 2024-02-18
    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/ijms25042407
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: A Comprehensive NMR Analysis of Serum and Fecal Metabolites in Familial Dysautonomia Patients Reveals Significant Metabolic Perturbations.

    Costello, Stephanann M / Cheney, Alexandra M / Waldum, Annie / Tripet, Brian / Cotrina-Vidal, Maria / Kaufmann, Horacio / Norcliffe-Kaufmann, Lucy / Lefcort, Frances / Copié, Valérie

    Metabolites

    2023  Volume 13, Issue 3

    Abstract: Central metabolism has a profound impact on the clinical phenotypes and penetrance of neurological diseases such as Alzheimer's (AD) and Parkinson's (PD) diseases, Amyotrophic Lateral Sclerosis (ALS) and Autism Spectrum Disorder (ASD). In contrast to the ...

    Abstract Central metabolism has a profound impact on the clinical phenotypes and penetrance of neurological diseases such as Alzheimer's (AD) and Parkinson's (PD) diseases, Amyotrophic Lateral Sclerosis (ALS) and Autism Spectrum Disorder (ASD). In contrast to the multifactorial origin of these neurological diseases, neurodevelopmental impairment and neurodegeneration in Familial Dysautonomia (FD) results from a single point mutation in the
    Language English
    Publishing date 2023-03-16
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662251-8
    ISSN 2218-1989
    ISSN 2218-1989
    DOI 10.3390/metabo13030433
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Gut microbiome dysbiosis drives metabolic dysfunction in Familial dysautonomia.

    Cheney, Alexandra M / Costello, Stephanann M / Pinkham, Nicholas V / Waldum, Annie / Broadaway, Susan C / Cotrina-Vidal, Maria / Mergy, Marc / Tripet, Brian / Kominsky, Douglas J / Grifka-Walk, Heather M / Kaufmann, Horacio / Norcliffe-Kaufmann, Lucy / Peach, Jesse T / Bothner, Brian / Lefcort, Frances / Copié, Valérie / Walk, Seth T

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 218

    Abstract: Familial dysautonomia (FD) is a rare genetic neurologic disorder caused by impaired neuronal development and progressive degeneration of both the peripheral and central nervous systems. FD is monogenic, with >99.4% of patients sharing an identical point ... ...

    Abstract Familial dysautonomia (FD) is a rare genetic neurologic disorder caused by impaired neuronal development and progressive degeneration of both the peripheral and central nervous systems. FD is monogenic, with >99.4% of patients sharing an identical point mutation in the elongator acetyltransferase complex subunit 1 (ELP1) gene, providing a relatively simple genetic background in which to identify modifiable factors that influence pathology. Gastrointestinal symptoms and metabolic deficits are common among FD patients, which supports the hypothesis that the gut microbiome and metabolome are altered and dysfunctional compared to healthy individuals. Here we show significant differences in gut microbiome composition (16 S rRNA gene sequencing of stool samples) and NMR-based stool and serum metabolomes between a cohort of FD patients (~14% of patients worldwide) and their cohabitating, healthy relatives. We show that key observations in human subjects are recapitulated in a neuron-specific Elp1-deficient mouse model, and that cohousing mutant and littermate control mice ameliorates gut microbiome dysbiosis, improves deficits in gut transit, and reduces disease severity. Our results provide evidence that neurologic deficits in FD alter the structure and function of the gut microbiome, which shifts overall host metabolism to perpetuate further neurodegeneration.
    MeSH term(s) Humans ; Mice ; Animals ; Dysautonomia, Familial/genetics ; Gastrointestinal Microbiome ; Dysbiosis/metabolism ; Neurons/metabolism ; Central Nervous System/metabolism
    Language English
    Publishing date 2023-01-13
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-35787-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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