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  1. Article ; Online: How Microbiota-Derived Metabolites Link the Gut to the Brain during Neuroinflammation.

    Rebeaud, Jessica / Peter, Benjamin / Pot, Caroline

    International journal of molecular sciences

    2022  Volume 23, Issue 17

    Abstract: Microbiota-derived metabolites are important molecules connecting the gut to the brain. Over the last decade, several studies have highlighted the importance of gut-derived metabolites in the development of multiple sclerosis (MS). Indeed, microbiota- ... ...

    Abstract Microbiota-derived metabolites are important molecules connecting the gut to the brain. Over the last decade, several studies have highlighted the importance of gut-derived metabolites in the development of multiple sclerosis (MS). Indeed, microbiota-derived metabolites modulate the immune system and affect demyelination. Here, we discuss the current knowledge about microbiota-derived metabolites implications in MS and in different mouse models of neuroinflammation. We focus on the main families of microbial metabolites that play a role during neuroinflammation. A better understanding of the role of those metabolites may lead to new therapeutical avenues to treat neuroinflammatory diseases targeting the gut-brain axis.
    MeSH term(s) Animals ; Brain/metabolism ; Gastrointestinal Microbiome ; Mice ; Microbiota ; Multiple Sclerosis/metabolism ; Neuroinflammatory Diseases
    Language English
    Publishing date 2022-09-04
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms231710128
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Lowering blood cholesterol does not affect neuroinflammation in experimental autoimmune encephalomyelitis.

    Vigne, Solenne / Duc, Donovan / Peter, Benjamin / Rebeaud, Jessica / Yersin, Yannick / Ruiz, Florian / Bressoud, Valentine / Collet, Tinh-Hai / Pot, Caroline

    Journal of neuroinflammation

    2022  Volume 19, Issue 1, Page(s) 42

    Abstract: Background: Multiple sclerosis (MS) is a chronic disabling disease of the central nervous system (CNS) commonly affecting young adults. There is increasing evidence that environmental factors are important in the development and course of MS. The ... ...

    Abstract Background: Multiple sclerosis (MS) is a chronic disabling disease of the central nervous system (CNS) commonly affecting young adults. There is increasing evidence that environmental factors are important in the development and course of MS. The metabolic syndrome (MetS) which comprises dyslipidemia has been associated with a worse outcome in MS disease. Furthermore, the lipid-lowering drug class of statins has been proposed to improve MS disease course. However, cholesterol is also rate-limiting for myelin biogenesis and promotes remyelination in MS animal models. Thus, the impact of circulating blood cholesterol levels during the disease remains debated and controversial.
    Methods: We assessed the role of circulating cholesterol on the murine model of MS, the experimental autoimmune encephalomyelitis (EAE) disease using two different approaches: (1) the mouse model of familial hypercholesterolemia induced by low-density lipoprotein receptor (LDLr) deficiency, and (2) the use of the monoclonal anti-PCSK9 neutralizing antibody alirocumab, which reduces LDLr degradation and consequently lowers blood levels of cholesterol.
    Results: Elevated blood cholesterol levels induced by LDLr deficiency did not worsen clinical symptoms of mice during EAE. In addition, we observed that the anti-PCSK9 antibody alirocumab did not influence EAE disease course, nor modulate the immune response in EAE.
    Conclusions: These findings suggest that blood cholesterol level has no direct role in neuro-inflammatory diseases and that the previously shown protective effects of statins in MS are not related to circulating cholesterol.
    MeSH term(s) Animals ; Encephalomyelitis, Autoimmune, Experimental/drug therapy ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ; Hypercholesterolemia/metabolism ; Mice ; Multiple Sclerosis ; Neuroinflammatory Diseases
    Chemical Substances Hydroxymethylglutaryl-CoA Reductase Inhibitors
    Language English
    Publishing date 2022-02-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 2156455-3
    ISSN 1742-2094 ; 1742-2094
    ISSN (online) 1742-2094
    ISSN 1742-2094
    DOI 10.1186/s12974-022-02409-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Endothelial cell-derived oxysterol ablation attenuates experimental autoimmune encephalomyelitis.

    Ruiz, Florian / Peter, Benjamin / Rebeaud, Jessica / Vigne, Solenne / Bressoud, Valentine / Roumain, Martin / Wyss, Tania / Yersin, Yannick / Wagner, Ingrid / Kreutzfeldt, Mario / Pimentel Mendes, Marisa / Kowalski, Camille / Boivin, Gael / Roth, Leonard / Schwaninger, Markus / Merkler, Doron / Muccioli, Giulio G / Hugues, Stephanie / Petrova, Tatiana V /
    Pot, Caroline

    EMBO reports

    2023  Volume 24, Issue 3, Page(s) e55328

    Abstract: The vasculature is a key regulator of leukocyte trafficking into the central nervous system (CNS) during inflammatory diseases including multiple sclerosis (MS). However, the impact of endothelial-derived factors on CNS immune responses remains unknown. ... ...

    Abstract The vasculature is a key regulator of leukocyte trafficking into the central nervous system (CNS) during inflammatory diseases including multiple sclerosis (MS). However, the impact of endothelial-derived factors on CNS immune responses remains unknown. Bioactive lipids, in particular oxysterols downstream of Cholesterol-25-hydroxylase (Ch25h), promote neuroinflammation but their functions in the CNS are not well-understood. Using floxed-reporter Ch25h knock-in mice, we trace Ch25h expression to CNS endothelial cells (ECs) and myeloid cells and demonstrate that Ch25h ablation specifically from ECs attenuates experimental autoimmune encephalomyelitis (EAE). Mechanistically, inflamed Ch25h-deficient CNS ECs display altered lipid metabolism favoring polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC) expansion, which suppresses encephalitogenic T lymphocyte proliferation. Additionally, endothelial Ch25h-deficiency combined with immature neutrophil mobilization into the blood circulation nearly completely protects mice from EAE. Our findings reveal a central role for CNS endothelial Ch25h in promoting neuroinflammation by inhibiting the expansion of immunosuppressive myeloid cell populations.
    MeSH term(s) Mice ; Animals ; Encephalomyelitis, Autoimmune, Experimental ; Endothelial Cells/metabolism ; Oxysterols/metabolism ; Neuroinflammatory Diseases ; Central Nervous System/metabolism ; Mice, Inbred C57BL
    Chemical Substances Oxysterols
    Language English
    Publishing date 2023-01-30
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.15252/embr.202255328
    Database MEDical Literature Analysis and Retrieval System OnLINE

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