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Article ; Online: [Gut environment and multiple sclerosis].

Miyake, Sachiko / Noto, Daisuke

2021 Volume 61, Issue 9, Page(s) 583–587

Abstract: Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) and T cell-mediated autoimmune processes are assumed to be involved in its pathogenesis. Recently, accumulating evidence has indicated that commensal ... ...

Abstract	Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) and T cell-mediated autoimmune processes are assumed to be involved in its pathogenesis. Recently, accumulating evidence has indicated that commensal bacteria interact with the host immune system and that the alteration of commensal bacteria composition, termed dysbiosis, is associated with various autoimmune diseases including CNS autoimmune diseases. The effect of gut microbiota on disease has been initially shown in experimental autoimmune encephalomyelitis (EAE), animal model of MS. Recent analysis of microbiota revealed dysbiosis in patients with MS including the reduction of short chain fatty acid (SCFA). Administration of SCFA ameliorates disease severity of EAE in association with the induction of regulatory T cells. Moreover metabolites of microbiota such as SCFA and tryptophan have been shown to influence glial functions in CNS. In this review, we introduce recent findings regarding the interaction between gut microbiota and MS both in EAE and MS.
MeSH term(s)	Animals ; Central Nervous System ; Disease Models, Animal ; Dysbiosis/etiology ; Humans ; Multiple Sclerosis ; Neuroglia
Language	Japanese
Publishing date	2021-08-26
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	604200-4
ISSN	1882-0654 ; 0009-918X
ISSN (online)	1882-0654
ISSN	0009-918X
DOI	10.5692/clinicalneurol.cn-001590
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Article ; Online: Gut dysbiosis and multiple sclerosis.

Noto, Daisuke / Miyake, Sachiko

Clinical immunology (Orlando, Fla.)

2020 Volume 235, Page(s) 108380

Abstract: Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS) and T cell-mediated autoimmune processes are assumed to be involved in its pathogenesis. Recently, accumulating evidence has indicated that commensal bacteria interact ...

Abstract	Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS) and T cell-mediated autoimmune processes are assumed to be involved in its pathogenesis. Recently, accumulating evidence has indicated that commensal bacteria interact with the host immune system and that the alteration of commensal bacteria composition, termed dysbiosis, is associated with various autoimmune diseases including CNS autoimmune diseases. In this review, we introduce recent findings regarding the association between gut microbiota and MS and related diseases and microbiota function in an animal model of MS.
MeSH term(s)	Animals ; Dysbiosis ; Gastrointestinal Microbiome/physiology ; Humans ; Multiple Sclerosis ; T-Lymphocytes/physiology
Language	English
Publishing date	2020-03-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2020.108380
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Article ; Online: Immunoglobulin directly enhances differentiation of oligodendrocyte-precursor cells and remyelination.

Li, Yaguang / Noto, Daisuke / Hoshino, Yasunobu / Mizuno, Miho / Yoshikawa, Soichiro / Miyake, Sachiko

Scientific reports

2023 Volume 13, Issue 1, Page(s) 9394

Abstract: Multiple sclerosis (MS) is an inflammatory demyelinating disease characterized by multiple lesions in the central nervous system. Although the role of B cells in MS pathogenesis has attracted much attention, but the detailed mechanisms remain unclear. To ...

Abstract	Multiple sclerosis (MS) is an inflammatory demyelinating disease characterized by multiple lesions in the central nervous system. Although the role of B cells in MS pathogenesis has attracted much attention, but the detailed mechanisms remain unclear. To investigate the effects of B cells on demyelination, we analyzed a cuprizone-induced demyelination model, and found that demyelination was significantly exacerbated in B cell-deficient mice. We next investigated whether immunoglobulin affected the myelin formation process using organotypic brain slice cultures and revealed that remyelination was improved in immunoglobulin-treated groups compared with the control group. Analysis of oligodendrocyte-precursor cell (OPC) monocultures showed that immunoglobulins directly affected on OPCs and promoted their differentiation and myelination. Furthermore, OPCs expressed FcγRI and FcγRIII, two receptors that were revealed to mediate the effects of IgG. To the best of our knowledge, this is the first study to demonstrate that B cells act in an inhibitory manner against cuprizone-induced demyelination, while immunoglobulins enhance remyelination following demyelination. Analysis of the culture system revealed that immunoglobulins directly act on OPCs to promote their differentiation and myelination. Future studies to elucidate the effects of immunoglobulins on OPCs in vivo and the detailed mechanisms of these effects may lead to new treatments for demyelinating diseases.
MeSH term(s)	Mice ; Animals ; Remyelination ; Oligodendroglia/pathology ; Cuprizone/pharmacology ; Cell Differentiation ; Immunoglobulins/pharmacology ; Multiple Sclerosis/pathology ; Mice, Inbred C57BL ; Myelin Sheath/physiology ; Disease Models, Animal
Chemical Substances	Cuprizone (5N16U7E0AO) ; Immunoglobulins
Language	English
Publishing date	2023-06-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-36532-3
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Article ; Online: Author Correction: Immunoglobulin directly enhances differentiation of oligodendrocyte-precursor cells and remyelination.

Li, Yaguang / Noto, Daisuke / Hoshino, Yasunobu / Mizuno, Miho / Yoshikawa, Soichiro / Miyake, Sachiko

Scientific reports

2023 Volume 13, Issue 1, Page(s) 12995

Language	English
Publishing date	2023-08-10
Publishing country	England
Document type	Published Erratum
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-40118-4
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Article ; Online: Dysregulated B cell differentiation towards antibody-secreting cells in neuromyelitis optica spectrum disorder.

Hoshino, Yasunobu / Noto, Daisuke / Sano, Shuhei / Tomizawa, Yuji / Yokoyama, Kazumasa / Hattori, Nobutaka / Miyake, Sachiko

Journal of neuroinflammation

2022 Volume 19, Issue 1, Page(s) 6

Abstract: Background: Anti-aquaporin 4 (AQP4) antibody (AQP4-Ab) is involved in the pathogenesis of neuromyelitis optica spectrum disorder (NMOSD). However, the mechanism involved in AQP4-Ab production remains unclear.: Methods: We analyzed the ... ...

Abstract	Background: Anti-aquaporin 4 (AQP4) antibody (AQP4-Ab) is involved in the pathogenesis of neuromyelitis optica spectrum disorder (NMOSD). However, the mechanism involved in AQP4-Ab production remains unclear. Methods: We analyzed the immunophenotypes of patients with NMOSD and other neuroinflammatory diseases as well as healthy controls (HC) using flow cytometry. Transcriptome analysis of B cell subsets obtained from NMOSD patients and HCs was performed. The differentiation capacity of B cell subsets into antibody-secreting cells was analyzed. Results: The frequencies of switched memory B (SMB) cells and plasmablasts were increased and that of naïve B cells was decreased in NMOSD patients compared with relapsing-remitting multiple sclerosis patients and HC. SMB cells from NMOSD patients had an enhanced potential to differentiate into antibody-secreting cells when cocultured with T peripheral helper cells. Transcriptome analysis revealed that the profiles of B cell lineage transcription factors in NMOSD were skewed towards antibody-secreting cells and that IL-2 signaling was upregulated, particularly in naïve B cells. Naïve B cells expressing CD25, a receptor of IL-2, were increased in NMOSD patients and had a higher potential to differentiate into antibody-secreting cells, suggesting CD25 Conclusions: To the best of our knowledge, this is the first study to demonstrate that B cells in NMOSD patients are abnormally skewed towards antibody-secreting cells at the transcriptome level during the early differentiation phase, and that IL-2 might participate in this pathogenic process. Our study indicates that CD25
MeSH term(s)	Adolescent ; Adult ; Aged ; Antibody-Producing Cells/immunology ; Antibody-Producing Cells/pathology ; B-Lymphocytes/immunology ; B-Lymphocytes/pathology ; Cell Differentiation/physiology ; Female ; Gene Expression Profiling ; Humans ; Immunoglobulin G/immunology ; Interleukin-2/immunology ; Male ; Middle Aged ; Multiple Sclerosis, Relapsing-Remitting/immunology ; Multiple Sclerosis, Relapsing-Remitting/pathology ; Neuromyelitis Optica/immunology ; Neuromyelitis Optica/pathology ; Signal Transduction/immunology ; Young Adult
Chemical Substances	Immunoglobulin G ; Interleukin-2
Language	English
Publishing date	2022-01-06
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/s12974-021-02375-w
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Article ; Online: Enhanced GATA4 expression in senescent systemic lupus erythematosus monocytes promotes high levels of IFNα production.

Kuga, Taiga / Chiba, Asako / Murayama, Goh / Hosomi, Kosuke / Nakagawa, Tomoya / Yahagi, Yoshiyuki / Noto, Daisuke / Kusaoi, Makio / Kawano, Fuminori / Yamaji, Ken / Tamura, Naoto / Miyake, Sachiko

Frontiers in immunology

2024 Volume 15, Page(s) 1320444

Abstract: Enhanced interferon α (IFNα) production has been implicated in the pathogenesis of systemic lupus erythematosus (SLE). We previously reported IFNα production by monocytes upon activation of the stimulator of IFN genes (STING) pathway was enhanced in ... ...

Abstract	Enhanced interferon α (IFNα) production has been implicated in the pathogenesis of systemic lupus erythematosus (SLE). We previously reported IFNα production by monocytes upon activation of the stimulator of IFN genes (STING) pathway was enhanced in patients with SLE. We investigated the mechanism of enhanced IFNα production in SLE monocytes. Monocytes enriched from the peripheral blood of SLE patients and healthy controls (HC) were stimulated with 2'3'-cyclic GAMP (2'3'-cGAMP), a ligand of STING. IFNα positive/negative cells were FACS-sorted for RNA-sequencing analysis. Gene expression in untreated and 2'3'-cGAMP-stimulated SLE and HC monocytes was quantified by real-time PCR. The effect of GATA binding protein 4 (GATA4) on IFNα production was investigated by overexpressing GATA4 in monocytic U937 cells by vector transfection. Chromatin immunoprecipitation was performed to identify GATA4 binding target genes in U937 cells stimulated with 2'3'-cGAMP. Differentially expressed gene analysis of cGAS-STING stimulated SLE and HC monocytes revealed the enrichment of gene sets related to cellular senescence in SLE. CDKN2A, a marker gene of cellular senescence, was upregulated in SLE monocytes at steady state, and its expression was further enhanced upon STING stimulation. GATA4 expression was upregulated in IFNα-positive SLE monocytes. Overexpression of GATA4 enhanced IFNα production in U937 cells. GATA4 bound to the enhancer region of IFIT family genes and promoted the expressions of IFIT1, IFIT2, and IFIT3, which promote type I IFN induction. SLE monocytes with accelerated cellular senescence produced high levels of IFNα related to GATA4 expression upon activation of the cGAS-STING pathway.
MeSH term(s)	Humans ; GATA4 Transcription Factor/genetics ; GATA4 Transcription Factor/metabolism ; Gene Expression ; Interferon Type I/metabolism ; Interferon-alpha/metabolism ; Lupus Erythematosus, Systemic/metabolism ; Monocytes/metabolism
Chemical Substances	GATA4 protein, human ; GATA4 Transcription Factor ; Interferon Type I ; Interferon-alpha
Language	English
Publishing date	2024-03-28
Publishing country	Switzerland
Document type	Journal Article ; 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.2024.1320444
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Article ; Online: Different Spatial and Temporal Roles of Monocytes and Monocyte-Derived Cells in the Pathogenesis of an Imiquimod Induced Lupus Model.

Nomura, Atsushi / Mizuno, Miho / Noto, Daisuke / Aoyama, Aki / Kuga, Taiga / Murayama, Goh / Chiba, Asako / Miyake, Sachiko

Frontiers in immunology

2022 Volume 13, Page(s) 764557

Abstract: Mounting evidence indicates the importance of aberrant Toll-like receptor 7 (TLR7) signaling in the pathogenesis of systemic lupus erythematosus (SLE). However, the mechanism of disease progression remains unclear. An imiquimod (IMQ)-induced lupus model ... ...

Abstract	Mounting evidence indicates the importance of aberrant Toll-like receptor 7 (TLR7) signaling in the pathogenesis of systemic lupus erythematosus (SLE). However, the mechanism of disease progression remains unclear. An imiquimod (IMQ)-induced lupus model was used to analyze the lupus mechanism related to the aberrant TLR7 signals. C57BL/6 mice and NZB/NZW mice were treated with topical IMQ, and peripheral blood, draining lymph nodes, and kidneys were analyzed focusing on monocytes and monocyte-related cells. Monocytes expressed intermediate to high levels of TLR7, and the long-term application of IMQ increased Ly6C
MeSH term(s)	Animals ; Cell Count ; Imiquimod ; Interleukin-6/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NZB ; Monocytes/metabolism ; Toll-Like Receptor 7/metabolism
Chemical Substances	Interleukin-6 ; Toll-Like Receptor 7 ; Imiquimod (P1QW714R7M)
Language	English
Publishing date	2022-03-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.764557
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Article: [Innate immunity and neuroimmune disease].

Noto, Daisuke / Miyake, Sachiko

Nihon rinsho. Japanese journal of clinical medicine

2015 Volume 73 Suppl 7, Page(s) 23–32

MeSH term(s)	Animals ; Autoimmune Diseases/immunology ; Central Nervous System Diseases/immunology ; Dendritic Cells/immunology ; Humans ; Immunity, Innate ; Killer Cells, Natural/immunology ; Receptors, Pattern Recognition/immunology
Chemical Substances	Receptors, Pattern Recognition
Language	Japanese
Publishing date	2015-09
Publishing country	Japan
Document type	Journal Article
ZDB-ID	390903-7
ISSN	0047-1852
ISSN	0047-1852
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Article ; Online: Unique primed status of microglia under the systemic autoimmune condition of lupus-prone mice.

Nomura, Atsushi / Noto, Daisuke / Murayama, Goh / Chiba, Asako / Miyake, Sachiko

Arthritis research & therapy

2019 Volume 21, Issue 1, Page(s) 303

Abstract: Background: Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the production of various autoantibodies. This disease causes disabling neuropsychiatric symptoms even in the absence of apparent inflammation in the central ... ...

Abstract	Background: Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the production of various autoantibodies. This disease causes disabling neuropsychiatric symptoms even in the absence of apparent inflammation in the central nervous system (CNS), but the mechanisms involved remain unknown. Innate immune-mediated inflammation has attracted attention as a pathogenic mechanism in neuropsychiatric diseases. Methods: We investigated the CNS of lupus-prone mice focusing on innate immunity. Three strains of lupus-prone mice, FcγRIIB Results: Flow cytometry analysis demonstrated the numbers of brain CD45 Conclusions: Our data indicated that microglia in lupus exhibit a unique primed phenotype characterized by the upregulated expressions of neurodegeneration-related genes and IFN-responsive genes. Interaction with peripheral cells and brain resident cells was presumed to orchestrate neuroinflammation. Targeting innate immune cells, such as microglia and monocytes, may be a promising therapeutic approach for neuropsychiatric SLE.
MeSH term(s)	Animals ; Autoimmunity/genetics ; Autoimmunity/immunology ; CD11 Antigens/genetics ; CD11 Antigens/immunology ; CD11 Antigens/metabolism ; Central Nervous System/immunology ; Central Nervous System/metabolism ; Central Nervous System/pathology ; Gene Expression/immunology ; Lectins, C-Type/genetics ; Lectins, C-Type/immunology ; Lectins, C-Type/metabolism ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/immunology ; Mice, Inbred C57BL ; Mice, Inbred MRL lpr ; Mice, Inbred NZB ; Mice, Inbred Strains ; Mice, Knockout ; Microglia/immunology ; Microglia/metabolism ; Monocytes/immunology ; Monocytes/metabolism ; Myeloid Cells/immunology ; Myeloid Cells/metabolism ; Receptors, IgG/deficiency ; Receptors, IgG/genetics ; Receptors, IgG/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
Chemical Substances	CD11 Antigens ; Fcgr2b protein, mouse ; Itgax protein, mouse ; Lectins, C-Type ; Receptors, IgG ; dectin 1
Language	English
Publishing date	2019-12-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2107602-9
ISSN	1478-6362 ; 1478-6354
ISSN (online)	1478-6362
ISSN	1478-6354
DOI	10.1186/s13075-019-2067-8
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Article ; Online: Butyrate suppresses demyelination and enhances remyelination.

Chen, Tong / Noto, Daisuke / Hoshino, Yasunobu / Mizuno, Miho / Miyake, Sachiko

Journal of neuroinflammation

2019 Volume 16, Issue 1, Page(s) 165

Abstract: Background: The association of gut microbiota and diseases of the central nervous system (CNS), including multiple sclerosis (MS), has attracted much attention. Although a previous analysis of MS gut microbiota revealed a reduction in species producing ... ...

Abstract	Background: The association of gut microbiota and diseases of the central nervous system (CNS), including multiple sclerosis (MS), has attracted much attention. Although a previous analysis of MS gut microbiota revealed a reduction in species producing short-chain fatty acids (SCFAs), the influence of these metabolites on demyelination and remyelination, the critical factors of MS pathogenesis, remains unclear. Methods: To investigate the relationship between demyelination and gut microbiota, we administered a mixture of non-absorbing antibiotics or SCFAs to mice with cuprizone-induced demyelination and evaluated demyelination and the accumulation of microglia. To analyze the direct effect of SCFAs on demyelination or remyelination, we induced demyelination in an organotypic cerebellar slice culture using lysolecithin and analyzed the demyelination and maturation of oligodendrocyte precursor cells with or without SCFA treatment. Results: The oral administration of antibiotics significantly enhanced cuprizone-induced demyelination. The oral administration of butyrate significantly ameliorated demyelination, even though the accumulation of microglia into demyelinated lesions was not affected. Furthermore, we showed that butyrate treatment significantly suppressed lysolecithin-induced demyelination and enhanced remyelination in an organotypic slice culture in the presence or absence of microglia, suggesting that butyrate may affect oligodendrocytes directly. Butyrate treatment facilitated the differentiation of immature oligodendrocytes. Conclusions: We revealed that treatment with butyrate suppressed demyelination and enhanced remyelination in an organotypic slice culture in association with facilitating oligodendrocyte differentiation. Our findings shed light on a novel mechanism of interaction between the metabolites of gut microbiota and the CNS and may provide a strategy to control demyelination and remyelination in MS.
MeSH term(s)	Animals ; Anti-Bacterial Agents/toxicity ; Butyrates/pharmacology ; Butyrates/therapeutic use ; Cell Differentiation/drug effects ; Cell Differentiation/physiology ; Cuprizone/toxicity ; Demyelinating Diseases/chemically induced ; Demyelinating Diseases/metabolism ; Demyelinating Diseases/prevention & control ; Gastrointestinal Microbiome/drug effects ; Gastrointestinal Microbiome/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Myelin Sheath/drug effects ; Myelin Sheath/metabolism ; Oligodendroglia/drug effects ; Oligodendroglia/metabolism ; Organ Culture Techniques ; Remyelination/drug effects ; Remyelination/physiology
Chemical Substances	Anti-Bacterial Agents ; Butyrates ; Cuprizone (5N16U7E0AO)
Language	English
Publishing date	2019-08-09
Publishing country	England
Document type	Journal Article
ISSN	1742-2094
ISSN (online)	1742-2094
DOI	10.1186/s12974-019-1552-y
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