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dc.contributor.authorOmura, S-
dc.contributor.authorSato, F-
dc.contributor.authorPark, A-M-
dc.contributor.authorFujita, M-
dc.contributor.authorKhadka, S-
dc.contributor.authorNakamura, Y-
dc.contributor.authorKatsuki, A-
dc.contributor.authorNishio, K-
dc.contributor.authorGavins, FNE-
dc.contributor.authorTsunoda, I-
dc.identifier.citationOmura S, Sato F, Park A-M, Fujita M, Khadka S, Nakamura Y, Katsuki A, Nishio K, Gavins FNE and Tsunoda I (2020) Bioinformatics Analysis of Gut Microbiota and CNS Transcriptome in Virus-Induced Acute Myelitis and Chronic Inflammatory Demyelination; Potential Association of Distinct Bacteria With CNS IgA Upregulation. Front. Immunol. 11:1138en_US
dc.descriptionThe Supplementary Material for this article can be found online at:
dc.description.abstract© 2020 Omura, Sato, Park, Fujita, Khadka, Nakamura, Katsuki, Nishio, Gavins and Tsunoda. Virus infections have been associated with acute and chronic inflammatory central nervous system (CNS) diseases, e.g., acute flaccid myelitis (AFM) and multiple sclerosis (MS), where animal models support the pathogenic roles of viruses. In the spinal cord, Theiler's murine encephalomyelitis virus (TMEV) induces an AFM-like disease with gray matter inflammation during the acute phase, 1 week post infection (p.i.), and an MS-like disease with white matter inflammation during the chronic phase, 1 month p.i. Although gut microbiota has been proposed to affect immune responses contributing to pathological conditions in remote organs, including the brain pathophysiology, its precise role in neuroinflammatory diseases is unclear. We infected SJL/J mice with TMEV; harvested feces and spinal cords on days 4 (before onset), 7 (acute phase), and 35 (chronic phase) p.i.; and examined fecal microbiota by 16S rRNA sequencing and CNS transcriptome by RNA sequencing. Although TMEV infection neither decreased microbial diversity nor changed overall microbiome patterns, it increased abundance of individual bacterial genera Marvinbryantia on days 7 and 35 p.i. and Coprococcus on day 35 p.i., whose pattern-matching with CNS transcriptome showed strong correlations: Marvinbryantia with eight T-cell receptor (TCR) genes on day 7 and with seven immunoglobulin (Ig) genes on day 35 p.i.; and Coprococcus with gene expressions of not only TCRs and IgG/IgA, but also major histocompatibility complex (MHC) and complements. The high gene expression of IgA, a component of mucosal immunity, in the CNS was unexpected. However, we observed substantial IgA positive cells and deposition in the CNS, as well as a strong correlation between CNS IgA gene expression and serum anti-TMEV IgA titers. Here, changes in a small number of distinct gut bacteria, but not overall gut microbiota, could affect acute and chronic immune responses, causing AFM- and MS-like lesions in the CNS. Alternatively, activated immune responses would alter the composition of gut microbiota.en_US
dc.description.sponsorshipNational Institute of General Medical Sciences COBRE Grant; Japan Society for the Promotion of Science; The Royal Society Wolfson Fellowship; Novartis Pharma Research Grantsen_US
dc.publisherFrontiers Mediaen_US
dc.subjectfecal microbiomeen_US
dc.subjectviral model for multiple sclerosisen_US
dc.subjectpattern matchingen_US
dc.subjectpredictive metagenome analysisen_US
dc.subjectgene expression profilesen_US
dc.titleBioinformatics Analysis of Gut Microbiota and CNS Transcriptome in Virus-Induced Acute Myelitis and Chronic Inflammatory Demyelination; Potential Association of Distinct Bacteria with CNS IgA upregulationen_US
dc.relation.isPartOfFrontiers in Immunology Mucosal Immunity-
Appears in Collections:Dept of Life Sciences Research Papers

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