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  1. AU="Rothfuchs, Antonio G"
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  1. Article ; Online: SARS-CoV-2 promotes microglial synapse elimination in human brain organoids.

    Samudyata / Oliveira, Ana O / Malwade, Susmita / Rufino de Sousa, Nuno / Goparaju, Sravan K / Gracias, Jessica / Orhan, Funda / Steponaviciute, Laura / Schalling, Martin / Sheridan, Steven D / Perlis, Roy H / Rothfuchs, Antonio G / Sellgren, Carl M

    Molecular psychiatry

    2022  Volume 27, Issue 10, Page(s) 3939–3950

    Abstract: Neuropsychiatric manifestations are common in both the acute and post-acute phase of SARS-CoV-2 infection, but the mechanisms of these effects are unknown. In a newly established brain organoid model with innately developing microglia, we demonstrate ... ...

    Abstract Neuropsychiatric manifestations are common in both the acute and post-acute phase of SARS-CoV-2 infection, but the mechanisms of these effects are unknown. In a newly established brain organoid model with innately developing microglia, we demonstrate that SARS-CoV-2 infection initiate neuronal cell death and cause a loss of post-synaptic termini. Despite limited neurotropism and a decelerating viral replication, we observe a threefold increase in microglial engulfment of postsynaptic termini after SARS-CoV-2 exposure. We define the microglial responses to SARS-CoV-2 infection by single cell transcriptomic profiling and observe an upregulation of interferon-responsive genes as well as genes promoting migration and synapse engulfment. To a large extent, SARS-CoV-2 exposed microglia adopt a transcriptomic profile overlapping with neurodegenerative disorders that display an early synapse loss as well as an increased incident risk after a SARS-CoV-2 infection. Our results reveal that brain organoids infected with SARS-CoV-2 display disruption in circuit integrity via microglia-mediated synapse elimination and identifies a potential novel mechanism contributing to cognitive impairments in patients recovering from COVID-19.
    MeSH term(s) Humans ; SARS-CoV-2 ; Organoids ; Microglia ; COVID-19 ; Brain ; Presynaptic Terminals
    Language English
    Publishing date 2022-10-05
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1330655-8
    ISSN 1476-5578 ; 1359-4184
    ISSN (online) 1476-5578
    ISSN 1359-4184
    DOI 10.1038/s41380-022-01786-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4812: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Nucleotide-binding oligomerization domain-2 (NOD2) regulates type-1 cytokine responses to Mycobacterium avium but is not required for host control of infection.

    Carvalho, Natália B / Oliveira, Fernanda S / Marinho, Fábio A V / de Almeida, Leonardo A / Fahel, Júlia S / Báfica, André / Rothfuchs, Antonio G / Zamboni, Dario S / Caliari, Marcelo V / Oliveira, Sérgio C

    Microbes and infection

    2015  Volume 17, Issue 5, Page(s) 337–344

    Abstract: Nucleotide-binding oligomerization domain-2 (NOD2) is an innate immune receptor that recognizes peptidoglycan-derived muramyl dipeptide from intracellular bacteria and triggers proinflammatory signals. In this study, we sought to evaluate the role played ...

    Abstract Nucleotide-binding oligomerization domain-2 (NOD2) is an innate immune receptor that recognizes peptidoglycan-derived muramyl dipeptide from intracellular bacteria and triggers proinflammatory signals. In this study, we sought to evaluate the role played by this receptor during early and late stages of infection with Mycobacterium avium in mice. We demonstrated that NOD2 knockout (KO) animals were able to control M. avium infection similarly to wild-type mice at all time points studied, even though IL-12 and TNF-α production was impaired in NOD2-deficient macrophages. At 100 days following infection with this bacterium, but not at 30 days post-infection, NOD2-deficient mice showed significantly diminished production of IFN-γ, as confirmed by reduced accumulation of IFN-γ and IL-12 mRNA in the spleens of KO mice. Additionally, a reduction in the size and in the number of lymphocytes/granulocytes of hepatic granulomas from NOD2 KO animals was observed only during late time points of M. avium infection. Taken together, these data demonstrate that NOD2 regulates type-1 cytokine responses to M. avium but is not required for the control of infection with this bacterium in vivo.
    MeSH term(s) Animals ; Cytokines/immunology ; Cytokines/metabolism ; Infection/immunology ; Mice ; Mice, Knockout ; Mycobacterium avium/cytology ; Mycobacterium avium/physiology ; Nod2 Signaling Adaptor Protein/immunology ; Nod2 Signaling Adaptor Protein/metabolism ; Receptors, Immunologic/immunology ; Receptors, Immunologic/metabolism
    Chemical Substances Card15 protein, mouse ; Cytokines ; Nod2 Signaling Adaptor Protein ; Receptors, Immunologic
    Language English
    Publishing date 2015-05
    Publishing country France
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1465093-9
    ISSN 1769-714X ; 1286-4579
    ISSN (online) 1769-714X
    ISSN 1286-4579
    DOI 10.1016/j.micinf.2015.03.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5014: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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