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  1. Article ; Online: HIV-1

    Bertacchi, Giulia / Posch, Wilfried / Wilflingseder, Doris

    Biomolecules

    2022  Volume 12, Issue 2

    Abstract: Nonadjacent immune cells communicate through a complex network of tunneling nanotubes (TNTs). TNTs can be hijacked by HIV-1, allowing it to spread between connected cells. Dendritic cells (DCs) are among the first cells to encounter HIV-1 at mucosal ... ...

    Abstract Nonadjacent immune cells communicate through a complex network of tunneling nanotubes (TNTs). TNTs can be hijacked by HIV-1, allowing it to spread between connected cells. Dendritic cells (DCs) are among the first cells to encounter HIV-1 at mucosal sites, but they are usually efficiently infected only at low levels. However, HIV-1 was demonstrated to productively infect DCs when the virus was complement-opsonized (HIV-C). Such HIV-C-exposed DCs mediated an improved antiviral and T-cell stimulatory capacity. The role of TNTs in combination with complement in enhancing DC infection with HIV-C remains to be addressed. To this aim, we evaluated TNT formation on the surface of DCs or DC/CD4
    MeSH term(s) Cell Communication ; Complement System Proteins/metabolism ; Dendritic Cells ; HIV Infections ; HIV-1/metabolism ; Humans ; Receptor, Anaphylatoxin C5a/therapeutic use ; T-Lymphocytes
    Chemical Substances C5AR1 protein, human ; Receptor, Anaphylatoxin C5a ; Complement System Proteins (9007-36-7)
    Language English
    Publishing date 2022-02-15
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701262-1
    ISSN 2218-273X ; 2218-273X
    ISSN (online) 2218-273X
    ISSN 2218-273X
    DOI 10.3390/biom12020313
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Guidelines for visualization and analysis of DC in tissues using multiparameter fluorescence microscopy imaging methods.

    Bayerl, Felix / Bejarano, David A / Bertacchi, Giulia / Doffin, Anne-Claire / Gobbini, Elisa / Hubert, Margaux / Li, Lijian / Meiser, Philippa / Pedde, Anna-Marie / Posch, Wilfried / Rupp, Luise / Schlitzer, Andreas / Schmitz, Marc / Schraml, Barbara U / Uderhardt, Stefan / Valladeau-Guilemond, Jenny / Wilflingseder, Doris / Zaderer, Viktoria / Böttcher, Jan P

    European journal of immunology

    2023  Volume 53, Issue 11, Page(s) e2249923

    Abstract: This article is part of the Dendritic Cell Guidelines article series, which provides a collection of state-of-the-art protocols for the preparation, phenotype analysis by flow cytometry, generation, fluorescence microscopy, and functional ... ...

    Abstract This article is part of the Dendritic Cell Guidelines article series, which provides a collection of state-of-the-art protocols for the preparation, phenotype analysis by flow cytometry, generation, fluorescence microscopy, and functional characterization of mouse and human dendritic cells (DC) from lymphoid organs and various non-lymphoid tissues. Here, we provide detailed procedures for a variety of multiparameter fluorescence microscopy imaging methods to explore the spatial organization of DC in tissues and to dissect how DC migrate, communicate, and mediate their multiple functional roles in immunity in a variety of tissue settings. The protocols presented here entail approaches to study DC dynamics and T cell cross-talk by intravital microscopy, large-scale visualization, identification, and quantitative analysis of DC subsets and their functions by multiparameter fluorescence microscopy of fixed tissue sections, and an approach to study DC interactions with tissue cells in a 3D cell culture model. While all protocols were written by experienced scientists who routinely use them in their work, this article was also peer-reviewed by leading experts and approved by all co-authors, making it an essential resource for basic and clinical DC immunologists.
    MeSH term(s) Humans ; Dendritic Cells ; Microscopy, Fluorescence/methods ; T-Lymphocytes
    Language English
    Publishing date 2023-01-09
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120108-6
    ISSN 1521-4141 ; 0014-2980
    ISSN (online) 1521-4141
    ISSN 0014-2980
    DOI 10.1002/eji.202249923
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 489: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
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  3. Article ; Online: C5aR inhibition of nonimmune cells suppresses inflammation and maintains epithelial integrity in SARS-CoV-2-infected primary human airway epithelia.

    Posch, Wilfried / Vosper, Jonathan / Noureen, Asma / Zaderer, Viktoria / Witting, Christina / Bertacchi, Giulia / Gstir, Ronald / Filipek, Przemyslaw A / Bonn, Günther K / Huber, Lukas A / Bellmann-Weiler, Rosa / Lass-Flörl, Cornelia / Wilflingseder, Doris

    The Journal of allergy and clinical immunology

    2021  Volume 147, Issue 6, Page(s) 2083–2097.e6

    Abstract: Background: Excessive inflammation triggered by a hitherto undescribed mechanism is a hallmark of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections and is associated with enhanced pathogenicity and mortality.: Objective: ... ...

    Abstract Background: Excessive inflammation triggered by a hitherto undescribed mechanism is a hallmark of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections and is associated with enhanced pathogenicity and mortality.
    Objective: Complement hyperactivation promotes lung injury and was observed in patients suffering from Middle East respiratory syndrome-related coronavirus, SARS-CoV-1, and SARS-CoV-2 infections. Therefore, we investigated the very first interactions of primary human airway epithelial cells on exposure to SARS-CoV-2 in terms of complement component 3 (C3)-mediated effects.
    Methods: For this, we used highly differentiated primary human 3-dimensional tissue models infected with SARS-CoV-2 patient isolates. On infection, viral load, viral infectivity, intracellular complement activation, inflammatory mechanisms, and tissue destruction were analyzed by real-time RT-PCR, high content screening, plaque assays, luminex analyses, and transepithelial electrical resistance measurements.
    Results: Here, we show that primary normal human bronchial and small airway epithelial cells respond to SARS-CoV-2 infection by an inflated local C3 mobilization. SARS-CoV-2 infection resulted in exaggerated intracellular complement activation and destruction of the epithelial integrity in monolayer cultures of primary human airway cells and highly differentiated, pseudostratified, mucus-producing, ciliated respiratory tissue models. SARS-CoV-2-infected 3-dimensional cultures secreted significantly higher levels of C3a and the proinflammatory cytokines IL-6, monocyte chemoattractant protein 1, IL-1α, and RANTES.
    Conclusions: Crucially, we illustrate here for the first time that targeting the anaphylotoxin receptors C3a receptor and C5a receptor in nonimmune respiratory cells can prevent intrinsic lung inflammation and tissue damage. This opens up the exciting possibility in the treatment of COVID-19.
    MeSH term(s) Bronchi/immunology ; Bronchi/pathology ; Bronchi/virology ; COVID-19/immunology ; COVID-19/pathology ; COVID-19/virology ; Cell Line ; Complement Activation ; Complement C3/immunology ; Cytokines/immunology ; Epithelial Cells/immunology ; Epithelial Cells/pathology ; Epithelial Cells/virology ; Humans ; Inflammation/immunology ; Inflammation/pathology ; Receptor, Anaphylatoxin C5a/immunology ; Respiratory Mucosa/immunology ; Respiratory Mucosa/pathology ; Respiratory Mucosa/virology ; SARS-CoV-2/immunology
    Chemical Substances C3 protein, human ; C5AR1 protein, human ; Complement C3 ; Cytokines ; Receptor, Anaphylatoxin C5a
    Language English
    Publishing date 2021-04-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2021.03.038
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uh III Zs.92: Show issues Location:
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