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  1. Article ; Online: Toll-like receptor-agonist-based therapies for respiratory viral diseases: thinking outside the cell.

    Girkin, Jason L N / Maltby, Steven / Bartlett, Nathan W

    European respiratory review : an official journal of the European Respiratory Society

    2022  Volume 31, Issue 164

    Abstract: Respiratory virus infections initiate in the upper respiratory tract (URT). Innate immunity is critical for initial control of infection at this site, particularly in the absence of mucosal virus-neutralising antibodies. If the innate immune response is ... ...

    Abstract Respiratory virus infections initiate in the upper respiratory tract (URT). Innate immunity is critical for initial control of infection at this site, particularly in the absence of mucosal virus-neutralising antibodies. If the innate immune response is inadequate, infection can spread to the lower respiratory tract (LRT) causing community-acquired pneumonia (as exemplified by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)/coronavirus disease 2019). Vaccines for respiratory viruses (influenza and SARS-CoV-2) leverage systemic adaptive immunity to protect from severe lung disease. However, the URT remains vulnerable to infection, enabling viral transmission and posing an ongoing risk of severe disease in populations that lack effective adaptive immunity.Innate immunity is triggered by host cell recognition of viral pathogen-associated molecular patterns
    MeSH term(s) Antiviral Agents ; COVID-19 ; Humans ; Immunity, Innate ; Lung ; SARS-CoV-2 ; Toll-Like Receptors
    Chemical Substances Antiviral Agents ; Toll-Like Receptors
    Language English
    Publishing date 2022-05-04
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1077620-5
    ISSN 1600-0617 ; 0905-9180
    ISSN (online) 1600-0617
    ISSN 0905-9180
    DOI 10.1183/16000617.0274-2021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3265: 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: A unique role for IL-13 in inducing esophageal eosinophilia through MID-1 and STAT6.

    Girkin, Jason L N / Sokulsky, Leon A / Starkey, Malcolm R / Hansbro, Philip M / Foster, Paul S / Collison, Adam M / Mattes, Joerg

    Frontiers in allergy

    2023  Volume 4, Page(s) 1248432

    Abstract: Introduction: Eosinophilic esophagitis (EoE) is associated with allergen-driven inflammation of the esophagus and an upregulated Th2 cytokine signature. Recombinant interleukin (IL)-13 (rIL-13) administration to mice induces some of the hallmark ... ...

    Abstract Introduction: Eosinophilic esophagitis (EoE) is associated with allergen-driven inflammation of the esophagus and an upregulated Th2 cytokine signature. Recombinant interleukin (IL)-13 (rIL-13) administration to mice induces some of the hallmark features of EoE, including increased eotaxin expression and eosinophil recruitment. Inflammation in EoE has previously been shown to depend on the expression of TRAIL and MID-1, which reduced protein phosphatase 2A (PP2A) activity. The relationship between IL-13 and TRAIL signalling in esophageal eosinophilia is currently unknown.
    Objective: To investigate the interaction between IL-13-driven eosinophil infiltration and TRAIL or MID-1 in the esophagus.
    Method: We administered rIL-13 to wild type (WT), TRAIL-deficient (
    Results: rIL-13 administration to mice increased TRAIL and MID-1 expression in the esophagus while reducing PP2A activity. TRAIL deficient, but not STAT6 deficient mice demonstrated increased MID-1 expression and PP2A reduction upon IL-13 challenge which correlated with eosinophil infiltration into the esophagus. Silencing MID-1 expression with siRNA completely ablated IL-13 induced eosinophil infiltration of the esophagus, restored PP2A activity, and reduced eotaxin-1 expression.
    Conclusion: IL-13-driven eosinophil infiltration of the esophagus induced eosinophilia and eotaxin-1 expression in a STAT6-dependent and MID-1-dependent manner. This study highlights a novel mechanism employed by IL-13 to perpetuate eosinophil infiltration.
    Language English
    Publishing date 2023-11-06
    Publishing country Switzerland
    Document type Journal Article
    ISSN 2673-6101
    ISSN (online) 2673-6101
    DOI 10.3389/falgy.2023.1248432
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Upper Respiratory Tract OC43 Infection Model for Investigating Airway Immune-Modifying Therapies.

    Girkin, Jason L N / Bryant, Nathan E / Loo, Su-Ling / Hsu, Alan / Kanwal, Amama / Williams, Teresa C / Maltby, Steven / Turville, Stuart G / Wark, Peter A B / Bartlett, Nathan W

    American journal of respiratory cell and molecular biology

    2023  Volume 69, Issue 6, Page(s) 614–622

    Abstract: Respiratory virus infections initiate and transmit from the upper respiratory tract (URT). Coronaviruses, including OC43, are a major cause of respiratory infection and disease. Failure to mount an effective antiviral immune response in the nasal mucosa ... ...

    Abstract Respiratory virus infections initiate and transmit from the upper respiratory tract (URT). Coronaviruses, including OC43, are a major cause of respiratory infection and disease. Failure to mount an effective antiviral immune response in the nasal mucosa increases the risk of severe disease and person-to-person transmission, highlighting the need for URT infection models to support the development of nasal treatments that improve coronavirus antiviral immunity. We aimed to determine if OC43 productively infected the mouse URT and would therefore be a suitable model to assess the efficacy and mechanism of action of nasal-targeting immune-modifying treatments. We administered OC43 via intranasal inoculation to wild-type Balb/c mice and assessed virus airway tropism (by comparing total respiratory tract vs. URT-only virus exposure) and characterized infection-induced immunity by quantifying specific antiviral cytokines and performing gene array assessment of immune genes. We then assessed the effect of immune-modulating therapies, including an immune-stimulating TLR2/6 agonist (INNA-X) and the immune-suppressing corticosteroid fluticasone propionate (FP). OC43 replicated in nasal respiratory epithelial cells, with peak viral RNA observed 2 days after infection. Prophylactic treatment with INNA-X accelerated expression of virus-induced IFN-λ and IFN-stimulated genes. In contrast, intranasal FP treatment increased nasal viral load by 2.4 fold and inhibited virus-induced IFN and IFN-stimulated gene expression. Prior INNA-X treatment reduced the immune-suppressive effect of FP. We demonstrate that the mouse nasal epithelium is permissive to OC43 infection and strengthen the evidence that TLR2 activation is a β-coronavirus innate immune determinant and therapeutic target.
    MeSH term(s) Humans ; Animals ; Mice ; Toll-Like Receptor 2 ; Respiratory Tract Infections/drug therapy ; Cytokines/metabolism ; Nasal Mucosa/metabolism ; Interferon Lambda
    Chemical Substances Toll-Like Receptor 2 ; Cytokines ; Interferon Lambda
    Language English
    Publishing date 2023-08-21
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2023-0202MA
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2851: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  4. Article ; Online: A Critical Role for the CXCL3/CXCL5/CXCR2 Neutrophilic Chemotactic Axis in the Regulation of Type 2 Responses in a Model of Rhinoviral-Induced Asthma Exacerbation.

    Sokulsky, Leon A / Garcia-Netto, Keilah / Nguyen, Thi Hiep / Girkin, Jason L N / Collison, Adam / Mattes, Joerg / Kaiko, Gerard / Liu, Chi / Bartlett, Nathan W / Yang, Ming / Foster, Paul S

    Journal of immunology (Baltimore, Md. : 1950)

    2020  Volume 205, Issue 9, Page(s) 2468–2478

    Abstract: Rhinovirus (RV) infections in asthmatic patients are often associated with asthma exacerbation, characterized by worsened airways hyperreactivity and increased immune cell infiltration to the airways. The C-X-C chemokines, CXCL3 and CXCL5, regulate ... ...

    Abstract Rhinovirus (RV) infections in asthmatic patients are often associated with asthma exacerbation, characterized by worsened airways hyperreactivity and increased immune cell infiltration to the airways. The C-X-C chemokines, CXCL3 and CXCL5, regulate neutrophil trafficking to the lung via CXCR2, and their expression in the asthmatic lung is associated with steroid-insensitive type 2 inflammatory signatures. Currently, the role of CXCL3 and CXCL5 in regulating neutrophilic and type 2 responses in viral-induced asthma exacerbation is unknown. Inhibition of CXCL3 or CXCL5 with silencing RNAs in a mouse model of RV-induced exacerbation of asthma attenuated the accumulation of CXCR2
    MeSH term(s) Animals ; Asthma/immunology ; Bronchial Hyperreactivity/immunology ; Chemokine CXCL5/immunology ; Chemokines, CXC/immunology ; Chemotaxis, Leukocyte/immunology ; Eosinophils/immunology ; Immunity, Innate/immunology ; Inflammation/immunology ; Lung/immunology ; Lymphocytes/immunology ; Male ; Mice ; Mice, Inbred BALB C ; Neutrophils/immunology ; Receptors, Interleukin-8B/immunology ; Rhinovirus/immunology
    Chemical Substances Chemokine CXCL5 ; Chemokines, CXC ; Cxcl3 protein, mouse ; Cxcl5 protein, mouse ; Cxcr2 protein, mouse ; Receptors, Interleukin-8B
    Language English
    Publishing date 2020-09-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.1901350
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ud II Zs.37: Show issues Location:
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