Fachbereich Veterinärmedizin



    TLR7 Contributes to the Rapid Progression but not to the Overall Fatal Outcome of Secondary Pneumococcal Disease Following Influenza A Virus Infection (2013)

    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Stegemann-Koniszewski, Sabine
    Gereke, Marcus
    Orrskog, Sofia
    Lienenklaus, Stefan
    Pasche, Bastian
    Bader, Sophie R (WE 12)
    Gruber, Achim D (WE 12)
    Akira, Shizuo
    Weiss, Siegfried
    Henriques-Normark, Birgitta
    Bruder, Dunja
    Gunzer, Matthias
    Journal of innate immunity; 5(1) — S. 84–96
    ISSN: 1662-8128
    DOI: 10.1159/000345112
    Pubmed: 23154432
    Institut für Tierpathologie

    Robert-von-Ostertag-Str. 15
    Gebäude 12
    14163 Berlin
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    Abstract / Zusammenfassung

    Increased risk for bacterial superinfections substantially contributes to the mortality caused by influenza A virus (IAV) epidemics. While the mechanistic basis for this lethal synergism is still insufficiently understood, immune modulation through the viral infection has been shown to be involved. Since the pattern-recognition receptor (PRR) toll-like receptor 7 (TLR7) is a major sensor for the viral genome, we studied how IAV recognition by TLR7 influences the development of secondary pneumococcal infection. In a mouse model of IAV, TLR7-deficient hosts induced a potent antiviral response and showed unchanged survival. In secondary pneumococcal infection during acute influenza, TLR7ko mice showed a fatal outcome similar to wild-type (WT) hosts, despite significantly delayed disease progression. Also, when bacterial superinfection occurred after virus clearance, WT and TLR7-deficient hosts showed similar mortality, even though we found the phagocytic activity of alveolar macrophages isolated from IAV-pre-infected hosts to be enhanced in TLR7ko over WT mice. Thus, we show that a virus-sensing PRR modulates the progression of secondary pneumococcal infection following IAV. However, the fatal overall outcome in WT as well as TLR7ko hosts suggests that processes distinct from TLR7-triggering override the contribution of this single PRR.