Articles by Sabine Stegemann-Koniszewski in JoVE
Flowcytometrische Isolatie van primaire Murine Type II alveolaire epitheelcellen voor Functionele en moleculaire studies Marcus Gereke1,2, Andrea Autengruber1,2, Lothar Gröbe3, Andreas Jeron2, Dunja Bruder1,2, Sabine Stegemann-Koniszewski1 1Research Group Immune Regulation, Helmholtz Centre for Infection Research, 2Research Group Infection Immunology, Institute of Medical Microbiology, Otto-von-Guericke University, 3Department of Experimental Immunology, Helmholtz Centre for Infection Research We beschrijven de snelle isolatie van primaire murine type II alveolaire epitheelcellen (AECII) door flowcytometrische negatieve selectie. Deze AECII vertonen hoge levensvatbaarheid en zuiverheid en zijn geschikt voor diverse functionele en moleculaire studies over hun rol bij luchtwegaandoeningen zoals auto of infectieziekten.
Other articles by Sabine Stegemann-Koniszewski on PubMed
TLR7 Contributes to the Rapid Progression but Not to the Overall Fatal Outcome of Secondary Pneumococcal Disease Following Influenza A Virus Infection Journal of Innate Immunity. Nov, 2012 | Pubmed ID: 23154432 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.