Excreted Cytoplasmic Proteins Contribute to Pathogenicity in Staphylococcus aureus

  • Patrick Ebner
    Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, Germany
  • Janina Rinker
    Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, Germany
  • Minh Thu Nguyen
    Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, Germany
  • Peter Popella
    Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, Germany
  • Mulugeta Nega
    Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, Germany
  • Arif Luqman
    Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, Germany
  • Birgit Schittek
    Department of Dermatology, University of Tübingen, Tübingen, Germany
  • Moreno Di Marco
    Department of Immunology, Interfaculty Institute for Cell Biology, University of Tübingen, Tübingen, Germany
  • Stefan Stevanovic
    Department of Immunology, Interfaculty Institute for Cell Biology, University of Tübingen, Tübingen, Germany
  • Friedrich Götz
    Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, Germany

説明

<jats:title>ABSTRACT</jats:title> <jats:p> Excretion of cytoplasmic proteins in pro- and eukaryotes, also referred to as “nonclassical protein export,” is a well-known phenomenon. However, comparatively little is known about the role of the excreted proteins in relation to pathogenicity. Here, the impact of two excreted glycolytic enzymes, aldolase (FbaA) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH), on pathogenicity was investigated in <jats:named-content content-type="genus-species">Staphylococcus aureus</jats:named-content> . Both enzymes bound to certain host matrix proteins and enhanced adherence of the bacterial cells to host cells but caused a decrease in host cell invasion. FbaA and GAPDH also bound to the cell surfaces of staphylococcal cells by interaction with the major autolysin, Atl, that is involved in host cell internalization. Surprisingly, FbaA showed high cytotoxicity to both MonoMac 6 (MM6) and HaCaT cells, while GAPDH was cytotoxic only for MM6 cells. Finally, the contribution of external FbaA and GAPDH to <jats:named-content content-type="genus-species">S. aureus</jats:named-content> pathogenicity was confirmed in an insect infection model. </jats:p>

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