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A new pathway of staphylococcal pathogenesis: Apoptosis-like death induced by staphopain B in human neutrophils and monocytes

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DOI

  • Jan Smagur, Department of Microbiology, University of Copenhagen
  • ,
  • Krzysztof Guzik, Jagiellonian University
  • ,
  • Lukasz Magiera, Jagiellonian University
  • ,
  • Malgorzata Bzowska, Jagiellonian University
  • ,
  • Milosz Gruca, Department of Microbiology, University of Copenhagen
  • ,
  • Ida B. Thøgersen
  • Jan J. Enghild
  • Jan Potempa, Department of Microbiology, University of Copenhagen
  • Department of Molecular Biology

Circulating neutrophils and monocytes form the first line of cellular defense against invading bacteria. Here, we describe a novel and specific mechanism of disabling and eliminating phagocytes by Staphylococcus aureus. Staphopain B (SspB) selectively cleaved CD11b on phagocytes, which rapidly acquired features of cell death. SspB-treated phagocytes expressed phosphatidylserine as well as annexin I and became permeable to propidium iodide, thus demonstrating distinctive features of both apoptosis and necrosis, respectively. The cell death observed was caspase and Syk tyrosine kinase independent, whilst cytochalasin D efficiently inhibited the staphopain-induced neutrophil killing. Neutrophil and monocyte cell death was not affected by integrin clustering ligands (ICAM-1 or fibrin) and was prevented, and even reversed, by IgG. This protective effect was dependent on the Fc fragment, collectively suggesting cooperation of the CD16 receptor and integrin Mac-1 (CD11b/CD18). We conclude that SspB, particularly in the presence of staphylococcal protein A, may reduce the number of functional phagocytes at infection sites, thus facilitating colonization and dissemination of S. aureus.

Original languageEnglish
JournalJournal of Innate Immunity
Volume1
Issue2
Pages (from-to)98-108
Number of pages11
ISSN1662-811X
DOIs
Publication statusPublished - 1 Jan 2009

    Research areas

  • Apoptosis, Immunoglobulin, Infection, Inflammation, Necrosis, Phagocytosis, Protease, Receptor, Staphylococcus aureus

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