Human IgG response to experimental colonization with S. aureus

  • Silva Holtfreter, Institute of Immunology and Transfusion Medicine, University of Greifswald, Germany, Germany
  • Hoai Nguyen, Institute of Immunology and Transfusion Medicine, University of Greifswald, Germany, Germany
  • Dr Heiman Wertheim, Oxford University Clinical Research Unit, National Institute of Infectious and Tropical Diseases Bach Mai Hospital, Hanoi, Viet, Vietnam
  • Dr Leif Steil, Department of Functional Genomics, Institute of Genetics, University of Greifswald, Germany, Germany
  • Dr Susanne Engelmann, Institute of Microbiology and Molecular Biology, University of Greifswald,, Germany
  • Alex van Belkum, Department of Medical Microbiology and Infectious Diseases, University Medical Center, Rotterdam, The Netherlands, The Netherlands
  • Dr Uwe Völker, Department of Functional Genomics, Institute of Genetics, University of Greifswald, Germany, Germany
  • Dr Barbara Bröker, Institute of Immunology and Transfusion Medicine, University of Greifswald, Germany, Germany

    • S. aureus carriers have an increased risk of developing nosocomial S. aureus bacteremia with their own strain. Interestingly, their prognosis is much better than that of noncarriers who develop nosocomial bacteremia. We propose that carriers raise an antibody response against their colonizing strain, which (partially) protects them from the complications of S. aureus infection. Accordingly, we previously showed that carriers mount an efficient and highly specific antibody response against the superantigens of their colonizing strain. This raises the question, whether colonization with S. aureus is sufficient to trigger an adaptive immune response.
    To investigate this, we colonized 16 healthy volunteers with S. aureus strain 8325-4, which was selected for safety reasons because of its low virulence, and obtained serum samples before and four weeks after colonization. The secreted staphylococcal proteins were separated by two-dimensional gel electrophoresis and quantitative immunoblots with the human sera were performed. There was a large inter-individual variability in spot patterns and spot intensities already before experimental colonization. The healthy volunteers harboured antibodies directed against a broad range of extracellular S. aureus proteins, which are likely due to previous encounters with S. aureus. A set of immunodominant proteins was bound by serum IgG from many different individuals (Hla, Hlb, Plc, SspA, SspB). Only rarely we observed additional spots or increased spot intensities after experimental colonization with S. aureus. Thus, short term colonization with low virulent strains (8325-4) is not sufficient to trigger strong antibody responses to S. aureus. This probably requires minor infections or more virulent strains.