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Clinical and Vaccine Immunology, November 2009, p. 1607-1614, Vol. 16, No. 11
1071-412X/09/$08.00+0 doi:10.1128/CVI.00263-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
Human Immune Proteome in Experimental Colonization with Staphylococcus aureus
,
Silva Holtfreter,1
Thi Thu Hoai Nguyen,1
Heiman Wertheim,2,3
Leif Steil,4
Harald Kusch,5
Quoc Phong Truong,4
Susanne Engelmann,5
Michael Hecker,5
Uwe Völker,4
Alex van Belkum,2 and
Barbara M. Bröker1*
Institute of Immunology and Transfusion Medicine,1 Interfaculty Institute of Genetics and Functional Genomics,4 Institute of Microbiology and Molecular Biology, University of Greifswald, Greifswald, Germany,5 Department of Medical Microbiology and Infectious Diseases, University Medical Center, Rotterdam, The Netherlands,2 Oxford University Clinical Research Unit, National Institute of Infectious and Tropical Diseases, Bach Mai Hospital, Hanoi, Vietnam3
Received 10 June 2009/ Returned for modification 28 July 2009/ Accepted 9 September 2009
More than 20% of adults are persistently colonized with Staphylococcus aureus. When hospitalized, these carriers have increased risks of infection with their own strains. However, a recent study demonstrated a lower incidence of bacteremia-related death among carriers than among noncarriers, raising the question whether the adaptive immune system plays a protective role. In fact, S. aureus carriers mount a highly specific neutralizing antibody response against superantigens of their colonizing strains. We now used 2-dimensional immunoblotting to investigate the profiles of antibodies from healthy individuals against S. aureus extracellular proteins. Moreover, we tested whether symptom-free experimental colonization of these individuals with an S. aureus strain of low virulence, 8325-4, is sufficient to induce an antibody response. Sera obtained before and 4 weeks after colonization were screened for immunoglobulin G (IgG) antibody binding to extracellular staphylococcal proteins. At baseline, most volunteers harbored IgG directed against conserved virulence factors, including alpha-hemolysin (Hla), beta-hemolysin (Hlb), phospholipase C (Plc), staphylococcal serine protease (SspA), and cysteine protease (SspB). However, the variability of spot patterns and intensities was striking and could be important in case of infection. Experimental nasal colonization with S. aureus 8325-4 did not elicit new antibodies or boost the humoral response. Thus, the high antibody prevalence in humans is likely not induced by short-term nasal colonization, and presumably minor infections are required to trigger anti-S. aureus antibody responses.
* Corresponding author. Mailing address: Institut für Immunologie und Transfusionsmedizin, Universität Greifswald, Neubau P, Sauerbruchstrasse, D-17487 Greifswald, Germany. Phone: 49 3834 86 55 95. Fax: 49 3834 86 54 90. E-mail: broeker{at}uni-greifswald.de
Published ahead of print on 16 September 2009.
Supplemental material for this article may be found at http://cvi.asm.org/.
Clinical and Vaccine Immunology, November 2009, p. 1607-1614, Vol. 16, No. 11
1071-412X/09/$08.00+0 doi:10.1128/CVI.00263-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»