IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
IAI.01530-07v1
76/4/1518    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Clarke, S. R.
Right arrow Articles by Foster, S. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Clarke, S. R.
Right arrow Articles by Foster, S. J.

 Previous Article  |  Next Article 

Infection and Immunity, April 2008, p. 1518-1526, Vol. 76, No. 4
0019-9567/08/$08.00+0     doi:10.1128/IAI.01530-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

IsdA Protects Staphylococcus aureus against the Bactericidal Protease Activity of Apolactoferrin{triangledown}

Simon R. Clarke{dagger} and Simon J. Foster*

Department of Molecular Biology and Biotechnology, University of Sheffield, Firth Court, Western Bank, Sheffield S10 2TN, United Kingdom

Received 19 November 2007/ Accepted 20 January 2008

An important facet of the Staphylococcus aureus host-pathogen interaction is the ability of the invading bacterium to evade host innate defenses, particularly the cocktail of host antimicrobial peptides. In this work, we showed that IsdA, a surface protein of S. aureus which is required for nasal colonization, binds to lactoferrin, the most abundant antistaphylococcal polypeptide in human nasal secretions. The presence of IsdA on the surface of S. aureus confers resistance to killing by lactoferrin. In addition, the bactericidal activity of lactoferrin was inhibited by addition of phenylmethylsulfonyl fluoride, implicating the serine protease activity of lactoferrin in the killing of S. aureus. Recombinant IsdA was a competitive inhibitor of lactoferrin protease activity. Reciprocally, antibody reactive to IsdA enhanced killing of S. aureus. Thus, IsdA can protect S. aureus against lactoferrin and acts as a protease inhibitor.

* Corresponding author. Mailing address: Department of Molecular Biology and Biotechnology, University of Sheffield, Firth Court, Western Bank, Sheffield S10 2TN, United Kingdom. Phone: 44 114 222 4411. Fax: 44 114 222 2800. E-mail: s.foster{at}sheffield.ac.uk

{triangledown} Published ahead of print on 28 January 2008.

Editor: V. J. DiRita

{dagger} Present address: School of Biological Sciences, University of Reading, Whiteknights, Reading RG6 6AJ, United Kingdom.

Infection and Immunity, April 2008, p. 1518-1526, Vol. 76, No. 4
0019-9567/08/$08.00+0     doi:10.1128/IAI.01530-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2008 by the American Society for Microbiology. All rights reserved.