This article is part of the Research Topic The <i>Staphylococci</i> and staphylococcal pathogenesis

Review ARTICLE

Front. Cell. Infect. Microbiol., 03 April 2012 | doi: 10.3389/fcimb.2012.00041

The iron-regulated staphylococcal lipoproteins

  • Department of Microbiology and Immunology, Western University, London, ON, Canada

Lipoproteins fulfill diverse roles in antibiotic resistance, adhesion, protein secretion, signaling and sensing, and many also serve as the substrate binding protein (SBP) partner to ABC transporters for the acquisition of a diverse array of nutrients including peptides, sugars, and scarcely abundant metals. In the staphylococci, the iron-regulated SBPs are significantly upregulated during iron starvation and function to sequester and deliver iron into the bacterial cell, enabling staphylococci to circumvent iron restriction imposed by the host environment. Accordingly, this subset of lipoproteins has been implicated in staphylococcal pathogenesis and virulence. Lipoproteins also activate the host innate immune response, triggered through Toll-like receptor-2 (TLR2) and, notably, the iron-regulated subset of lipoproteins are particularly immunogenic. In this review, we discuss the iron-regulated staphylococcal lipoproteins with regard to their biogenesis, substrate specificity, and impact on the host innate immune response.

Keywords: Staphylococcus, lipoproteins, iron-regulated, iron acquisition, substrate binding protein, TLR2, Fur

Citation: Sheldon JR and Heinrichs DE (2012) The iron-regulated staphylococcal lipoproteins. Front. Cell. Inf. Microbio. 2:41. doi: 10.3389/fcimb.2012.00041

Received: 18 January 2012; Paper pending published: 04 February 2012;
Accepted: 13 March 2012; Published online: 04 April 2012.

Edited by:

Martin J. McGavin, University of Western Ontario, Canada

Reviewed by:

Fabio Bagnoli, Novartis Vaccines, Italy
John Helmann, Cornell University, USA

Copyright: © 2012 Sheldon and Heinrichs. This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.

*Correspondence: David E. Heinrichs, Department of Microbiology and Immunology, Western University, Dental Sciences Building, Room 3014, London, N6A 5C1 ON, Canada. e-mail: deh@uwo.ca

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