Iron regulated surface determinant B (IsdB) promotes Staphylococcus aureus adherence to and internalization by non-phagocytic human cells
Zapotoczna, Marta (Author), Jevnikar, Zala (Author), Miajlović, Helen (Author), Kos, Janko (Author), Foster, Timothy J. (Author)

URLURL - Presentation file, Visit http://onlinelibrary.wiley.com/doi/10.1111/cmi.12097/pdf This link opens in a new window

Staphylococcus aureus is a human pathogen that causes invasive and recurring infections. The ability to internalize into and persist within host cells is thought to contribute to infection. Here we report a novel role for the well characterized iron regulated surface determinant B (IsdB) protein which we have shown can promote adhesion of 293T, HeLa cells and platelets to immobilized bacteria independently of its ability to bind haemoglobin. IsdB bound to the active form of the platelet integrin ŽIIbŽ3, both on platelets and when the integrin was expressed ectopically in CHO cells. IsdB also promoted bacterial invasion into human cells. This was clearly demonstrated with bacteria lacking fibronectin-binding proteins (FnBPs), which are known to promote invasion in the presence of fibronectin, However, IsdB also contributed significantly to invasion by cells expressing FnBPs in the presence of serum. Thus IsdB appears to be able to interact with the broader family of integrins that bind ligands with the RGD motif and to act as a back up mechanism to promote interactions with mammalian cells.

Keywords:Staphylococcus aureus, Isd proteins, S. aureus invasion, S. aureus adherence
Work type:Not categorized (r6)
Tipology:1.01 - Original Scientific Article
Organization:FFA - Faculty of Pharmacy
Number of pages:str. 1026-1041
Numbering:Vol. 15, no. 6
ISSN on article:1462-5814
DOI:10.1111/cmi.12097 Link is opened in a new window
COBISS.SI-ID:3379569 Link is opened in a new window
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Record is a part of a journal

Title:Cellular microbiology
Shortened title:Cell. microbiol.
Publisher:Blackwell Science
COBISS.SI-ID:554773 This link opens in a new window

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