Open AccessFibronectin‐binding protein acts as Staphylococcus aureus invasin via fibronectin bridging to integrin α 5 β 1
Author(s) -
Sinha Bhanu,
François Patrice P.,
Nüße Oliver,
Foti Michelangelo,
Hartford Orla M.,
Vaudaux Pierre,
Foster Timothy J.,
Lew Daniel P.,
Herrmann Mathias,
Krause KarlHeinz
Publication year - 1999
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1046/j.1462-5822.1999.00011.x
Subject(s) - fibronectin , biology , staphylococcus aureus , bacterial adhesin , microbiology and biotechnology , integrin , cell , bacteria , escherichia coli , extracellular matrix , gene , biochemistry , genetics
The ability of Staphylococcus aureus to invade mammalian cells may explain its capacity to colonize mucosa and to persist in tissues after bacteraemia. To date, the underlying molecular mechanisms of cellular invasion by S. aureus are unknown, despite its high prevalence and difficulties in treatment. Here, we show cellular invasion as a novel function for an S. aureus adhesin, previously implicated solely in attachment. S. aureus , but not S. epidermidis , invaded epithelial 293 cells in a temperature‐ and F‐actin‐dependent manner. Formaldehyde‐fixed and live bacteria were equally invasive, suggesting that no active bacterial process was involved. All clinical S. aureus isolates analysed, but only a subset of laboratory strains, were invasive. Fibronectin‐binding proteins (FnBPs) acted as S. aureus invasins, because: (i) FnBP deletion mutants of invasive laboratory strains lost invasiveness; (ii) expression of FnBPs in non‐invasive strains conferred invasiveness; and (iii) the soluble isolated fibronectin‐binding domain of FnBP (D1–D4) completely blocked invasion. Integrin α 5 β 1 served as host cell receptor, which interacted with staphylococcal FnBPs through cellular or soluble fibronectin. FnBP‐deficient mutants lost invasiveness for epithelial cells, endothelial cells and fibroblasts. Thus, fibronectin‐dependent bridging between S. aureus FnBPs and host cell integrin α 5 β 1 is a conserved mechanism for S. aureus invasion of human cells. This may prove useful in developing new therapeutic and vaccine strategies for S. aureus infections.