scholarly journals Protein F1 and Streptococcus pyogenes Resistance to Phagocytosis

2007 ◽  
Vol 75 (6) ◽  
pp. 3188-3191 ◽  
Author(s):  
Kendra A. Hyland ◽  
Beinan Wang ◽  
P. Patrick Cleary

ABSTRACT Streptococcus pyogenes is a major cause of pharyngitis in humans and encodes several fibronectin-binding proteins. M protein and protein F1 (PrtF1/SfbI) are differentially regulated by CO2 and O2, respectively, and both mediate the invasion of epithelial cells. This study examined whether PrtF1/SfbI shares other properties with M protein. Expression of the PrtF1/SfbI protein by an M-negative mutant conferred resistance to phagocytosis and partial inhibition of C3 deposition on the S. pyogenes surface.

2004 ◽  
Vol 72 (7) ◽  
pp. 4302-4308 ◽  
Author(s):  
Sonja Oehmcke ◽  
Andreas Podbielski ◽  
Bernd Kreikemeyer

ABSTRACT The serum opacity factor (SOF) of Streptococcus pyogenes is a serotyping tool and pathogenesis factor. Using SOF-coated latex beads in cell adherence assays and antiserum directed against SOF in S. pyogenes-HEp-2 cell adherence inhibition experiments, we demonstrate SOF involvement in the fibronectin-mediated adherence of S. pyogenes to epithelial cells. SOF exclusively targets the 30-kDa N-terminal region of fibronectin. The interaction revealed association and dissociation constants 1 order of magnitude lower than those of other S. pyogenes fibronectin-binding proteins.


2002 ◽  
Vol 70 (7) ◽  
pp. 3865-3873 ◽  
Author(s):  
Mary C. McElroy ◽  
David J. Cain ◽  
Christine Tyrrell ◽  
Timothy J. Foster ◽  
Christopher Haslett

ABSTRACT Fibronectin-binding proteins mediate Staphylococcus aureus internalization into nonphagocytic cells in vitro. We have investigated whether fibronectin-binding proteins are virulence factors in the pathogenesis of pneumonia by using S. aureus strain 8325-4 and isogenic mutants in which fibronectin-binding proteins were either deleted (DU5883) or overexpressed [DU5883(pFnBPA4)]. We first demonstrated that fibronectin-binding proteins mediate S. aureus internalization into alveolar epithelial cells in vitro and that S. aureus internalization into alveolar epithelial cells requires actin rearrangement and protein kinase activity. Second, we established a rat model of S. aureus-induced pneumonia and measured lung injury and bacterial survival at 24 and 96 h postinoculation. S. aureus growth and the extent of lung injury were both increased in rats inoculated with the deletion mutant (DU5883) in comparison with rats inoculated with the wild-type (8325-4) and the fibronectin-binding protein-overexpressing strain DU5883(pFnBPA4) at 24 h postinfection. Morphological evaluation of infected lungs at the light and electron microscopic levels demonstrated that S. aureus was present within neutrophils from both 8325-4- and DU5883-inoculated lungs. Our data suggest that fibronectin-binding protein-mediated internalization into alveolar epithelial cells is not a virulence mechanism in a rat model of pneumonia. Instead, our data suggest that fibronectin-binding proteins decrease the virulence of S. aureus in pneumonia.


2000 ◽  
Vol 38 (1) ◽  
pp. 389-392
Author(s):  
Alison M. Goodfellow ◽  
Megan Hibble ◽  
Susanne R. Talay ◽  
Bernd Kreikemeyer ◽  
Bart J. Currie ◽  
...  

ABSTRACT Fibronectin binding proteins play an important role in the adherence and invasion of group A streptococci (GAS). Genotypically distinct GAS isolates were screened for the presence and expression of two streptococcal fibronectin binding protein genes, sfbI and sfbII . Of the tested strains, 64 and 36% were shown to harbor and express the sfbI and sfbII genes, respectively. All sfbII -positive strains tested were also positive for sfbI , but only 28% of the sfbII -negative strains were positive for sfbI . High levels of immunoglobulin G antibodies to both SfbI and SfbII were found in sera from 80 subjects with defined streptococcal infections.


Microbiology ◽  
2012 ◽  
Vol 158 (3) ◽  
pp. 781-790 ◽  
Author(s):  
Sarah E. Maddocks ◽  
Marta Salinas Lopez ◽  
Richard S. Rowlands ◽  
Rose A. Cooper

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